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Absorption 2.1.7. Cannabidiol

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24.06.2018

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  • Absorption 2.1.7. Cannabidiol
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  • Much of the early cannabinoid data are based on radiolabeled cannabinoids yielding highly .. Cannabidiol Absorption. Cannabidiol (CBD) is a natural, . Absorption Smoking Oral Oromucosal Rectal Transcutaneous Intravenous Cannabidiol Absorption Distribution. A cannabinoid is one of a class of diverse chemical compounds that acts on cannabinoid . CBD can interfere with the uptake of adenosine, which plays an important role in biochemical processes, such as energy transfer. It may play a role in.

    Absorption 2.1.7. Cannabidiol

    Mean THC concentrations in urine specimens from seven subjects, collected after each had smoked a single marijuana cigarette 3. Using a modified analytical method with E. We found that OH-THC may be excreted in the urine of chronic cannabis users for a much longer period of time, beyond the period of pharmacodynamic effects and performance impairment.

    Compared to other drugs of abuse, analysis of cannabinoids presents some difficult challenges. Complex specimen matrices, i. Care must be taken to avoid low recoveries of cannabinoids due to their high affinity to glass and plastic containers, and to alternate matrix-collection devices [ - ].

    Whole-blood cannabinoid concentrations are approximately one-half the concentrations found in plasma specimens, due to the low partition coefficient of drug into erythrocytes [ 96 ][ ][ ].

    THC Detection times in plasma of 3. In the latter study, the terminal half-life of THC in plasma was determined to be ca. This inactive metabolite was detected in the plasma of all subjects by 8 min after the start of smoking. The half-life of the rapid-distribution phase of THC was estimated to be 55 min over this short sampling interval. The relative percentages of free and conjugated cannabinoids in plasma after different routes of drug administration are unclear.

    Even the efficacy of alkaline- and enzymatic-hydrolysis procedures to release analytes from their conjugates is not fully understood [ 24 ][ 77 ][ 93 ][ ][ ][ ][ - ]. In general, the concentrations of conjugate are believed to be lower in plasma, following intravenous or smoked administration, but may be of much greater magnitude after oral intake. There is no indication that the glucuronide conjugates are active, although supporting data are lacking.

    Peak concentrations and time-to-peak concentrations varied sometimes considerably between subjects. Most THC plasma data have been collected following acute exposure; less is known of plasma THC concentrations in frequent users. No difference in terminal half-life in frequent or infrequent users was observed. There continues to be controversy in the interpretation of cannabinoid results from blood analysis, some general concepts having wide support.

    It is well-established that plasma THC concentrations begin to decline prior to the time of peak effects, although it has been shown that THC effects appear rapidly after initiation of smoking [ 15 ].

    Individual drug concentrations and ratios of cannabinoid metabolite to parent drug concentration have been suggested as potentially useful indicators of recent drug use [ 24 ][ ]. This is in agreement with results reported by Mason and McBay [ 96 ], and those by Huestis et al. Measurement of cannabinoid analytes with short time courses of detection e. This correlates well with the suggested concentration of plasma THC, due to the fact that THC in hemolyzed blood is approximately one-half the concentration of plasma THC [ ].

    Accurate prediction of the time of cannabis exposure would provide valuable information in establishing the role of cannabis as a contributing factor to events under investigation. Two mathematical models for the prediction of time of cannabis use from the analysis of a single plasma specimen for cannabinoids were developed [ ]. More recently, the validation of these predictive models was extended to include estimation of time of use after multiple doses of THC and at low THC concentrations 0.

    Some 38 cannabis users each smoked a cigarette containing 2. The predicted times of cannabis smoking, based on each model, were then compared to the actual smoking times. The most accurate approach applied a combination of models I and II. All time estimates were correct for 77 plasma specimens, with THC concentrations of 0. The models provide an objective, validated method for assessing the contribution of cannabis to accidents or clinical symptoms. These models also appeared to be valuable when applied to the small amount of data from published studies of oral ingestion available at the time.

