INTERACTIONS WITH OTHER DRUGS & Cannabis studies completed
Overview
Some people use marijuana for recreational purposes, to create a sense of well being or to alter the senses. It is either taken by mouth or smoked (inhaled).
Marijuana is also taken by mouth for medicinal purposes. A cannabinoid from marijuana, tetrahydrocannabinol (THC), is used in the prescription-only, FDA-approved product dronabinol (Marinol) for the treatment of weight loss or appetite loss due to AIDS and for nausea and vomiting caused by cancer chemotherapy.
Cannabinoids are at least as effective as some conventional medications for nausea, including prochlorperazine (Compazine), metoclopramide (Reglan), chlorpromazine (Compazine), and thiethylperazine (Torecan).
Cannabinoids from marijuana also appear to be similar to codeine for treatment of pain. However, extreme sleepiness and other central nervous system effects make cannabinoids undesirable as painkillers.
Other cannabinoids from marijuana have also been used by mouth to treat symptoms of multiple sclerosis (MS).
Some people inhale cannabis for medicinal purposes. Cannabis is smoked for nausea, glaucoma, appetite stimulation, mucous membrane inflammation, leprosy, fever, dandruff, hemorrhoids, obesity, asthma, urinary tract infections, cough, anorexia
associated with weight loss in AIDS patients, pain, and multiple
sclerosis. It is also inhaled to weaken the immune system after kidney
transplant to lessen the chance of transplant rejection.
Avoid confusion with hemp, a distinct variety of Cannabis sativa cultivated for its fiber and seeds, which contains less than 1% THC.
Science and Research
2012 - Study ~ Changes of Blood Endocannabinoids during Anaesthesia: a Special Case for Fatty Acid Amide Hydrolase Inhibition by Propofol?
2012 - Study ~ Effects
of amphetamine on dopamine release in the rat nucleus accumbens shell
region depend on cannabinoid CB1 receptor activation.
2011 - Study ~ Cannabidiol Attenuates Cisplatin-Induced Nephrotoxicity by Decreasing Oxidative/Nitrosative Stress, Inflammation, and Cell Death
2011 - Study ~ Cannabidiol Attenuates Cisplatin-Induced Nephrotoxicity by Decreasing Oxidative/Nitrosative Stress, Inflammation, and Cell Death
2011 - Study ~ Combined effects of acute, very-low-dose ethanol and delta(9)-tetrahydrocannabinol in healthy human volunteers
2011 - Study ~ Inhibition of monoacylglycerol lipase (MAGL) attenuates NSAID-induced gastric hemorrhages in mice.
2011 - Study ~ Cannabinoid system and cyclooxygenases inhibitors
2011 - Study ~ Possible involvement of the endocannabinoid system in memory modulation effect of general anesthetics
2011 - Study ~ Role of GLT-1 transporter activation in prevention of cannabinoid tolerance by the beta-lactam antibiotic, ceftriaxone, in mice.
2011 - Study ~ Cannabis in Palliative Medicine: Improving Care and Reducing Opioid-Related Morbidity
2011 - Study ~ Cannabinoid-opioid interaction in chronic pain.
2011 - Study ~ A combined preclinical therapy of cannabinoids and temozolomide against glioma.
2011 - Study ~ The safety of modafinil in combination with oral Δ9-tetrahydrocannabinol in humans.
2011 - Study ~ The G protein-coupled cannabinoid-1 (CB(1)) receptor of mammalian brain: Inhibition by phthalate esters in vitro.
2011 - Study ~ Combined effects of THC and caffeine on working memory in rats.
2011 - Study ~ Pretreatment with Δ9-tetrahydrocannabinol (THC) increases cocaine-stimulated activity in adolescent but not adult male rats
2011 - Study ~ Previous exposure to delta9-tetrahydrocannibinol enhances locomotor responding to but not self-administration of amphetamine.
2011 - Study ~ THC-methadone and THC-naltrexone interactions on discrimination, antinociception, and locomotion in rats.
2011 - Study ~ Pharmacokinetics of a combination of Δ9-tetrahydro-cannabinol and celecoxib in a porcine model of hemorrhagic shock.
2011 - Study ~ Low-volume binary drug therapy for the treatment of hypovolemia.
2011 - Study ~ Efavirenz interference in urine screening immunoassays for tetrahydrocannabinol.
2011 - Study ~ Clozapine
and SCH 23390 prevent the spatial working memory disruption induced by
Δ9-THC administration into the medial prefrontal cortex.
2011 - News ~ Pharmaceutical Drug-Herb Interaction List
2010 - Study ~ THC Prevents MDMA Neurotoxicity in Mice.
2010 - Study ~ Attenuation of morphine antinociceptive tolerance by a CB(1) receptor agonist and an NMDA receptor antagonist: Interactive effects.
2010 - Study ~ Influence of ethanol on cannabinoid pharmacokinetic parameters in chronic users
2010 - Study ~ Methamphetamine neurotoxicity increases brain expression and alters behavioral functions of CB₁ cannabinoid receptors.
2010 - Study ~ The safety of modafinil in combination with oral Δ9-tetrahydrocannabinol in humans
2010 - Study ~ Opioid antagonism enhances marijuana's effects in heavy marijuana smokers.
2010 - Study ~ The analgesic potential of cannabinoids.
2010 - Study - Probable Interaction Between Warfarin and Marijuana Smoking
2010 - Study - Adolescent cannabis use increases risk for cocaine-induced paranoia
2010 - News ~ Chocolate: The Good, the Bad and the Angry
2010 - News ~ Cocoa and the Search for Dietary Cannabinoids
2010 - News ~ Cannabis-enhancing plant to be marketed worldwide as new drug
2010 - News ~ Acetaminophen Synergizes Through the CB1 Receptor
2009 - Study ~ Effects of Cannabinoids on Caffeine Contractures in Slow and Fast Skeletal Muscle Fibers of the Frog
2009 - Study ~ Cannabinoid receptor-independent cytotoxic effects of cannabinoids in human colorectal carcinoma cells: synergism with 5-fluorouracil.
2009 - Study ~ Pharmacological synergism between cannabinoids and paclitaxel in gastric cancer cell lines.
2009 - Study ~ Delayed onset of seizures and toxicity associated with recreational use of Bromo-dragonFLY.
