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)

The effects of giving propiopromazine alone and of electroanesthesia-propiopromazine treatment on thermoregulation (body temperature regulation) were studied in 3 sheep at ambient temperatures of 5, 25, and 35 C. Measures of thermoregulation during a 120-minute treatment and 120-treatment recovery period included rectal temperature, respiratory frequency, respiratory evaporative heat loss, metabolic heat production, multiple skin temperatures, and shivering. During cold exposure (5 C), both the propiopromazine administration and the electroanesthesia-propiopromazine treatment resulted in hypothermia which was attributed to increased peripheral and respiratory heat losses, a transient inhibition of shivering thermogenesis, and a reduction in metabolic heat production. At 35 C ambient temperature, both resulted in hyperthermia caused principally by a reduction in respiratory evaporative heat loss. The effects of electroanesthesia-propiopromazine treatment on thermoregulation appeared to be additive at both the cold (5 C) and the hot (35 C) environments, in that simultaneous administration resulted in a more profound thermoregulatory impairment. Nevertheless, shifts in body temperature during electroanesthesia are partly attributable to phenothiazine premedication.
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PMID:Effects of electroanesthesia and a phenothiazine tranquilizer on thermoregulation in the sheep. 1 89

Hypothermic protection of myocardia during E.C.C. has been estimated on a 35 dogs experimental series and on a clinical series of 700 acquired cardiopathies of adult, including 400 valvular replacements and 300 aorto-coronary by-pass. Experimental results have been estimated by biochemic and morphologic controls done on myocardic samples took up by drillbiopsy. The biochemical study includes among others a dosing of the high-energy phosphorus compounds (P.C. and A.T.P.). Morphological study was done by optic and electronic microscopy. Results made clear the superiority of the hypothermic ischemia at 10 degrees C on the continued perfusion at 32 degrees C with fibrillative heart. An hypothermic protection method with successively cold perfusion of the coronary system and a heart immersion in a salted solution at 4 degrees C has been utilized during valvular and coronary surgery on human in 700 cases. The total mortality was of 5,8 p. 100. The rate of post-operative infarcts was 2,4 p. 100. Incidence of intra-ventricular conduction troubles has been 1,1 p. 100. There was no relation between mortality and morbidity of myocardic origin and the lasting of the ischemic clamp, which were of 21 mn up to 165 mn. The low incidence of complications of myocardic origin is due to the hypothermic protection of the myocardia.
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PMID:[Protection of the myocardium by hypothermia during extracorporeal circulation. Experimental and clinical study]. 1 26

Intraperitoneal administration of a peripheral decarboxylase inhibitor benserazide (Ro4-4602) to unanesthetized rats produced alterations in body temperature which depended on ambient temperature. In the cold, hypothermia was brought about by a decrease in metabolic heat production. At room temperature, a dose-dependent hypothermia was preceded by a slight hyperthermia. The hypothermia was due to an increase in skin temperature (tail) and a decrease in metabolic heat production, while the hyperthermia was due to a decrease in skin temperatures (both tail and footsole) and an increase in metabolic heat production. In the heat, hyperthermia responses to benserazide were associated with decrease in skin temperature (both tail and footsole). Benserazide treatment produced no significant change in brain 5-HT content. Chlorpromazine-induced hypothermia was greatly enhanced after pretreatment of the animals with benserazide at room temperature (22 degrees).
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PMID:The effects of a decarboxylase inhibitor, benserazide, on both thermoregulation and chlorpromazine-induced hypothermia in rats. 3 39

The semisynthetic ergot derivative lisuride induced dose- and time-dependent hypothermia in rats placed in a cold environment (+4 degrees C). As regards dosage, lisuride was more than 100 times more effective in this test model than bromocriptine. The effect of both drugs could be reduced by pretreatment with the dopamine antagonist haloperidol, which indicated a dopaminergic action of both drugs. In contrast, the hypothermic effect of lisuride could not be impaired by pretreatment with sulpiride, whilst the effects of bromocriptine were clearly antagonized by this drug. This results could be explained by a different affinity of these drugs to the same receptors, or, more likely, by a different mechanism of action by which lisuride and bromocriptine activate dopaminergic systems.
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PMID:Hypothermic action of lisuride in rats and differences to bromocriptine in the antagonistic effect of neuroleptics. 3 72

The R(-) and S(+)-isomers of 2,5-dimethoxy-4-methylamphetamine (DOM) produce a dose-dependent hypothermia in rats kept in the cold (6 degrees C). 2 This hypothermia was linearly dependent upon ambient temperature and the R(-)-isomer was considerably more potent than the S(+)-isomer. 3 A statistically significant tachyphylaxis was observed when R(-)-DOM was administered on two successive days. The response seven days after the second injection was similar to that on the first day of injection. 4 The hypothermia induced by R(-) and S(+)-DOM was antagonized by methysergide but not by p-chlorophenylalanine (PCPA) or pimozide. Methysergide, PCPA or pimozide alone did not elicit hypothermia at the doses used. The results indicate that R(-) and S(+)-DOM act at post-synaptic 5-hydroxytryptamine receptors.
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PMID:Stereospecific actions of 2,5-dimethoxy-4-methylamphetamine (DOM) on colonic temperature in the rat at various ambient temperatures. 13 54

