| Potencial terapéutico de cannabis y cannabinoides |
The therapeutic potential of cannabis and cannabinoids.
Grotenhermen F, Müller-Vahl K.
nova-Institut GmbH, Chemiepark Knapsack, Hürth.
Dtsch Arztebl Int. 2012 Jul;109(29-30):495-501. Epub 2012 Jul 23.
Abstract
BACKGROUND:
Cannabis-based medications have been a topic of intense study since the endogenous cannabinoid system was discovered two decades ago. In 2011, for the first time, a cannabis extract was approved for clinical use in Germany. METHODS: Selective literature review. RESULTS: Cannabis-based medications exert their effects mainly through the activation of cannabinoid receptors (CB1 and CB2). More than 100 controlled clinical trials of cannabinoids or whole-plant preparations for various indications have been conducted since 1975. The findings of these trials have led to the approval of cannabis-based medicines (dronabinol, nabilone, and a cannabis extract [THC:CBD=1:1]) in several countries. In Germany, a cannabis extract was approved in 2011 for the treatment of moderate to severe refractory spasticity in multiple sclerosis. It is commonly used off label for the treatment of anorexia, nausea, and neuropathic pain. Patients can also apply for government permission to buy medicinal cannabis flowers for self-treatment under medical supervision. The most common side effects of cannabinoids are tiredness and dizziness (in more than 10% of patients), psychological effects, and dry mouth. Tolerance to these side effects nearly always develops within a short time. Withdrawal symptoms are hardly ever a problem in the therapeutic setting. CONCLUSION:
There is now clear evidence that cannabinoids are useful for the treatment of various medical conditions
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3442177/pdf/Dtsch_
Arztebl_Int-109-0495.pdf
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| Marihuana médica; despejando el humo |
Medical marijuana: clearing away the smoke.
Grant I, Atkinson JH, Gouaux B, Wilsey B.
Center for Medicinal Cannabis Research; University of California, San Diego; San Diego, CA, USA.
Open Neurol J. 2012;6:18-25. doi: 10.2174/1874205X01206010018. Epub 2012 May 4.
Abstract
Recent advances in understanding of the mode of action of tetrahydrocannabinol and related cannabinoid in-gredients of marijuana, plus the accumulating anecdotal reports on potential medical benefits have spurred increasing re-search into possible medicinal uses of cannabis. Recent clinical trials with smoked and vaporized marijuana, as well as other botanical extracts indicate the likelihood that the cannabinoids can be useful in the management of neuropathic pain, spasticity due to multiple sclerosis, and possibly other indications. As with all medications, benefits and risks need to be weighed in recommending cannabis to patients. We present an algorithm that may be useful to physicians in determining whether cannabis might be recommended as a treatment in jurisdictions where such use is permitted.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358713/pdf/TONEUJ-6-18.pdf
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| Facilitación de la liberación de sustancia P de la médula espinal de las ratas por el receptor cannabionoide CB1, medida como la internalización del receptor neuroquinina 1. |
Cannabinoid CB1 receptor facilitation of substance P release in the rat spinal cord, measured as neurokinin 1 receptor internalization.
Zhang G, Chen W, Lao L, Marvizón JC.
Veteran Affairs Greater Los Angeles Healthcare System, Los Angeles, CA 90073, USA.
Eur J Neurosci. 2010 Jan;31(2):225-37. doi: 10.1111/j.1460-9568.2009.07075.x. Epub 2010 Jan 13.
Abstract
The contribution of CB1 receptors in the spinal cord to cannabinoid analgesia is still unclear. The objective of this study was to investigate the effect of CB1 receptors on substance P release from primary afferent terminals in the spinal cord. Substance P release was measured as neurokinin 1 (NK1) receptor internalization in lamina I neurons. It was induced in spinal cord slices by dorsal root stimulation and in live rats by a noxious stimulus. In spinal cord slices, the CB1 receptor antagonists AM251, AM281 and rimonabant partially but potently inhibited NK1 receptor internalization induced by electrical stimulation of the dorsal root. This was due to an inhibition of substance P release and not of NK1 receptor internalization itself, because AM251 and AM281 did not inhibit NK1 receptor internalization induced by exogenous substance P. The CB1 receptor agonist ACEA increased NK1 receptor internalization evoked by dorsal root stimulation. The effects of AM251 and ACEA cancelled each other. In vivo, AM251 injected intrathecally decreased NK1 receptor internalization in spinal segments L5 and L6 induced by noxious hind paw clamp. Intrathecal AM251 also produced analgesia to radiant heat stimulation of the paw. The inhibition by AM251 of NK1 receptor internalization was reversed by antagonists of mu-opioid and GABA(B) receptors. This indicates that CB1 receptors facilitate substance P release by inhibiting the release of GABA and opioids next to primary afferent terminals, producing disinhibition. This results in a pronociceptive effect of CB1 receptors in the spinal cord.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2857979/pdf/nihms-189750.pdf Atentamente Anestesiología y Medicina del Dolor www.anestesia-dolor.org
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