2009 - Study ~ An unusual cause of syncope
2009 - Study - Cannabis Coadministration Potentiates the Effects of "Ecstasy" on Heart Rate and Temperature in Humans
2009 - Study - Induction dose of propofol in patients using cannabis
2009 - Study - Interaction of the cannabinoid and opioid systems in the modulation of nociception
2009 - Study - Cannabis coadministration potentiates the effects of "ecstasy" on heart rate and temperature in human
2009 - Study - Cannabinoids, Opioids and MDMA: Neuropsychological Interactions Related to Addiction
2009 - News - Smoking Pot, Cigarettes Ups COPD Risk
2009 - Study ~ Enhancing the in vitro cytotoxic activity of Δ9-tetrahydrocannabinol in leukemic cells through a combinatorial approach
2008 - Study - Enhancing the in vitro cytotoxic activity of Δ9-tetrahydrocannabinol in leukemic cells through a combinatorial approach
2008 - Study ~ Repeated Cannabinoid Injections into the Rat Periaqueductal Gray Enhances Subsequent Morphine Antinociception
2008 - Study ~ Priapism, ecstasy, and marijuana: is there a connection?
2008 - Study ~ Propofol Sedation Is Reduced by {Delta}9-Tetrahydrocannabinol in Mice
2008 - Study ~ Additive
Interaction of the Cannabinoid Receptor I Agonist
Arachidonyl-2-chloroethylamide with Etomidate in a Sedation Model in
Mice
2008 - Study ~ Interaction of plant cannabinoids with the multidrug transporter ABCC1 (MRP1).
2007 - Study - Synergy between Delta(9)-tetrahydrocannabinol and morphine in the arthritic rat
2007 - Study ~ Opioid Antagonism of Cannabinoid Effects: Differences between Marijuana Smokers and Nonmarijuana Smokers
2007 - Study - Medicinal cannabis does not influence the clinical pharmacokinetics of irinotecan and docetaxel
2007 - Study ~ Antinociceptive Synergy Between the Cannabinoid Receptor Agonist WIN 55,212-2 and Bupivacaine in the Rat Formalin Test
2007 - Study - The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids
2007 - Study ~ Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats.
2007 - Study ~ Additive Effects of Timolol and Cannabinoids on Intraocular Pressure in a Rat Glaucoma Model
2007 - Study ~ Propranolol effects on acute marihuana intoxication in man
2007 - News - Cannabinoids, in combination with (NSAIDS), produce a synergistic analgesic effect
2007 - News ~ Science: The use of cannabis does not influence the efficacy of two anti-cancer drugs, a clinical study finds
2006 - Study ~ Modulation of paraoxon toxicity by the cannabinoid receptor agonist WIN 55,212-2.
2006 - Study ~ Benefits of an add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain - a randomized controlled trial.
2006 - Study - Synergistic affective analgesic interaction between delta-9-tetrahydrocannabinol and morphine
2006 - Study - Add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain
2006 - News ~ Cannabinoids Enhance Analgesic Effects Of Anti-Inflammatory Drugs, Study Says
2004 - Study - Cyclic Antidepressants
2004 - Study ~ Cannabinoids prevent the acute hyperthermia and partially protect against the 5-HT depleting effects of MDMA ("Ecstasy") in rats.
2004 - Study ~ Cannabis Abuse is Not a Risk Factor for Treatment Outcome in Methadone Maintenance Treatment: a 1-year Prospective Study in an Israeli Clinic.
2003 - Study - Cannabis reduces opioid dose in the treatment of chronic non-cancer pain
2003 - Study ~ Haloperidol, but not clozapine, produces dramatic catalepsy in delta9-THC-treated rats: possible clinical implications.
2003 - Study ~ Manipulation of the endocannabinoid system by a general anaesthetic.
2003 - Study ~ Modulation of oral morphine antinociceptive tolerance and naloxone-precipitated withdrawal signs by oral Delta 9-tetrahydrocannabinol.
2003 - Study ~ Topical cannabinoid enhances topical morphine antinociception.2002 - Study ~ Decrease in efficacy and potency of nonsteroidal anti-inflammatory drugs by chronic delta(9)-tetrahydrocannabinol administration.
2001 - Study ~ Protective effects of cannabinoid receptor ligands analogous to anandamide against cocaine toxicity.
2000 - Study ~ Involvement
of central and peripheral cannabinoid receptors in the regulation of
heart resistance to arrhythmogenic effects of epinephrine.
1999 - Study ~ Case report: adverse effects of taking tricyclic antidepressants and smoking marijuana.
1996 - Study ~ Marijuana and chocolate.
1995 - Study ~ Anandamide and delta 9-THC dilation of cerebral arterioles is blocked by indomethacin
1994 - Study ~ Marihuana smoking increases plasma cocaine levels and subjective reports of euphoria in male volunteers.
1992 - Study ~ Marihuana attenuates the rise in plasma ethanol levels in human subjects.
1991 - Study - Dronabinol and prochlorperazine in combination for treatment of cancer chemotherapy-induced nausea and vomiting.
1991 - Study ~ Flashback Following Use of Cannabis--a Review
1987 - Study ~ Respiratory effects of cocaine "freebasing" among habitual users of marijuana with or without tobacco
1983 - Study ~ Adverse Interaction Between Disulfiram and Marijuana: a Case Report.
1983 - Study ~ ANALGESIC INTERACTION BETWEEN NITROUS OXIDE AND DELTA-9-TETRAHYDEROCANNABINOL IN THE RAT
1983 - Study ~ Adverse Interaction Between Disulfiram and Marijuana: a Case Report.
1983 - Study ~ ANALGESIC INTERACTION BETWEEN NITROUS OXIDE AND DELTA-9-TETRAHYDEROCANNABINOL IN THE RAT
1981 - Study ~ Tetrahydrocannabinol potentiates reserpine-induced hypokinesia.
1980 - Study ~ Effects of drugs on behavior in pigeons tolerant to delta 9-tetrahydrocannabinol.
1978 - Study ~ Enhanced Biotransformation of Theophylline in Marihuana and Tobacco Smokers.
1977 - Study ~ Cannabidiol --antiepileptic drug comparisons and interactions in experimentally induced seizures in rats.
1977 - Study ~ The effect of delta 9-tetrahydrocannabinol, cannabidiol, and cannabinol on the anaesthesia induced by various anaesthetic agents in mice.
1977 - Study ~ Propranolol Effects on Acute Marihuana Intoxication in Man.
1976 - Study ~ The Effects of Delta-9-Tetrahydrocannabinol (Cannabis) on Cardiac Performance with and without Beta Blockade
1975 - Study - The analgesic properties of delta-9-tetrahydrocannabinol and codeine
1975 - Study ~ Combination of delta9-tetrahydrocannabinol with oxymorphone or pentobarbital: Effects on ventilatory control and cardiovascular dynamics.
1975 - Study ~ Interactions in man of delta-9-tetrahydrocannabinol. II. Cannabinol and cannabidiol.
