Drugs online research references
Neurosci Biobehav Rev. 1991 Fall;15(3):349-62.
Anticonvulsants for poisoning by the organophosphorus compound soman: pharmacological mechanisms.
Shih TM, Koviak TA, Capacio BR.
Pharmacology Division, U.S. Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD 21010-5425.
Exposure to high doses of organophosphorus nerve agents such as soman, even with carbamate pretreatment, produces a variety of toxic cholinergic signs, including secretions, convulsions and death. Evidence suggests that soman-induced convulsions may be associated with postexposure brain neuropathology. The purpose of this study was to investigate the pharmacologic mechanism of action of soman-induced convulsions and of anticonvulsant drugs. Various classes of compounds were evaluated for their efficacy in preventing soman-induced convulsions in rats pretreated with the oxime HI-6 to increase survival time, along with various doses of the test compounds (IM) either in the absence or presence of atropine sulfate (16 mg/kg, IM) 30 minutes prior to a soman challenge dose (180 micrograms/kg, SC; equivalent to 1.6 x LD50) that produced 100% convulsions. Without atropine sulfate, only tertiary anticholinergics (scopolamine, trihexyphenidyl, biperiden, benactyzine, benztropine, azaprophen and aprophen), caramiphen, carbetapentane and MK-801 were effective anticonvulsants. In the presence of atropine sulfate, the benzodiazepines (diazepam, midazolam, clonazepam, loprazolam and alprazolam), mecamylamine, flunarizine, diphenylhydantoin, clonidine, CGS 19755 and Organon 6370 studied were effective. We have examined the possibility that diazepam may exert some of its anticonvulsant effects through cholinergic mechanisms and found that a reduced release of ACh into synapses after diazepam and atropine treatment may account for diazepam's anticonvulsant activity against soman. We also found that at anticonvulsant doses biperiden and trihexyphenidyl each significantly reversed the effects of soman on striatal levels of DOPAC and HVA, the metabolites of dopamine, and have concluded that in addition to actions on muscarinic receptors, the anticonvulsant effects of these anticholinergics in soman poisoning may be partially related to their actions on the striatal dopaminergic system. These findings allow us to postulate that central muscarinic cholinergic mechanisms are primarily involved in eliciting the convulsions following exposure to soman and that subsequent recruitment of other excitatory neurotransmitter systems and loss of inhibitory control may be responsible for sustaining the convulsions and for producing the subsequent brain damage. Future studies to confirm these neuropharmacological mechanisms are proposed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1683477&dopt=Abstract
Rev Med Interne. 1995;16(3):187-90.
[Datura stramonium poisoning: the diagnosis is clinical, treatment is symptomatic]
[Article in French]
Roblot F, Montaz L, Delcoustal M, Gaboriau E, Chavagnat JJ, Morichaud G, Pourrat O, Scepi M, Patte D.
Service accueil-urgences, CHU La Miletrie, Poitiers, France.
Datura stramonium is a hallucinogenic plant found in urban or rural areas. It contains three main toxic alkaloids: atropine, scopolamine, and hyosciamine. Consumption of any part of the plant can result in severe anticholinergic toxicity. Clinical symptoms are those seen in atropine poisoning, particularly hallucinations and mydriasis. Prognostic is good in this study. Patients always require hospitalisation because of agitated behavior. Symptomatic treatment is efficient. Clinicians should be aware of the potential abuse of botanicals such as jimson weed to avoid excessive investigations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7740228&dopt=Abstract
Am J Physiol. 1986 Jul;251(1 Pt 1):G51-5.
Vasoactive intestinal polypeptide provokes acetylcholine release from the myenteric plexus.
Kusunoki M, Tsai LH, Taniyama K, Tanaka C.
Effects of vasoactive intestinal polypeptide (VIP) on the release of acetylcholine (ACh) from longitudinal muscle strips with myenteric plexus (LM) preparations were examined in the guinea pig small intestine. VIP (10(-10) to 10(-6) M) induced a concentration-dependent contraction of LM preparation. The VIP-induced contractions seem to be related to three components, the scopolamine-sensitive, the scopolamine-insensitive, the tetrodotoxin-sensitive, and the tetrodotoxin-insensitive contractions. VIP (10(-10) to 10(-6) M) induced a concentration-dependent increase in the release of [3H]ACh from LM preparations preloaded with [3H]choline. The VIP-evoked [3H]ACh release was inhibited by removal of Ca2+ from the perfusion medium and by treatment with tetrodotoxin but not by scopolamine and hexamethonium. The spontaneous and VIP-evoked [3H]ACh release was not affected by phentolamine, propranolol, methysergide, diphenhydramine, cimetidine, bicuculline, or [D-Pro2, D-Trp7,9]substance P. The result demonstrates that VIP induces contractions of longitudinal smooth muscle directly and indirectly by the stimulation of both cholinergic neurons and noncholinergic excitatory neurons.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3728677&dopt=Abstract
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