    Additional studies were performed to determine if the predictive models could estimate last usage after multiple oral doses, a route of administration more popular with the advent of cannabis therapies. Each of twelve subjects in one group received a single oral dose of dronabinol 10 mg of synthetic THC. In another protocol, six subjects received four different oral daily doses, divided into thirds, and administered with meals for five consecutive days.

    There was a d washout period between each dosing regimen. The daily doses were 0. The actual times between ingestion of THC and blood collection spanned 0. These results provide further evidence of the usefulness of the predictive models in estimating the time of last oral THC ingestion following single or multiple doses. Detection of cannabinoids in urine is indicative of prior cannabis exposure, but the long excretion half-life of THC-COOH in the body, especially in chronic cannabis users, makes it difficult to predict the timing of past drug use.

    This individual had used cannabis heavily for more than ten years. However, a naive user's urine may be found negative by immunoassay after only a few hours following smoking of a single cannabis cigarette [ ].

    Assay cutoff concentrations and the sensitivity and specificity of the immunoassay affect drug-detection times. A positive urine test for cannabinoids indicates only that drug exposure has occurred. The result does not provide information on the route of administration, the amount of drug exposure, when drug exposure occurred, or the degree of impairment. THC-COOH concentration in the first specimen after smoking is indicative of how rapidly the metabolite can appear in urine.

    Thus, THC-COOH concentrations in the first urine specimen are dependent upon the relative potency of the cigarette, the elapsed time following drug administration, smoking efficiency, and individual differences in drug metabolism and excretion. The mean times of peak urine concentration were 7. Although peak concentrations appeared to be dose-related, there was a twelvefold variation between individuals. Drug detection time, or the duration of time after drug administration in which the urine of an individual tests positive for cannabinoids, is an important factor in the interpretation of urine drug results.

    Detection time is dependent on pharmacological factors e. Mean detection times in urine following smoking vary considerably between subjects, even in controlled smoking studies, where cannabis dosing is standardized and smoking is computer-paced. During the terminal elimination phase, consecutive urine specimens may fluctuate between positive and negative, as THC-COOH concentrations approach the cutoff concentration.

    It may be important in drug-treatment settings or in clinical trials to differentiate between new drug use and residual excretion of previously used cannabinoids. After smoking a cigarette containing 1. This had the effect of producing much longer detection times for the last positive specimen. Normalization of cannabinoid concentration to urine creatinine concentration aids in the differentiation of new from prior cannabis use, and reduces the variability of drug measurement due to urine dilution.

    Due to the long half-life of drug in the body, especially in chronic cannabis users, toxicologists and practitioners are frequently asked to determine if a positive urine test represents a new episode of drug use or represents continued excretion of residual drug. Random urine specimens contain varying amounts of creatinine, depending on the degree of concentration of the urine.

    Hawks first suggested creatinine normalization of urine test results to account for variations in urine volume in the bladder [ ]. Whereas urine volume is highly variable due to changes in liquid, salt, and protein intake, exercise, and age, creatinine excretion is much more stable. If the increase is greater than or equal to the threshold selected, then new use is predicted.

    This approach has received wide attention for potential use in treatment and employee-assistance programs, but there was limited evaluation of the usefulness of this ratio under controlled dosing conditions. Huestis and Cone conducted a controlled clinical study of the excretion profile of creatinine and cannabinoid metabolites in a group of six cannabis users, who smoked two different doses of cannabis, separated by weekly intervals [ ].

    As seen in Fig. Being able to differentiate new cannabis use from residual THC-COOH excretion in urine would be highly useful for drug treatment, criminal justice, and employee assistance drug testing programs.

    The ratio times of the creatinine normalized later specimen divided by the creatinine normalized earlier specimen were evaluated for determining the best ratio to predict new cannabis use. The most accurate ratio To further substantiate the validity of the derived ROC curve, urine-cannabinoid-metabolite and creatinine data from another controlled clinical trial that specifically addressed water dilution as a means of specimen adulteration were evaluated [ ].

