Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, the thermal responses induced by intraventicular administration of pyrogen prostaglandin E1, the brain monoamines norepinephrine and serotonin, and the antipyretic sodium acetylsalicylate (aspirin) were measured in conscious rabbits to assess the possible involvement of these substances in fever production. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to the administration of these drugs were measured. The results showed that sodium acetylsalicylate, an inhibitor of prostaglandin synthetase, antagonizes the norepinephrine induced fever but not the prostaglandin fever. The data also showed that the serotonin induced hypothermia was reversed by prostaglandin administration. Thus, the fact strongly suggest that the prostaglandin E1 serves as a fever-prducing mediator in the central nervous system. Also, the norepinephrine fever and serotonin hpyothermia, respectively, may be associated with an increase and a decrease in prostaglandin synthesis in the brain.
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PMID:Brain monoamines act through the prostaglandin release to influence the body temperature. 1 25

The influence of pretreatment with 5.0 or 10.0 mg/kg of indomethacin, a prostaglandin synthetase inhibitor, on the alterations in body temperature produced by 3.0 and 4.0 g/kg of ethanol, was studied in food-deprived and free-feeding rats. A partial antagonism of ethanol's hypothermic effect resulted from indomethacin pretreatments and this effect was found to be ethanol dose-dependent. This result could account for the conflicting reports in the literature on the effectiveness of indomethacin in antagonizing ethanol-induced hypothermia. Indomethacin (5.0 mg/kg) also antagonized ethanol-induced hypoglycemia in 48 hr starved rats. The relationship between two effects of ethanol, hypothermia and hypoglycemia, is discussed.
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PMID:Hypoglycemia and hypothermia induced by ethanol: antagonism by indomethacin. 378 36

The present study investigates the results of pretreatment with five prostaglandin (PG) synthetase inhibitors on effects of morphine on body temperature, pupillary diameter, body movement and production of exophthalmos in rat. Hyperthermia, induced by a low dose of morphine, was inhibited in animals pretreated with any of the PG synthetase inhibitors. However, PG synthetase inhibitors had no clear effect on hypothermia induced by higher doses of morphine. The duration of morphine-induced catalepsy was attenuated by pretreatment with the PG synthetase inhibitors in a dose-related manner. The exophthalmos induced by all doses of morphine was either shortened in duration or inhibited by sulindac, paracetamol or ibuprofen. Morphine-induced mydriasis was either attenuated or inhibited by paracetamol, ibuprofen or meclofenamic acid. The results suggest that endogenous PGs play a role in morphine-induced hyperthermia, catalepsy, exophthalmos and mydriasis whereas a physiological role for PGs in morphine-induced hypothermia was not indicated.
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PMID:Effect of prostaglandin synthetase inhibitors on non-analgesic actions of morphine. 640 56

Previous studies in our laboratory have demonstrated that inhibition of prostaglandin biosynthesis through pretreatment with aspirin and other prostaglandin synthetase inhibitors (PGSI) significantly reduces CNS sensitivity to a hypnotic dose of ethanol. Indomethacin, a potent PGSI, was administered to male LS, SS, and HS/Ibg mice (65 +/- 10 days of age) 15 min prior to administration of a hypnotic dose of ethanol or pentobarbital. Doses of indomethacin used were identical to those previously reported as optimally antagonizing ethanol-induced sleep. Another group received a vehicle-control injection, while a third group also received a control injection, but were placed in a incubator maintained at 30 +/ 1 degrees C. Body temperatures were recorded periodically for several hours. Both indomethacin and incubation significantly reduced hypothermia induced by ethanol and pentobarbital. Incubation increased sleep time after ethanol, but did not affect pentobarbital sleep time. These results suggest that the hypnotic and hypothermic effects of ethanol, although possibly mediated through prostaglandins, apparently are not causally linked.
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PMID:Prostaglandin synthetase inhibitors antagonize hypothermia induced by sedative hypnotics. 679 Dec 32

The intraperitoneal administration of lipopolysaccharide from Salmonella typhimurium (1 mg/kg) caused a fall in the rat colonic temperature of about 2 degrees C at an ambient temperature of 22 +/- 3 degrees C. The hypothermia induced by the lipopolysaccharide was abated in a dose-dependent manner by the administration of indomethacin. Other inhibitors of prostaglandin synthetase such as aspirin, flufenamic acid, and phenylbutazone had effects similar to those of indomethacin. When various prostaglandins were injected intracerebroventricularly, only prostaglandin D2 caused a dose-dependent fall in the colonic temperature at doses between 1.2 and 6 nmol/kg. Microinjection of prostaglandin D2 into the preoptic area caused hypothermia of about 1 degree C. However, injection of prostaglandin D2 into the posterior hypothalamus had little effect on the colonic temperature. The hypothermia caused by prostaglandin D2 was not abated by the administration of indomethacin. The amount of prostaglandin D2 increased significantly in the preoptic/hypothalamic region of rat brain 1 hr after the intraperitoneal administration of the lipopolysaccharide, whereas such increase was not observed in rats pretreated with indomethacin. The in vitro incubation of the preoptic/hypothalamic slices with the lipopolysaccharide also increased the amount of prostaglandin D2. These results suggest that the intraperitoneal administration of the lipopolysaccharide induces the release of prostaglandin D2 in the preoptic/hypothalamic area of rat brain and that the latter compound is involved in the hypothermic response of rats to the lipopolysaccharide.
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PMID:Role of prostaglandin D2 in the hypothermia of rats caused by bacterial lipopolysaccharide. 696 2