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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of environmental temperature on body temperature and neuroendocrine parameters were evaluated following a single acute dose (60 micrograms/kg) of soman. Plasma levels of corticosterone, glucose, and free fatty acids, as well as acetylcholinesterase activity in plasma, erythrocytes, and brain were determined over a 96-hr time course in rats maintained at 23-25, 14-16, and 3-5 degrees C. Considerable inhibition of plasma and erythrocyte acetylcholine hydrolysis activity was observed after administration of soman at all three environmental temperatures. The degree of hypothermia in all soman-treated rats in each environment tested was associated with the amount of brain acetylcholinesterase inhibition. In animals maintained at 23-25 and 14-16 degrees C, changes in plasma corticosterone levels were influenced by central acetylcholine hydrolysis. Hyperglycemia was found only in rats with greater than 45% brain inhibition regardless of environmental temperature. However, the plasma concentration of glucose over the 96 hr test period varied in relation to the hydrolysis of acetylcholine in soman-treated rats. Recovery of plasma acetylcholinesterase was more rapid at lower environmental temperatures. A greater inhibition of central acetylcholinesterase was found in soman-treated rats exposed to 3-5 degrees C. Soman may be more toxic at low environmental temperatures.
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PMID:Effects of environmental temperature on hypothermia and neuroendocrine changes induced by soman. 236 72

The hormonal changes were estimated after poisoning with an extremely toxic organophosphate, soman (pinacolyl methylphosphonofluoridate). Soman produced a significant (p less than or equal to 0.05) increase in serum corticosterone, thyroxine, and triidothyronine concentrations at 3, 6, and 9 hr after poisoning. However, by 22 hr the levels were not significantly different from control. Plasma ACTH levels were decreased at 3 hr after soman at 100 micrograms/kg but not after 287 micrograms/kg. Serum testosterone levels were decreased significantly (p less than or equal to 0.01) 6 and 9 hr after soman poisoning but had returned to control levels by 22 hr. Soman (100 micrograms/kg) produced an immunosuppressive response when administered at 24 hr after an antigen (sheep red blood cells). However, a similar response was obtained in adrenalectomized mice suggesting that some other mechanism other than elevated corticosterone was responsible for the immunosuppressive effect. Soman poisoning produced an intense hypothermia. It is possible that the hormonal changes noted after soman poisoning are due to a reduction in metabolism and excretion, a result of the hypothermia and not a direct action of soman.
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PMID:Hormonal consequences of organophosphate poisoning. 300 1

The neurotoxicity and lethality of Soman and Sarin, after single and repeated treatment at 50-60% of their LD50 doses in rats were investigated. Single treatment with Soman (100 micrograms/kg) and Sarin (120 micrograms/kg) produced severe tremors, convulsions and hypothermia, in some rats only, while the others did not show toxicity, i.e. an all or none effect. Soman and Sarin (100-120 micrograms/kg) caused, respectively, 89-93% and 26-48% inhibition of AChE at 6 hr and 56-68% and 17-39% inhibition at 24 h after single injections. Repeated treatment with Soman (90 micrograms/kg) and Sarin (100 micrograms/kg) at 4 day intervals caused variable incidences of neurotoxicity and increasing mortalities, and after ten injections the survival rates were 31 and 54%, and AChE inhibition was 86 and 75%, respectively. It is suggested, that the variable neurotoxicity of and the low tolerance to of these compounds are partly related to peripheral dispositional mechanisms. Furthermore, the profile of toxicity of these anticholinesterase agents should be differentiated from, but not generalized with, that of the other anticholinesterase organophosphates.
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PMID:Variability of neurotoxicity of and lack of tolerance to the anticholinesterases soman and sarin in the rat. 402 23

The object of the study was to determine the pharmacological nature of pinacolyl methylphosphonofluoridate (soman)-induced hypothermia in mice. This was accomplished by examining the soman hypothermia dose response and the effect of various pharmacological antagonists in comparison to the hypothermia responses of muscarinic and nicotinic cholinergic agonists such as oxotremorine and nicotine and another anticholinesterase, physostigmine. Core temperature in mice was monitored by telemetry. In general, atropine antagonized oxotremorine, physostigmine, and soman hypothermia but not nicotine hypothermia whereas mecamylamine antagonized nicotine hypothermia but not that produced by the other agonists. Soman hypothermia was not affected significantly by various pharmacological antagonists, suggesting that other neurotransmitters were not involved in the expression of soman hypothermia. Soman hypothermia appears to be due to muscarinic receptor stimulation and can be effectively antagonized, but not completely, by the use of atropine. Acetylcholinesterase oxime reactivators, such as HI-6 and toxogonin, were ineffective in antagonizing soman-induced hypothermia and reactivating hypothalamic acetylcholinesterase, whereas HI-6 was effective in reactivating soman-inhibited diaphragm acetylcholinesterase when administered up to 10 min after soman, indicating that aging of the soman-inhibited acetylcholinesterase had not occurred. Soman hypothermia appears to be primarily a muscarinic receptor-related event.
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PMID:Pharmacological nature of soman-induced hypothermia in mice. 845 Dec 71