1974 - Study - Interaction of cannabis and general anaesthetic agents in mice
1973 - Study ~ Cardiovascular and respiratory effects of cannabis extracts and 1-tetra-hydrocannabinol
( 1-THC).
1972 - Study - Effect of cannabis and certain of its constituents on pentobarbitone sleeping time and phenazone metabolism
1972 - Study ~ Proceedings: Effects of chronic and acute cannabis treatment upon thiopentone anaesthesia in rabbits.
1970 - Study ~ INTERACTIONS OF Δ1-TETRAHYDROCANNABINOL WITH BARBITURATES AND METHAMPHETAMINE
Cyclic Antidepressants
On October 15, 2004, the FDA has concluded that antidepressant medications increase the risk of suicidal thinking and behavior in children and adolescents with depression and other psychiatric disorders. If you have questions or concerns, discuss them with your health care provider
"What I remember most about being depressed was always being exhausted. I could never get to sleep at night, and when I did, I had nightmares. Then I'd wake up in the morning and have to drag myself to work. And in all that time—four or five years, I guess—I never once enjoyed anything. I was actually planning my own suicide when my doctor referred me to a psychiatrist who put me on imipramine. For the first time in years, I finally began to get some pleasure out of life."
—Sam, 43
Before the SSRIs, tricyclics were the first line of defense against encroaching depression, and had been ever since imipramine's release in 1958 under the brand name Tofranil.
Today, tricyclics are a less popular choice than the new generation of antidepressants, but they're still an important weapon in the antidepressant arsenal for a subset of people who don't respond to anything else.
Before tricyclics were developed, psychiatrists treating severely depressed clients had only two real choices: amphetamines or electroshock therapy.
Imipramine was discovered by Swiss scientists searching for a successful schizophrenia treatment; it turned out that imipramine didn't do much for schizophrenia at all. What it did do very well was perk up depressed patients.
Common Cyclic Antidepressants
Lower doses are used with elderly patients)
Drug | Usual Effective Daily Dose |
---|---|
Amitriptyline (Elavil, Endep, Emitrip, Enovil) | 150–300 mg |
Amoxapine (Asendin) | 150–400 mg |
Clomipramine (Anafranil) | 100–150 mg |
Desipramine (Norpramin, Pertofrane) | 100–300 mg |
Doxepin (Adapin, Sinequan) | 75–300 mg |
Imipramine (Janimine, Tipramine, Tofranil, Tofranil-PM) | 150–300 mg |
Maprotiline (Ludiomil) | 75–150 mg |
Nortriptyline (Pamelor, Aventyl) | 50–150 mg |
Protriptyline (Vivactil) | 15–60 mg |
Trimipramine (Surmontil) | 75–150 mg |
With the discovery of imipramine, doctors finally had a drug that relieved a person's underlying depression.
When scientists realized how effective imipramine was—about 70 percent of depressed patients responded to this drug—they flocked to the laboratories in search of similar drugs based on imipramine's three-ring ("tricyclic") antihistaminic chemical structure.
Before long, laboratories all over the country began churning out tricyclic clones, each one a little different from, but none any better than, imipramine itself.
A later-developed drug in this class, maprotiline (Ludiomil), had four rings and was therefore called "tetracyclic." Taken together, the tricyclics and tetracyclics are known as "heterocyclics" or "cyclics."
But while all these cyclics were effective, not one provided the perfect solution to depression for which scientists had been searching.
Dronabinol and prochlorperazine in combination
Title | Dronabinol and prochlorperazine in combination for treatment of cancer chemotherapy-induced nausea and vomiting. | |
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Author(s) | Lane M, Vogel CL, Ferguson J, Krasnow S, Saiers JL, Hamm J | |
Journal, Volume, Issue | Journal of Pain and Symptom Management 1991;6:352-359 | |
Major outcome(s) | prochlorperazine better than THC, both drugs combined better than both alone | |
Indication | Nausea/vomiting;Cancer;Cancer chemotherapy | Abstract |
Medication | Delta-9-THC | Dronabinol (Marinol, Roxane Laboratories, Columbus, OH) and prochlorperazine were tested alone and in combination in a randomized, double-blind, parallel group, multicenter study. Patients were randomized to receive either 1) dronabinol 10 mg every 6 hr plus placebo; 2) placebo plus prochlorperazine 10 mg every 6 hr; or 3) dronabinol and prochlorperazine, each 10 mg every 6 hr. Antiemetic treatment was begun 24 hr prior to and continued for 24 hr after the last dose of chemotherapy; all was given orally. Only 29% of patients in group 3 versus 47% in group 1 and 60% in group 2 experienced nausea after chemotherapy. In addition, the median duration per episode and severity of nausea were significantly less with combination therapy. Vomiting occurred after chemotherapy in 41%, 55%, and 35% of patients in groups 1, 2, and 3, respectively. The median duration per episode of vomiting was 1 min in group 3 versus two in group 1 and four in group 2. Side effects, primarily CNS, were more common in group 1 than in group 2; addition of prochlorperazine to dronabinol appeared to decrease the frequency of dysphoric effects seen with the latter agent. The combination was significantly more effective than was either single agent in controlling chemotherapy-induced nausea and vomiting.
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Route(s) | Oral | |
Dose(s) | ||
Duration (days) | 10 mg every 6 hr | |
Participants | 67 patients on various cancer chemotherapie | |
Design | Controlled study | |
Type of publication | ||
Address of author(s) | ||
Full text | ![]() |
Cannabinoids, in combination with (NSAIDS), produce a synergistic analgesic effect
Ankara, Turkey: Cannabinoids, when administered in combination with non-steroidal anti-inflammatory drugs (NSAIDS), produce a synergistic analgesic effect, according to preclinical data published in the February issue of the journal Anesthesia & Analgesia.