    Sensitivity, specificity, accuracy, and false positives and negatives were These data indicate that selection of a threshold to evaluate sequential creatinine-normalized urine drug concentrations can improve the ability to distinguish residual excretion from new drug usage. Cannabinoids were detectable for 93 d after cessation of smoking, with a decreasing ratio of cannabinoids to creatinine over time. An excretion half-life of 32 d was determined. When cannabinoid concentrations had not been normalized to creatinine concentrations, a number of false positive indications of new drug use would have occurred.

    Within this range, cannabinoid excretion is more variable, most likely based on the slow and variable release of stored THC from fat tissue.

    The factors governing release of THC stores are not known. Additional research is being performed to attempt to determine appropriate ratio cutoffs for reliably predicting new drug use in heavy, chronic users. Oral fluid also is a suitable specimen for monitoring cannabinoid exposure, and is being evaluated for driving under the influence of drugs, drug treatment, workplace drug testing, and for clinical trials [ - ].

    The oral mucosa is exposed to high concentrations of THC during smoking, and serves as the source of THC found in oral fluid. Only minor amounts of drug and metabolites diffuse from the plasma into oral fluid [ ]. Following intravenous administration of radiolabeled THC, no radioactivity could be demonstrated in oral fluid [ ]. Oral fluid collected with the Salivette collection device was positive for THC in 14 of these 22 participants.

    Several hours after smoking, the oral mucosa serves as a depot for release of THC into the oral fluid. In addition, as detection limits continue to decrease with the development of new analytical instrumentation, it may be possible to measure low concentrations of THC-COOH in oral fluid.

    Detection times of cannabinoids in oral fluid are shorter than in urine, and more indicative of recent cannabis use [ ][ ]. Oral-fluid THC concentrations temporally correlate with plasma cannabinoid concentrations and behavioral and physiological effects, but wide intra- and inter-individual variation precludes the use of oral-fluid concentrations as indicators of drug impairment [ ][ ]. THC may be detected at low concentrations by radioimmunoassay for up to 24 h after use. After these times, occasional positive oral-fluid results were interspersed with negative tests for up to 34 h.

    They suggested that the ease and non-invasiveness of sample collection made oral fluid a useful alternative matrix for detection of recent cannabis use. Oral-fluid samples also are being evaluated in the European Union's Roadside Testing Assessment ROSITA project to reduce the number of individuals driving under the influence of drugs and to improve road safety.

    The ease and non-invasiveness of oral-fluid collection, reduced hazards in specimen handling and testing, and shorter detection window are attractive attributes to the use of this specimen for identifying the presence of potentially performance-impairing drugs. They determined that, with a limit of quantification of 0. As mentioned above, oral-fluid specimens tested positive for up to 34 h. Positive oral-fluid cannabinoid tests were not obtained more than 2 h after last use, suggesting that much lower cutoff concentrations were needed to improve sensitivity.

    Detection of cannabinoids in oral fluid is a rapidly developing field; however, there are many scientific issues to resolve.

    One of the most important is the degree of absorption of the drug to oral-fluid collection devices. Recently, there has been renewed interest in oral-fluid drug testing for programs associated with drug treatment, workplace, and driving under the influence of drugs. Small and inconsistent specimen volume collection, poor extraction of cannabinoids from the collection device, low analyte concentrations for cannabinoids, and the potential for external contamination from environmental smoke are limitations to this monitoring method.

    Recently, independent evaluations of the extraction of cannabinoids from the collection device [ - ] and measurement of oral-fluid THC-COOH in concentrations as low as picograms per milliliter appear to adequately address these potential problems. The extraction efficiency of the buffer was reported to be between Specimens collected almost immediately after smoking cannabis, i. Some 95 specimens This limitation has curtailed the use of oral-fluid testing to monitor cannabis use.

    First, oral-fluid collection devices were contaminated when opened within the smoke-filled car. When the specimens were collected outside of the car, immediately following smoking, specimens from passive smokers were negative. Environmental cannabis smoke can contaminate collection devices, unless specimens are collected outside the area of smoke contamination.

    To date, there are no published data on the excretion of cannabinoids in sweat following controlled THC administration, although our laboratory at NIH is conducting such research.