1. The role of 5-hydroxytryptamine (5-HT) in temperature regulation and in fever in the rabbit has been investigated. 2. Intrahypothalamic microinjections of 5-HT in the conscious rabbit alters body temperature in a dose-dependent manner. 3. Low doses (5-5nmol) of 5-Ht and control saline injections produced a small, non-significant increase in temperature, with a long latency. 4. Doses of 14 nmol 5-HT produce a hyperthermia with a 45 min delay; while microinjections of 28 nmol result in a biphasic response; an initial short hypothermia is followed later by a hyperthermia. 5. Depleting the rabbit's brain of 5-HT by pretreatment with p-chlorophenylalanine (PCPA) fails to affect its body temperature at thermoneutral temperatures but significantly impairs the ability to thermoregulate against a cold stress. 6. PCPA pretreatment did not, however, impair the febrile response to bacterial pyrogen and prostaglandin E1. 7. These results reveal a dissociation between the effects of 5-HT depletion on temperature regulation, and on fever. The site of action of 5-HT in temperature regulation must be proximal to the fever input, but distal to the convengence of peripheral and hypothalamic temperature inputs.
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PMID:A dissociation between temperature regulation and fever in the rabbit. 14 Feb 37

1. Samples of cerebrospinal fluid (c.s.f.) have been taken from the cisterna magna of unanaesthetized cats, whilst rectal temperature was recorded, during exposure of the animals to various ambient temperatures and during fever induced by pyrogen. The concentration of adenosine 3', 5'-monophosphate (cyclic AMP) in samples of c.s.f. has been assayed. 2. Cats exposed to low ambient temperatures (-2 to +2 degrees C) for 3 h maintained body temperature by both behavioural and autonomic heat gain activity. Exposure of cats to high ambient temperatures (44 - 45 degrees C) for 3.5 h caused a rise in body temperatures of about 2.5 degrees C, despite behavioural and autonomic heat loss activity. Neither cold nor heat stress had a significant effect on c.s.f. cyclic AMP. 3. Fever induced by intravenous Shigella dysenteriae (2 and 20 mug/kg) was associated with a dose-related increase in the concentration of cyclic AMP in c.s.f. Paracetamol (75 mg/kg) injected I.P. before the onset of fever, suppressed the increase in both temperature and c.s.f. cyclic AMP in response to pyrogen. Paracetamol (50 and 100 mg/kg), injected after the onset of fever, caused a fall in temperature, which was not associated with a decrease in the concentration of cyclic AMP in c.s.f. 4. Fever induced in cats by intravenous Shigella dysenteriae (20 mug/kg) was associated with an increase in the concentration of cyclic AMP in plasma as well as in c.s.f. 5. The sodium salt of cyclic AMP (0.1-10 mg/kg) injected I.V. into unanaesthetized cats caused a dose-related hypothermia, which was associated with autonomic heat loss activity and a dose-related increase in the concentration of cyclic AMP in cisternal c.s.f., which was not mimicked by adenosine. 6. It is concluded that the raised concentrations of cyclic AMP in c.s.f., in response to pyrogen I.V., do not mediate fever in the cat and that the concentration of cyclic AMP in cisternal c.s.f. may be affected by changes in the plasma concentration of the nucleotide.
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PMID:Cyclic adenosine 3', 5'-monophosphate in cerebrospinal fluid during thermoregulation and fever. 19 Mar 83

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
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PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

The effectiveness of cooling the subendocardial myocardium by five different methods was evaluated in a group of 100 patients. The most effective and consistent method to cool the heart was by total body hypothermia with the heat exchanger in the cardiopulmonary bypass system. Myocardial temperature became equal to vena caval blood temperature after only a one minute lag. The least effective methods of myocardial cooling were those in which a bath of chilled fluid enveloped the outside surface of the heart, with and without aortic cross-clamping. The drop in ventricular septal temperature was so small that topical hypothermia, by itself, may be worthless. Two methods in wich chilled fluid was perfused through the coronary system produced a significant lowering of myocardial temperature. One of these methods employs coronary perfusion with a cold cardioplegic solution in addition to total body hypothermia. It is our current choice for myocardial protection during cross-clamping of the ascending aorta.
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PMID:The effectiveness of topical cardiac hypothermia. 29 2

A group of 176 patients undergoing cardiac surgery utilizing a technique of rapid core hypothermic cardioplegia with a hyperosmotic solution is presented. A cold, 2 to 4 degrees C hyperosmotic (396 mOsm) perfusate, injected under pressure, induced cardiac arrest without fibrillation within 2 to 4 seconds in every instance. At the end of each procedure, flushing of the cold solution out of the coronary system re-establishes spontaneous normal sinus cardiac rhythm in 96% (119 of 124) of coronary surgical procedures, 69% (11 of 16) of aortic valve replacements, 62% (10 of 16) of mitral valve replacements, 55% (five of nine) of aortic valve replacements combined with multiple coronary grafting, 57% (four of seven) of mitral valve replacement combined with multiple coronary grafting, and in 50% (two of four) of double valve replacements. Combined core and topical hypothermia with ice slush used in valve replacements and combined valve with coronary operations allowed periods of total ischemia up to 134 minutes without signs of detectable myocardial damage.
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PMID:Cardioplegia without fibrillation or defibrillation in cardiac surgery. 30 Sep 6


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