A research team at the Trakya University in Turkey investigated the analgesic interaction between cannabinoids and NSAIDS in mice. "Analysis showed additive interactions between [cannabinoids] and [NSAIDS] when they were co-administered systematically in an inflammatory visceral pain model," investigators concluded. "The combination of cannabinoids and NSAIDS may have utility in the pharmacotherapy of pain."
http://www.norml.org/index.cfm?Group_ID=6819
Add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain
Title | [Benefits of an add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain - a randomized controlled trial.] [Article in German] | |
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Author(s) | Pinsger M, Schimetta W, Volc D, Hiermann E, Riederer F, Polz W. | |
Journal, Volume, Issue | Wien Klin Wochenschr. 2006 Jun;118(11-12):327-35. | |
Major outcome(s) | Nabilone caused a significant reduction in pain and improvement of quality of life. | |
Indication | Pain | Abstract |
Medication | Nabilone | OBJECTIVE: The aim of this study was to investigate the efficacy and efficiency of an add-on treatment with the synthetic cannabinomimetic nabilone on patients with chronic pain. Of major interest were the evaluation of the influence the treatment had on pain and on quality of life as well as the subjective assessment of positive effects and side effects by the study participants. METHODS: The placebo-controlled double-blinded pilot study was divided into a 14 week cross-over period (two 4 week medication phases plus wash-out phases) followed by a 16 week medication switch period with free choice of the study drugs (drug A and drug B) by the study participants. The principal inclusion criterion was chronic therapy-resistant pain in causal relationship with a pathologic status of the skeletal and locomotor system. The study participants chose the dosage of the study drug themselves (between 1 und 4 capsules/day, in the case of nabilone this corresponds to (1/4)-1 mg/day). Pain intensity was assessed by a visual analogue scale (VAS), quality of life by the Mezzich & Cohen QOL-score. RESULTS: Altogether, 30 patients were included and analyzed. From the results, it is obvious that throughout the cross-over periods the nabilone treatment was superior (medians [25%-; 75%-percentiles]: nabilone/placebo): decrease of the average spinal pain intensity within the last 4 weeks (DeltaVAS) 0.9 [0.0; 2.0] / 0.5 [0.0; 1.7], decrease of the current spinal pain intensity (DeltaVAS) 0.6 [0.0; 2.5] / 0.0 [-1.0, 1.0] (p = .006), decrease of the average headache intensity within the last 4 weeks (DeltaVAS) 1.0 [-1.0; 2.4] / 0.2 [-0.9; 1.0], increase of the number of days without headache within the last 4 weeks 2.0 [0.0; 6.5] / 0.0 [-5.0; 4.0], increase of the quality of life (DeltaQOL-Score) 5.0 [0.8; 10.8] / 2.0 [-2.3; 8.0]. In the medication switch period, the number of study participants who favoured nabilone (nabilone intake >/=85% of all medication days) was more than 4 times higher than those who favoured placebo. The number of days with nabilone intake was clearly higher than the number with placebo intake (medians: 89% vs. 11% of all medication days, p = .003). CONCLUSION: In summary, the study results allow the conclusion that a majority of patients with chronic pain classify nabilone intake in addition to the standard treatment as a measure with a positive individual benefit-riskratio. Thus, this kind of treatment may be an interesting and attractive enrichment of analgetic therapy concepts. |
Route(s) | Oral | |
Dose(s) | 0,25-1mg | |
Duration (days) | 210 | |
Participants | 30 patients with chronic pain | |
Design | Controlled study | |
Type of publication | Medical journal | |
Address of author(s) | Confraternitat, Privatklinik Josefstadt, Wien, Austria, m.pinsger@nextra.at. | |
Full text | ![]() |
Synergistic affective analgesic interaction between delta-9-tetrahydrocannabinol and morphine
Title | Synergistic affective analgesic interaction between delta-9-tetrahydrocannabinol and morphine. | |
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Author(s) | Roberts JD, Gennings C, Shih M. | |
Journal, Volume, Issue | Eur J Pharmacol 2006;530(1-2):54-8. | |
Major outcome(s) | There was a synergistic effect between THC and morphine on the affective component of pain but not on the sensory component | |
Indication | Pain | Abstract |
Medication | Delta-9-THC | Evidence for an analgesic interaction between delta-9-tetrahydrocannabinol (Delta(9)-THC) and morphine was sought using an experimental pain model applied to normal volunteers. The study incorporated a double blinded, four treatment, four period, four sequence, crossover design. Subjects received Delta(9)-THC 5 mg orally or placebo and 90 min later morphine 0.02 mg/kg intravenously or placebo. Fifteen minutes later subjects rated the pain associated with the application of thermal stimuli to skin using two visual analog scales, one for the sensory and one for the affective aspects of pain. Among sensory responses, neither morphine nor Delta(9)-THC had a significant effect at the doses used, and there was no significant interaction between the two. Among affective responses, although neither morphine nor Delta(9)-THC had a significant effect, there was a positive analgesic interaction between the two (p=0.012), indicating that the combination had a synergistic affective analgesic effect. The surprisingly limited reported experimental experience in humans does not support a role for Delta(9)-THC as an analgesic or as an adjunct to cannabinoid analgesia, except for our finding of synergy limited to the affective component of pain. Comparison of our results with those of others suggests that extrapolation from experimental pain models to the clinic is not likely to be a straight-forward process. Future studies of Delta(9)-THC or other cannabinoids in combination with opiates should focus upon clinical rather than experimental pain. |
Route(s) | Oral | |
Dose(s) | 5 mg | |
Duration (days) | 1 | |
Participants | Healthy subjects | |
Design | Controlled study | |
Type of publication | Medical journal | |
Address of author(s) | Massey Cancer Center and the Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA | |
Full text |
The analgesic properties of delta-9-tetrahydrocannabinol and codeine
Title | The analgesic properties of delta-9-tetrahydrocannabinol and codeine. | |
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Author(s) | Noyes R Jr, Brunk SF, Avery DAH, Canter AC | |
Journal, Volume, Issue | Clinical Pharmacology and Therapeutics 1975;18(1):84-89 | |
Major outcome(s) | milde analgesic effect; with 20 mg THC strong adverse effects | |
Indication | Cancer; Pain | Abstract |
Medication | Delta-9-THC | The administration of single oral doses of delta-9- tetrahydrocannabinol (THC) to patients with cancer pain demonstrated a mild analgesic effect. At a dose of 20 mg, however, THC induced side effects that would prohibit its therapeutic use including somnolence, dizziness, ataxia, and blurred vision. Alarming adverse reactions were also observed at this dose. THC, 10 mg, was well tolerated and, despite its sedative effect, may analgesic potential. |
Route(s) | Oral | |
Dose(s) | 10-20 mg | |
Duration (days) | ||
Participants | 36 cancer patients | |
Design | Controlled study | |
Type of publication | ||
Address of author(s) | ||
Full text |
Synergy between Delta(9)-tetrahydrocannabinol and morphine in the arthritic rat
Cox ML, Haller VL, Welch SP
Eur J Pharmacol 2007 Apr 20.
We have shown in past isobolographic studies that a small amount of Delta(9)-tetrahydrocannabinol (Delta(9)-THC) can enhance morphine antinociception in mice. However, previous studies of the Delta(9)-THC/morphine interaction were performed using normal mice or rats and evaluated acute thermal antinociception.
