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)

Captopril, an angiotensin converting enzyme inhibitor, was evaluated for a potential antidepressive activity in several animal models. The drug administered in doses of 3-30 mg/kg ip neither affected the reserpine- or apomorphine-induced hypothermia in mice nor reduced the immobility time in the forces swimming test in mice and rats. Moreover, captopril administered repeatedly (10 mg/kg ip, twice daily for 14 days) neither changed the density or affinity of cortical beta-adrenoceptors nor modified the nomifensine-induced locomotor hyperactivity in rats. These results suggest that captopril has no antidepressant-like activity in animal models.
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PMID:Captopril lacks the antidepressant-like activity in animal models. 166 33

The effect of captopril on energy-rich phosphates and pH during normothermic ischemic arrest, hypothermic cardioplegic arrest and subsequent reperfusion was investigated in the isolated rat heart using 31P-nuclear magnetic resonance. The hearts remained in the probe during all perfusion procedures and captopril (80 ml.l-1) treatment was started directly after cannulation. After normothermic ischemic arrest (15 min), the ATP content of captopril-treated hearts was not significantly different from that of untreated hearts (53 +/- 9% and 52 +/- 8%, respectively). Accumulation of inorganic phosphate at the end of ischemia was significantly less in treated hearts, suggesting a higher end-ischemic nucleotide content in treated hearts. Hypothermic cardioplegic arrest (St. Thomas' Hospital solution, 4 degrees C) lasted for 3 h at 10 degrees C. Adenosine triphosphate in untreated hearts was significantly lower at the end of ischemia; 36 +/- 6% compared to 53 +/- 9% for untreated hearts. Adenosine triphosphate in untreated hearts recovered to 76 +/- 9% after normothermic ischemia and to 72 +/- 7% after hypothermic ischemia at the end of 30 min reperfusion. Captopril significantly improved adenosine triphosphate recovery in both treated groups; 89 +/- 4% after normothermic and 83 +/- 4% hypothermic ischemia. We conclude that captopril has a beneficial effect on recovery of adenosine triphosphate both after normothermic and after hypothermic ischemia.
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PMID:Captopril improves recovery of adenosine triphosphate during reperfusion of the ischemic isolated rat heart; a 31-phosphorus-nuclear magnetic resonance study. 306 91

The effects of 1-[(S)-3-acetylthio-2-methylpropanoyl]-L-prolyl-L-phenylalanine (alacepril, DU-1219), an orally active angiotensin converting enzyme inhibitor, on the central nervous and sensory systems and on several other functions were compared with those of captopril in the experimental animals. Alacepril at the high oral dose of 600 mg/kg prolonged the hexobarbital sleeping time and potentiated the reserpine-induced hypothermia in mice. However, alacepril at the same dose did not affect the general behavior, convulsions induced by maximal electroshock, pentetrazol and strychnine, active avoidance in mice and body temperature in rats. In addition, alacepril (200 mg/kg i.v.) has little effect on general behavior in mice. Captopril at over 107 mg/kg p.o. produced eyelid closure and at 320 mg/kg prolonged the hexobarbital sleeping time. A metabolite of alacepril, desacetylalacepril (DU-1227) (200 mg/kg i.v.), caused salivation in mice. Alacepril and DU-1227 at 60 mg/kg i.v. were without effect on flexor reflex and spontaneous electroencephalogram (EEG) in cats, while captopril at the equimolar dose depressed the flexor reflex and showed a tendency to increase the beta 2-band relative power of the cortical EEG. Alacepril and captopril neither affected the writhing syndrome induced by acetic acid nor that by phenylquinone in mice. Local anesthetic and irritant activities in rabbits and effect on neuromuscular junction in anesthetized rats were not observed with the two compounds. Alacepril at the oral dose of 0.1 mg/kg potentiated the carrageenin-induced edema in rats. However, the effect was one third that of captopril. Alacepril and captopril did not affect the increased vascular permeability by acetic acid in mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:General pharmacology of the novel angiotensin converting enzyme inhibitor alacepril. 2nd communication: Effects on central nervous and sensory systems and on the other functions. 351 78

The influence of captopril and enalapril on acute toxicity of ethanol, ethanol-induced hypothermia, ethanol sleeping time has been investigated in mice. Moreover, the combined effect of captopril and enalapril on spontaneous locomotor activity in mice has been examined. The captopril (5 and 20 mg/kg) and enalapril (5 and 20 mg/kg) were injected intraperitoneally i.p. The drugs were given as single or repeated doses for 10 days. It has been shown that the captopril and enalapril administered in single doses decreases, but chronic administration increases acute toxicity of ethanol. Captopril and enalapril in single doses enhanced, but chronic administration inhibits hypothermic effect of ethanol. Captopril and enalapril reduces ethanol sleeping time. Captopril and enalapril administered for 10 days and enalapril in a single dose 20 mg/kg decreases ethanol induced hyperactivity.
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PMID:Influence of captopril and enalapril on some central effects of ethanol. 1202 17