    Sweat testing is being applied to monitor cannabis use in drug treatment, criminal justice, workplace drug testing, and clinical studies [ ][ ]. In , Balabanova and Schneider used radioimmunoassay to detect cannabinoids in apocrine sweat [ ].

    Generally, the patch is worn for 7 d, and then exchanged for a new patch once each week during visits to the treatment clinic or parole officer. Theoretically, this permits constant monitoring of drug use throughout the week, extending the window of drug detection and improving test sensitivity.

    As with oral-fluid testing, this is a developing analytical technique, with much to be learned about the pharmacokinetics of cannabinoid excretion in sweat, potential re-absorption of THC by the skin, possible degradation of THC on the patch, and adsorption of THC onto the patch-collection device. Understanding the pharmacokinetics of THC excretion also is important for the interpretation of hair cannabinoid tests, as sweat has been shown to contribute to the amount of drug found in hair see below.

    Several investigators have evaluated the sensitivity and specificity of different screening assays for detecting cannabinoids in sweat [ ][ ]. The same investigators also evaluated forehead swipes with cosmetic pads for monitoring cannabinoids in sweat from individuals suspected of driving under the influence of drugs [ ].

    There are multiple mechanisms for the incorporation of cannabinoids in hair. THC and its metabolites may be incorporated into the hair bulb that is surrounded by capillaries. Drug may also diffuse into hair from sebum secreted onto the hair shaft, and from sweat excreted onto the skin surface. Drug may also be incorporated into hair from the environment. Cannabis is primarily smoked, providing an opportunity for environmental contamination of hair with THC in cannabis smoke.

    Basic drugs such as cocaine and methamphetamine concentrate in hair due to ionic bonding to melanin, the pigment in hair that determines hair color. The more neutral and lipophilic THC is not strongly bound to melanin, resulting in much lower concentrations of THC in hair as compared to other drugs of abuse. An advantage of measuring THC-COOH in hair is that this compound is not present in cannabis smoke, avoiding the issue of passive exposure from the environment.

    Analysis of cannabinoids in hair is challenging due to the high analytical sensitivity required. It is difficult to conduct controlled cannabinoid-administration studies on the disposition of cannabinoids in hair because of the inability to differentiate administered drug from previously self-administered cannabis.

    If isotopically labeled drug were administered, it would be possible to identify newly administered drug in hair. There are advantages to monitoring drug use with hair testing, including a wide window of drug detection, a less invasive specimen-collection procedure, and the ability to collect a second specimen at a later time.

    However, one of the weakest aspects of testing for cannabinoids in hair is the low sensitivity of drug detection in this alternate matrix. In the only controlled cannabinoid dosing study published to date, Huestis et al. Hair specimens were collected from each subject at the time of admittance to a closed research unit, following smoking of two cigarettes containing 2. Pre- and post-dose detection rates did not differ statistically. Therefore, all 53 specimens were considered as one group.

    For specimens with detectable cannabinoids, concentrations ranged from 3. All participants showed positive urine cannabinoid tests at the time of hair collection. An understanding of human cannabinoid pharmacokinetics is important for the development and monitoring of new therapeutic medications and to the interpretation of cannabinoid test results in a wide variety of biological matrices, including blood, plasma, urine, oral fluid, sweat, and hair.

    With the advent of new preparations containing THC, CBD, and other cannabinoids, and new administration routes, additional research is needed. Also, controlled drug-administration studies that provide the scientific database for interpreting cannabinoid concentrations in biological fluids and tissues are increasingly difficult to conduct due to safety and ethical concerns, and because of the high costs of performing human research.

    However, these data are essential for appropriate application of pharmacotherapies, and for drug testing in treatment, workplace, and forensic cases. National Center for Biotechnology Information , U. Author manuscript; available in PMC Jun 2.

    Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Chem Biodivers. See other articles in PMC that cite the published article. Introduction A multitude of roles for the endogenous cannabinoid system has been proposed by recent research efforts.

    Open in a separate window. Pharmacokinetics of Cannabinoids 2. Smoking Route of drug administration and drug formulation determine the rate of drug absorption.