Less is known about cannabinoid and opioid interactions involved in mechanical nociception and in chronic inflammatory pain models, such as Freund's complete adjuvant-induced arthritic model. One fixed-ratio combination was chosen for testing the interaction between Delta(9)-THC and morphine in the Freund's adjuvant-induced arthritic model.
This combination represented a 1:1 ratio of the drugs and thus consisted of equieffective doses ranging from 0.1 to 5 mg/kg Delta(9)-THC and from 0.1 to 5 mg/kg morphine. The combination ED(50) value for the fixed ratios (total dose) in relation to the ED(50) value of the drugs alone was determined.
The isobolographic analysis indicated a synergistic interaction between Delta(9)-THC and morphine in both the non-arthritic and the arthritic rats.
Since Freund's adjuvant-induced alteration in endogenous opioid tone has been previously shown, our data indicate that such changes did not preclude the use of Delta(9)-THC and morphine in combination. As with acute preclinical pain models in which the Delta(9)-THC/morphine combination results in less tolerance development, the implication of the study for chronic pain conditions is discussed.
Cannabis reduces opioid dose in the treatment of chronic non-cancer pain
Title | Cannabis reduces opioid dose in the treatment of chronic non-cancer pain. | |
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Author(s) | Lynch ME, Clark AJ. | |
Journal, Volume, Issue | J Pain Symptom Manage. 2003 Jun;25(6):496-8. | |
Major outcome(s) | Improvement in pain, spasticity, bladder spasm, and sleep. | |
Indication | Pain | Abstract |
Medication | Cannabis |
No abstract available. Ambulation was significantly compromised by the joint pain and leg spasticity. She was wheelchair dependent, and also suffered from severe insomnia and fatigue, which she attributed to the combination of pain, bladder spasm, and leg spasticity. Physical examination revealed paraparesis, weakness in the left upper extremity, tremor involving both hands, intranuclear ophthalmoplegia and l’Hermitte’s sign. Previous treatment included steroids, physiotherapy, acupuncture, interdisciplinary pain management, intramuscular injections of botulinum toxin, amitritryptiline, fluoxetine, amantadine, acetaminophen with codeine, oxycodone, nonsteroidal anti-inflammatory drugs (NSAIDS), and baclofen. The patients’ medications prior to access to smoked marijuana consisted of long-acting morphine 75 mg per day, tizanidine 24 mg per day, and sertraline 150 mg at bedtime. In spite of these treatments, the patient did not obtain adequate control of her pain, spasticity, or sleep.
Over the next six months, the morphine was reduced to 45 mg per day, tizanidine to 6 mg once per day, and setraline to between 100 mg and 150 mg at bedtime. The patient reported improvement in pain, spasticity, bladder spasm, and sleep. The patient denied any adverse side effects, other than she felt somewhat “high” if she smoked more than 4 puffs per dose. She was able to adjust the dose so that this did not occur. The patient received legal access in the autumn of 2000 and continues to use marijuana.
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Route(s) | Inhalation | |
Dose(s) | ||
Duration (days) | ||
Design | Uncontrolled case report | |
Type of publication | Medical journal | |
Address of author(s) | Queen Elizabeth II Health Sciences Center, Dalhousie University, Halifax, Nova Scotia, Canada | |
Full text |
Medicinal cannabis does not influence the clinical pharmacokinetics of irinotecan and docetaxel
Title | Medicinal cannabis does not influence the clinical pharmacokinetics of irinotecan and docetaxel. | |
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Author(s) | Engels FK, de Jong FA, Sparreboom A, Mathot RA, Loos WJ, Kitzen JJ, de Bruijn P, Verweij J, Mathijssen RH. | |
Journal, Volume, Issue | Oncologist 2007;12(3):291-300. | |
Major outcome(s) | Cannabis did not influence the pharmacokinetics of the two anti-cancer drugs | |
Indication | Cancer;Cancer chemotherapy | Abstract |
Medication | Cannabis | OBJECTIVE: To date, data regarding the potential of cannabinoids to modulate cytochrome P450 isozyme 3A (CYP3A) activity are contradictory. Recently, a standardized medicinal cannabis product was introduced in The Netherlands. We anticipated an increased use of medicinal cannabis concurrent with anticancer drugs, and undertook a drug-INTERACTION study to evaluate the effect of concomitant medicinal cannabis on the pharmacokinetics of irinotecan and docetaxel, both subject to CYP3A-mediated biotransformation. PATIENTS AND METHODS: Twenty-four cancer patients were treated with i.v. irinotecan (600 mg, n = 12) or docetaxel (180 mg, n = 12), followed 3 weeks later by the same drugs concomitant with medicinal cannabis (200 ml herbal tea, 1 g/l) for 15 consecutive days, starting 12 days before the second treatment. Blood samples were obtained up to 55 hours after dosing and analyzed for irinotecan and its metabolites (SN-38, SN-38G), respectively, or docetaxel. Pharmacokinetic analyses were performed during both treatments. Results are reported as the mean ratio (95% confidence interval [CI]) of the observed pharmacokinetic parameters with and without concomitant medicinal cannabis. RESULTS: Medicinal cannabis administration did not significantly influence exposure to and clearance of irinotecan (1.04; CI, 0.96-1.11 and 0.97; CI, 0.90-1.05, respectively) or docetaxel (1.11; CI, 0.94-1.28 and 0.95; CI, 0.82-1.08, respectively). CONCLUSION: Coadministration of medicinal cannabis, as herbal tea, in cancer patients treated with irinotecan or docetaxel does not significantly influence the plasma pharmacokinetics of these drugs. The evaluated variety of medicinal cannabis can be administered concomitantly with both anticancer agents without dose adjustments. |
Route(s) | Oral | |
Dose(s) | 200 ml cannabis tea | |
Duration (days) | 15 | |
Participants | 24 cancer patients treated with irinotecan or docetaxel | |
Design | Open study | |
Type of publication | Medical journal | |
Address of author(s) | Department of Medical Oncology, Erasmus MC University Medical Center Rotterdam - Daniel den Hoed Cancer Center, Rotterdam, The Netherlands. | |
Full text |
Interaction of cannabis and general anaesthetic agents in mice
Br J Pharmacol. 1974 April; 50(4): 593–599. | PMCID: PMC1776719 |
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Cannabis Coadministration Potentiates the Effects of "Ecstasy" on Heart Rate and Temperature in Humans
Dumont G, Kramers C, Sweep F, Touw D, van Hasselt J, de Kam M, van Gerven J, Buitelaar J, Verkes R
Clin Pharmacol Ther 2009 May 13.
This study assessed the acute physiologic effects over time of (co)administration of Delta9-tetrahydrocannabinol (Delta9-THC) (the main psychoactive compound of cannabis) and 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") in 16 healthy volunteers.
Pharmacokinetics and cardiovascular, temperature, and catecholamine responses were assessed over time.
Both single-drug conditions robustly increased heart rate, and coadministration showed additive effects.
MDMA increased epinephrine and norepinephrine concentrations, whereas THC did not affect the catecholamine response.
Coadministration of MDMA and THC attenuated the increase of norepinephrine concentrations relative to administration of MDMA alone.
These results show that THC mediates heart rate increase independent of sympathetic (catecholaminergic) activity, probably through direct cannabinoid receptor type 1 (CB(1)) agonism in cardiac tissue. Furthermore, THC coadministration did not prevent MDMA-induced temperature increase, but it delayed the onset and prolonged the duration of temperature elevation.
These effects may be of particular relevance for the cardiovascular safety of ecstasy users who participate in energetic dancing in nightclubs with high ambient temperature.Clinical Pharmacology & Therapeutics (2009); advance online publication 13 May 2009. doi:10.1038/clpt.2009.62.
Enhancing the in vitro cytotoxic activity of Δ9-tetrahydrocannabinol in leukemic cells through a combinatorial approach
Author(s)
LIU Wai M. ; SCOTT Katherine A. ; SHAMASH Jonathan ; JOEL Simon ; POWLES Thomas B. ;Abstract
Δ9-Tetrahydrocannabinol (THC) is the active metabolite of cannabis, which has demonstrable cytotoxic activity in vitro.
In support of our previously published data, we have investigated the interactions between THC and anti-leukemia therapies and studied the role of the signalling pathways in mediating these effects.
Results showed clear synergistic interactions between THC and the cytotoxic agents in leukemic cells.
Additionally, exposure of cells to sub lethal levels of THC (1 μM) sensitised cells to these cytotoxic agents, by reducing IC50 values by ∼ 50%. Sensitisation appeared to be dependent upon the ability of THC to down regulate phosphorylated ERK, as cells dominantly expressive of MEK were not sensitised to the cytotoxic drugs by equi-molar amounts of THC.
Overall, these results demonstrate for the first time that a combination approach with THC and established cytotoxic agents may enhance cell death in vitro. Additionally the MAPK/ERK pathway appears responsible in part for these effects.
Journal Title
Leukemia & lymphoma ISSN 1042-8194Source / Source
2008, vol. 49, no9, pp. 1800-1809 [10 page(s) (article)]
The multidrug transporter ABCG2 (BCRP) is inhibited by plant-derived cannabinoids
Br J Pharmacol. 2007 Nov;152(5):815-24. Epub 2007 Oct 1. SourceThe Discipline of Pharmacology, The University of Sydney, Sydney, New South Wales, Australia. AbstractBACKGROUND AND PURPOSE:Cannabinoids are used therapeutically for the palliation of the adverse side effects associated with cancer chemotherapy. However, cannabinoids also inhibit both the activity and expression of the multidrug transporter, P-glycoprotein in vitro. Here we address the interaction of cannabinol (CBN), cannabidiol (CBD) and delta 9-tetrahydrocannabinol (THC) with the related multidrug transporter, ABCG2. EXPERIMENTAL APPROACH:Cannabinoid inhibition of Abcg2/ABCG2 was assessed using flow cytometric analysis of substrate accumulation and ATPase activity assays. The cytotoxicity and chemosensitization by cannabinoids was determined with cell viability assays. Expression of cannabinoid and vanilloid receptors was assessed using reverse transcriptase polymerase chain reaction, and cannabinoid modulation of ABCG2 expression was examined using immunoblotting. KEY RESULTS:CBN, CBD and THC increased the intracellular accumulation of the Abcg2/ABCG2 substrate, mitoxantrone, in an over-expressing cell line. The THC metabolite, (-)-11-nor-9-carboxy-delta 9-THC was much less potent. The plant cannabinoids inhibited both basal and substrate stimulated ATPase activity of human ABCG2. Cannabinoid cytotoxicity occurred in the absence of known cannabinoid cell surface receptors, and only at concentrations higher than those required for Abcg2/ABCG2 inhibition. Sub-toxic concentrations of the cannabinoids resensitized the overexpressing cell line to the cytotoxic effect of Abcg2/ABCG2 substrates, mitoxantrone and topotecan. This occurred in the absence of any effect on ABCG2 expression. CONCLUSIONS AND IMPLICATIONS:Cannabinoids are novel Abcg2/ABCG2 inhibitors, reversing the Abcg2-mediated multidrug-resistant phenotype in vitro. This finding may have implications for the co-administration of cannabinoids with pharmaceuticals that are ABCG2 substrates.
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Efficacy of dronabinol alone and in combination
Title | Efficacy of dronabinol alone and in combination with ondansetron versus ondansetron alone for delayed chemotherapy-induced nausea and vomiting. | |
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Author(s) | Meiri E, Jhangiani H, Vredenburgh JJ, Barbato LM, Carter FJ, Yang HM, Baranowski V. | |
Journal, Volume, Issue | Curr Med Res Opin 2007;23(3):533-43. | |
Major outcome(s) | Dronabinol was as effective as ondansetron in reducing nausea and vomiting. Combination therapy was not more effective. | |
Indication | Nausea/vomiting;Cancer;Cancer chemotherapy | Abstract |
Medication | Delta-9-THC | OBJECTIVE: To compare the efficacy and tolerability of dronabinol, ondansetron, or the combination for delayed chemotherapy-induced nausea and vomiting (CINV) in a 5-day, double-blind, placebo-controlled study. RESEARCH DESIGN AND METHODS: Patients receiving moderately to highly emetogenic chemotherapy received dexamethasone (20 mg PO), ondansetron (16 mg IV) and either placebo or dronabinol (2.5 mg) prechemotherapy on day 1. Patients randomized to active treatment (dronabinol and/or ondansetron) also received dronabinol (2.5 mg) after chemotherapy on day 1. On day 2, fixed doses of placebo, dronabinol (10 mg), ondansetron (16 mg), or combination therapy were administered. On days 3-5, patients received placebo, flexible doses of dronabinol (10-20 mg), ondansetron (8-16 mg), or dronabinol and ondansetron (10-20 mg dronabinol, 8-16 mg ondansetron). MAIN OUTCOME MEASURES: Total response (TR = nausea intensity <5 mm on visual analog scale, no vomiting/retching, no rescue antiemetic), nausea (occurrence and intensity) and vomiting/retching episodes. RESULTS: Sixty-four patients were randomized; 61 analyzed for efficacy. TR was similar with dronabinol (54%), ondansetron (58%), and combination therapy (47%) versus placebo (20%). Nausea absence was significantly greater in active treatment groups (dronabinol, 71%; ondansetron, 64%; combination therapy, 53%) versus placebo (15%; p < 0.05 vs. placebo for all). Nausea intensity and vomiting/retching were lowest in patients treated with dronabinol. Active treatments were well tolerated. The low number of patients due to slow enrollment limits the interpretation of these data. CONCLUSIONS: Dronabinol or ondansetron was similarly effective for the treatment of CINV. Combination therapy with dronabinol and ondansetron was not more effective than either agent alone. Active treatments were well tolerated. |
Route(s) | Oral | |
Dose(s) | 10-20 mg | |
Duration (days) | 5 | |
Participants | 64 patients undergoing chemotherapy | |
Design | Controlled study | |
Type of publication | Medical journal | |
Address of author(s) | Bethesda Memorial Hospital, Comprehensive Cancer Care Center, Boynton Beach, FL 33435-7995, USA. mdeyal@hotmail.com | |
Full text |
Induction dose of propofol in patients using cannabis
Flisberg P, Paech MJ, Shah T, Ledowski T, Kurowski I, Parsons R
Support, Non-U.S. Gov't]
Eur J Anaesthesiol 2009 Mar; 26(3):192-5.