    Oral There are fewer studies on the disposition of THC and its metabolites after oral administration of cannabis as compared to the smoked route.

    Oromucosal Due to the chemical complexity of cannabis plant material compared to synthetic THC, extracts of cannabis that capture the full range of cannabinoids are being explored as therapeutic medications. Rectal Several different suppository formulations were evaluated in monkeys to determine the matrix that maximizes bioavailability and reduces first-pass metabolism [ 40 ][ 41 ]; THC-hemisuccinate provided the highest bioavailability of Transcutaneous Another route of cannabinoid exposure that avoids first-pass metabolism and improves THC bioavailability is topical administration [ 43 ].

    Intravenous Although THC is not abused by the intravenous route, pharmacodynamic and pharmacokinetic cannabinoid research has employed this technique. Cannabidiol Absorption Cannabidiol CBD is a natural, non-psychoactive [ 49 ][ 50 ] constituent of Cannabis sativa , but possesses pharmacological activity, which is explored for therapeutic applications. Distribution THC Plasma concentrations decrease rapidly after the end of smoking due to rapid distribution into tissues and metabolism in the liver.

    Extrahepatic Metabolism Other tissues, including brain, intestine, and lung, may contribute to the metabolism of THC, although alternate hydroxylation pathways may be more prominent [ 86 ][ - ]. Metabolism of Cannabidiol CBD Metabolism is similar to that of THC, with primary oxidation of C 9 to the alcohol and carboxylic acid [ 8 ][ ], as well as side-chain oxidation [ 88 ][ ].

    Terminal Elimination Half-Lives of THC-COOH Another common problem with studying the pharmacokinetics of cannabinoids in humans is the need for highly sensitive procedures to measure low cannabinoid concentrations in the terminal phase of excretion, and the requirement for monitoring plasma concentrations over an extended period to adequately determine cannabinoid half-lives. Cannabinoid—Glucuronide Conjugates Specimen preparation for cannabinoid testing frequently includes a hydrolysis step to free cannabinoids from their glucuronide conjugates.

    Interpretation of Cannabinoid Concentrations in Biological Fluids 3. Plasma Concentrations Compared to other drugs of abuse, analysis of cannabinoids presents some difficult challenges. Prediction Models for Estimation of Cannabis Exposure There continues to be controversy in the interpretation of cannabinoid results from blood analysis, some general concepts having wide support.

    Urine Concentrations Detection of cannabinoids in urine is indicative of prior cannabis exposure, but the long excretion half-life of THC-COOH in the body, especially in chronic cannabis users, makes it difficult to predict the timing of past drug use.

    THC-COOH Detection Windows in Urine Drug detection time, or the duration of time after drug administration in which the urine of an individual tests positive for cannabinoids, is an important factor in the interpretation of urine drug results.

    Normalization of Cannabinoid Urine Concentrations to Urine Creatinine Concentrations Normalization of cannabinoid concentration to urine creatinine concentration aids in the differentiation of new from prior cannabis use, and reduces the variability of drug measurement due to urine dilution.

    Oral-Fluid Testing Oral fluid also is a suitable specimen for monitoring cannabinoid exposure, and is being evaluated for driving under the influence of drugs, drug treatment, workplace drug testing, and for clinical trials [ - ].

    Cannabinoids in Sweat To date, there are no published data on the excretion of cannabinoids in sweat following controlled THC administration, although our laboratory at NIH is conducting such research.

    Cannabinoids in Hair There are multiple mechanisms for the incorporation of cannabinoids in hair. Conclusions An understanding of human cannabinoid pharmacokinetics is important for the development and monitoring of new therapeutic medications and to the interpretation of cannabinoid test results in a wide variety of biological matrices, including blood, plasma, urine, oral fluid, sweat, and hair.

    Claussen U, Korte F. Chemical, Pharmacologic and Therapeutic Aspects. Agurell S, Leander K. Pharmacokinetics and Pharmacodynamics of Psychoactive Drugs. Barnett G, Chiang CN, editors. Mechoulam R, Hanus L.

    Harder S, Rietbrock S. Russo E, Guy GW. Pharmacology, Toxicology, and Therapeutic Potential. Grotenhermen F, Russo E, editors. Proceedings of the Oxford Symposium on Cannabis. Kreuz DS, Axelrod J. Kelly P, Jones RT. Blackard C, Tennes K. The Pharmacology of Marijuana.

    Braude MC, Szara S, editors. Raven Press; New York: Ben-Zvi Z, Burstein S. Harvey DJ, Mechoulam R. Krishna DR, Klotz U. The Pharmacology of Marihuana. Johansson E, Halldin MM.

    Advances in Analytical Toxicology. Biomedical Publications; Foster City: Advances in Analytical Toxicology II. Year Book Medical Publishers; Chicago: August 29 — September 2, Chemical, Pharmacologic, and Therapeutic Aspects. Harcourt Brace Jonanovich; Orlando: Fraser AD, Worth D. Balabanova S, Schneider E. Samyn N, van Haeren C. October 31 — November 4, Hair Analysis in Forensic Toxicology: In , a third, ether -type endocannabinoid, 2-arachidonyl glyceryl ether noladin ether , was isolated from porcine brain.

    It binds primarily to the CB 1 receptor, and only weakly to the CB 2 receptor. A fifth endocannabinoid, virodhamine, or O -arachidonoyl-ethanolamine OAE , was discovered in June In rats, virodhamine was found to be present at comparable or slightly lower concentrations than anandamide in the brain , but 2- to 9-fold higher concentrations peripherally.

    Recent evidence has highlighted lysophosphatidylinositol as the endogenous ligand to novel endocannabinoid receptor GPR55 , making it a strong contender as the sixth endocannabinoid.

    Endocannabinoids serve as intercellular ' lipid messengers ', signaling molecules that are released from one cell and activating the cannabinoid receptors present on other nearby cells. Although in this intercellular signaling role they are similar to the well-known monoamine neurotransmitters such as dopamine , endocannabinoids differ in numerous ways from them. For instance, they are used in retrograde signaling between neurons.

    Furthermore, endocannabinoids are lipophilic molecules that are not very soluble in water. They are not stored in vesicles and exist as integral constituents of the membrane bilayers that make up cells. They are believed to be synthesized 'on-demand' rather than made and stored for later use. The mechanisms and enzymes underlying the biosynthesis of endocannabinoids remain elusive and continue to be an area of active research.

    The endocannabinoid 2-AG has been found in bovine and human maternal milk. A review by Matties et al. It is proposed that the competition of leptin and cannabinoids for Tlc1 is implicated in energy homeostasis. They are, in effect, released from the postsynaptic cell and act on the presynaptic cell, where the target receptors are densely concentrated on axonal terminals in the zones from which conventional neurotransmitters are released.

    Activation of cannabinoid receptors temporarily reduces the amount of conventional neurotransmitter released. This endocannabinoid-mediated system permits the postsynaptic cell to control its own incoming synaptic traffic. The ultimate effect on the endocannabinoid-releasing cell depends on the nature of the conventional transmitter being controlled.

    For instance, when the release of the inhibitory transmitter GABA is reduced, the net effect is an increase in the excitability of the endocannabinoid-releasing cell. On the converse, when release of the excitatory neurotransmitter glutamate is reduced, the net effect is a decrease in the excitability of the endocannabinoid-releasing cell.

    Endocannabinoids are hydrophobic molecules. They cannot travel unaided for long distances in the aqueous medium surrounding the cells from which they are released and therefore act locally on nearby target cells.

    Hence, although emanating diffusely from their source cells, they have much more restricted spheres of influence than do hormones , which can affect cells throughout the body. Historically, laboratory synthesis of cannabinoids was often based on the structure of herbal cannabinoids, and a large number of analogs have been produced and tested, especially in a group led by Roger Adams as early as and later in a group led by Raphael Mechoulam.