BACKGROUND AND OBJECTIVE: An estimated 150 million people worldwide use cannabis.
The effect of cannabis on anaesthetic requirements in humans does not appear to have been studied.
METHODS: In this prospective, randomized, single-blinded study, 30 male patients using cannabis more than once per week (group C) and 30 nonusers (group NC), aged 18-50 years, were induced with propofol 1.5, 2, 2.5, 3 or 3.5 mg kg.
Additional doses were given when required. The primary outcome was the 50% effective dose of propofol and successful induction was determined by loss of consciousness with a bispectral index value of less than 60 and satisfactory insertion of a laryngeal mask. Propofol requirements to achieve these outcomes were recorded.
RESULTS: The dose required to achieve the target bispectral index value was not significantly higher in group C, but group C required a significantly higher propofol dose to achieve laryngeal mask insertion (314.0 +/- 109.3 vs. 263.2 +/- 69.5 mg, P < 0.04). The estimated effective propofol induction dose in 50-95% of patients did not significantly differ between groups.
CONCLUSION: We conclude that cannabis use increases the propofol dose required for satisfactory clinical induction when inserting a laryngeal mask.
More from this journalEuropean journal of anaesthesiolog
Smoking Pot, Cigarettes Ups COPD Risk
WebMD Health News

April 13, 2009 -- People who smoke both cigarettes and marijuana have a greater risk for developing the progressive lung disease COPD than cigarette smokers who don't smoke pot, a new study shows.
Smokers in the study who reported using both tobacco and marijuana were three times as likely as nonsmokers to have clinically confirmed COPD (chronic obstructive pulmonary disease); people who smoked only cigarettes had a slightly lower risk.
The study is among the first to suggest a synergistic relationship between marijuana and tobacco use among older people who are most at risk for COPD.
"This effect suggests that smoking marijuana may act as a primer, or sensitizer, in the airways to amplify the adverse effects of tobacco on respiratory health," says study researcher Wan C. Tan, MD, of the University of British Columbia and St. Paul's Hospital in Vancouver, Canada.
COPD Risk
About 12 million Americans are currently living with a diagnosis of COPD; an equal number are believed to have the disease and not know it, according to the National Heart, Lung and Blood Institute.
In the U.S, the term COPD includes both emphysema and chronic bronchitis. With COPD, breathing becomes more difficult over time.
Largely caused by cigarette smoking, COPD is the fourth leading cause of death in the U.S.
While the link between tobacco and COPD is well established, far less is known about the impact of marijuana use on the lungs.
Some studies have found that even short-term heavy marijuana smoking can worsen lung function, while others have not shown this association.
Even less is known about the combined effects of smoking cigarettes and pot, Tan tells WebMD.
The study by Tan and colleagues included 878 residents of Vancouver, Canada participating in a larger investigation examining COPD prevalence.
Participants were considered tobacco smokers if they had smoked at least 365 cigarettes in their lifetime, and were considered marijuana smokers if they reported having ever smoked pot. The researchers defined "substantial" marijuana use as having smoked at least 50 marijuana cigarettes.
The average cigarette smoker in the study had smoked for 16 years, while the self-described pot smokers had smoked an average of 84 marijuana cigarettes.
When COPD was clinically confirmed though a diagnostic method known as spirometric testing:
- The incidence of COPD among participants who smoked cigarettes alone was 2.7 times higher than among nonsmokers.
- The incidence of COPD was 2.9 times higher among participants with a history of smoking both cigarettes and pot, even after controlling for other risk factors for the pulmonary disease.
- COPD risk among people who smoked marijuana, but not tobacco, was slightly higher than among nonsmokers, but the increase was not statistically significant.
The study appears in the April 14 issue of the Canadian Medical Association Journal.
Probable Interaction Between Warfarin and Marijuana Smoking
Yamreudeewong W, Wong HK, Brausch LM, Pulley KR
Probable Interaction Between Warfarin and Marijuana Smoking (July/August). [JOURNAL ARTICLE]
Ann Pharmacother 2009 Jun 16.
OBJECTIVE: To report a probable interaction between warfarin and marijuana smoking, resulting in increased international normalized ratio (INR) values and bleeding complications.
CASE SUMMARY: A 56-year-old white male had been receiving chronic warfarin therapy for 11 years after mechanical heart valve replacement. He was admitted to the hospital with a diagnosis of upper gastrointestinal bleeding. Upon admission, his INR value was supratherapeutic at 10.41, and his hemoglobin level was 6.6 g/dL.
He received 4 units of fresh frozen plasma and one 10-mg dose of oral vitamin K; his INR was 1.8 the next day. He was discharged 7 days after admission. Fifteen days after hospital discharge, he was readmitted with a constant nosebleed and increased bruising.
His INR value was 11.55. After treatment, he was discharged with an INR value of 1.14. The patient smoked marijuana more frequently throughout the period of these 2 hospitalizations due to his depression.
He was counseled by the pharmacist on the potential interaction of warfarin and marijuana. The patient decided to stop smoking marijuana after the third counseling session. During the 9 months that he did not smoke marijuana, his INR values ranged from 1.08 to 4.40 with no significant bleeding complications.
DISCUSSION: Marijuana may increase warfarin anticoagulant effect by inhibiting its metabolism, and to a lesser extent, displacing warfarin from protein-binding sites. Other causes (eg, nonadherence) of the patient's increased INR were ruled out. Using the Horn Drug Interaction Probability Scale, our patient's warfarin- marijuana interaction appeared to be probable.