    Newer compounds are no longer related to natural cannabinoids or are based on the structure of the endogenous cannabinoids. Synthetic cannabinoids are particularly useful in experiments to determine the relationship between the structure and activity of cannabinoid compounds, by making systematic, incremental modifications of cannabinoid molecules. When synthetic cannabinoids are used recreationally, they present significant health dangers to users. From Wikipedia, the free encyclopedia.

    Part of a series on Cannabis Arts Culture. Drug culture Illegal drug trade Psychedelia. Cannabinoid receptor type 1.

    Cannabinoid receptor type 2. Endocannabinoids [ edit ] Further information on the roles and regulation of the endocannabinoids: This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. Journal of Medicinal Chemistry. Journal of Natural Products. Pain, nausea and vomiting, spasticity, and harms". A Cellular and Molecular Approach. Progress in Lipid Research.

    Incorporation experiments with 13 C-labeled glucoses". European Journal of Biochemistry. US Patent application number: British Journal of Pharmacology. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. Retrieved 6 October American Journal of Botany. Journal of Pharmacology and Experimental Therapeutics. Current Topics in Medicinal Chemistry. Cannabinoid type 2 receptor-dependent and -independent immunomodulatory effects" PDF. The Journal of Biological Chemistry.

    Journal of Chromatography A. Drug Testing and Analysis. The British Journal of Psychiatry. Because they are extremely lipid soluble, cannabinoids accumulate in fatty tissues, reaching peak concentrations in days. They are then slowly released back into other body compartments, including the brain. Because of the sequestration in fat, the tissue elimination half-life of THC is about 7 days, and complete elimination of a single dose may take up to 30 days.

    Retrieved 3 December Therapeutics and Clinical Risk Management. Retrieved 29 November Retrieved 30 November US Food and Drug Administration. Retrieved 14 January Retrieved 12 January Cancer Chemotherapy and Pharmacology. Retrieved 25 June The Journal of Supercritical Fluids. Annual Review of Neuroscience. Quantification Of molecular species and their degradation upon imbibition".

    Possible implications for mollusc physiology and sea food industry". Biochimica et Biophysica Acta. Pharmacology Biochemistry and Behavior. European Journal of Pharmacology. The Journal of Pharmacology and Experimental Therapeutics.

    Experimental Biology and Medicine. Archived from the original on Histamine receptor agonist Histamine receptor antagonist H 1 H 2 H 3. Opioid modulator Opioid receptor agonist Opioid receptor antagonist Enkephalinase inhibitor. Cofactor see Enzyme cofactors Precursor see Amino acids. Cannabinoid receptor modulators cannabinoids by pharmacology List of:

    Cannabinoid

    Approach to making causal inferences. Neurobiology of cannabis effects in adolescence. .. absorption of THC by the lungs. One increasingly. In this report the term “cannabis” will be used instead of marijuana or other Cannabis smokers typically inhale deeply and hold their breath to ensure maximum absorption of THC by the lungs. .. Approach to making causal inferences. THC is rapidly absorbed after the inhalation of cannabis smoke. Rate of . Somatic adverse effects of THC [51]. Acute atropine-like adverse effects such as.

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    Comments

    Kenny1994

    Approach to making causal inferences. Neurobiology of cannabis effects in adolescence. .. absorption of THC by the lungs. One increasingly.

    exel1

    In this report the term “cannabis” will be used instead of marijuana or other Cannabis smokers typically inhale deeply and hold their breath to ensure maximum absorption of THC by the lungs. .. Approach to making causal inferences.

    ZloyRoma3

    THC is rapidly absorbed after the inhalation of cannabis smoke. Rate of . Somatic adverse effects of THC [51]. Acute atropine-like adverse effects such as.

    renato23

    Oromucosal: sublingual sprays and tinctures absorbed through cheek/oral (7). Eye pressure sensation. (1). Tinnitus (ringing in the ears). (6).

    hawkey017

    Healthcare Practitioner Perceptions of Benefit from Medical Cannabis. Oromucosal: sublingual sprays and tinctures absorbed through cheek/oral mucosa. (7). Eye pressure sensation. (1). Tinnitus (ringing in the ears) . (6).

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