CONCLUSIONS: To our knowledge, there have been no other reported cases of warfarin-marijuana interaction.
While more clinical reports would be useful to confirm this interaction, clinicians should be aware of its probability so as to manage patients appropriately.
The Annals of pharmacotherapy [Ann Pharmacother]
Cannabinoids, Opioids and MDMA: Neuropsychological Interactions Related to Addiction
Source
Laboratori de Neurofarmacologia, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra and Institut Municipal d'Investigació Mèdica (IMIM), Barcelona, Spain. patricia.robledo@upf.edu
Abstract
3,4-methylenedioxymethamphetamine (MDMA, "ecstasy") is an amphetamine derivative with psychostimulant properties.
This substance is widely used around the world by young adults in recreational settings. One of the most remarkable characteristic of ecstasy users is the concurrent consumption of several other drugs of abuse including psychostimulants, alcohol, tobacco, LSD, cannabis and opioids.
This poly-drug pattern of use is now prompting research towards understanding how the combination of MDMA with cannabis and opioids could affect neuropsychobiological processes related to addiction.
As with other drugs of abuse, behavioural evidence has been presented supporting the role of the endocannabinoid system as a modulator of the rewarding/reinforcing properties of MDMA.
On the other hand, the neurochemical substrate for the complex interactions between the endocannabinoid system and MDMA is poorly understood. MDMA also modulates the activity of the dynorphinergic and enkephalinergic systems in several brain structures related to addiction, as it has been shown for other psychostimulants.
The work regarding the contribution of micro- and delta-opioid receptors in the rewarding effects of MDMA shows differential results in pharmacological studies in rats, with respect to studies using knock-out mice. The present review describes the behavioural and neurochemical interactions between MDMA, cannabinoids and opioids with respect to addiction processes.
Cannabis coadministration potentiates the effects of "ecstasy" on heart rate and temperature in humans
Clin Pharmacol Ther. 2009 Aug;86(2):160-6. Epub 2009 May 13
Source
Department of Psychiatry, Donders Institute for Brain, Cognition, and Behavior, Radboud University Nijmegen Medical Centre, Nijmegen,
The Netherlands. g.j.h.dumont@psy.umcn.nl
Abstract
This study assessed the acute physiologic effects over time of (co)administration of Delta9-tetrahydrocannabinol (Delta9-THC) (the main psychoactive compound of cannabis) and 3,4-methylenedioxymethamphetamine (MDMA or "ecstasy") in 16 healthy volunteers.
Pharmacokinetics and cardiovascular, temperature, and catecholamine responses were assessed over time. Both single-drug conditions robustly increased heart rate, and coadministration showed additive effects. MDMA increased epinephrine and norepinephrine concentrations, whereas THC did not affect the catecholamine response. Coadministration of MDMA and THC attenuated the increase of norepinephrine concentrations relative to administration of MDMA alone.
These results show that THC mediates heart rate increase independent of sympathetic (catecholaminergic) activity, probably through direct cannabinoid receptor type 1 (CB(1)) agonism in cardiac tissue.
Furthermore, THC coadministration did not prevent MDMA-induced temperature increase, but it delayed the onset and prolonged the duration of temperature elevation.
These effects may be of particular relevance for the cardiovascular safety of ecstasy users who participate in energetic dancing in nightclubs with high ambient temperature.
Interaction of the cannabinoid and opioid systems in the modulation of nociception
Int Rev Psychiatry. 2009 Apr;21(2):143-51
Source
Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia 23298-0524, USA. swelch@vcu.edu
Abstract
Read More: http://informahealthcare.com/doi/abs/10.1080/09540260902782794
Effect of cannabis and certain of its constituents on pentobarbitone sleeping time and phenazone metabolism
Br J Pharmacol. 1972 February; 44(2): 250–261. | PMCID: PMC1666020 |

Adolescent cannabis use increases risk for cocaine-induced paranoia
Author(s) | Kalayasiri R, Gelernter J, Farrer L, Weiss R, Brady K, Gueorguieva R, Kranzler HR, Malison RT |
Institution | Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. |
Source | Drug Alcohol Depend 2010 Mar 1; 107(2-3):196-201. |
Abstract | Cannabis can produce and/or exacerbate psychotic symptoms in vulnerable individuals. Early exposure to cannabis, particularly in combination with genetic factors, increases the risk of a subsequent, primary, psychotic disorder. Because paranoia is a common feature of stimulant abuse and cocaine-dependent individuals frequently endorse a history of cannabis abuse, we examined whether early cannabis exposure, in conjunction with polymorphic variation in the catechol-O-methyl transferase gene (COMT Val158Met), influences the risk for cocaine-induced paranoia (CIP).
Logistic regression and generalized estimating equations' analyses were used to examine the role of adolescent-onset cannabis use (< or =15 years of age) on CIP risk, both controlling for previously implicated CIP risk factors and familial relationships, and considering potential interactions with COMT Val158Met genotype.
There were no effects of COMT genotype or genotype by early cannabis onset interactions. A modest (OR=1.4) and nearly significant (p=0.053) effect of CIP status in probands on CIP status in siblings was also noted.
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Pub Type(s) | Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't |
PubMed ID | 19944543
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Induction dose of propofol in patients using cannabis
Flisberg P, Paech MJ, Shah T, Ledowski T, Kurowski I, Parsons R
Research Support, Non-U.S. Gov't]
Eur J Anaesthesiol 2009 Mar; 26(3):192-5.
BACKGROUND AND OBJECTIVE:
An estimated 150 million people worldwide use cannabis. The effect of cannabis on anaesthetic requirements in humans does not appear to have been studied.
METHODS:
In this prospective, randomized, single-blinded study, 30 male patients using cannabis more than once per week (group C) and 30 nonusers (group NC), aged 18-50 years, were induced with propofol 1.5, 2, 2.5, 3 or 3.5 mg kg.
Additional doses were given when required. The primary outcome was the 50% effective dose of propofol and successful induction was determined by loss of consciousness with a bispectral index value of less than 60 and satisfactory insertion of a laryngeal mask.
Propofol requirements to achieve these outcomes were recorded.
RESULTS:
The dose required to achieve the target bispectral index value was not significantly higher in group C, but group C required a significantly higher propofol dose to achieve laryngeal mask insertion (314.0 +/- 109.3 vs. 263.2 +/- 69.5 mg, P < 0.04).
The estimated effective propofol induction dose in 50-95% of patients did not significantly differ between groups.
CONCLUSION:
We conclude that cannabis use increases the propofol dose required for satisfactory clinical induction when inserting a laryngeal mask.
European journal of anaesthesiology