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 responses of fed, fasted, and hyperthyroid (T4) Sprague-Dawley male rats to 50 mg 1,1-dichloroethylene (1,1-DCE)/kg were compared. Hyperthyroid rats received three sc injections of thyroxine (100 micrograms/100 g) at 48-hr intervals; all other rats were sham-injected. 1,1-DCE was given po in mineral oil 24 hr after the last T4 dose; controls received only mineral oil. Animals were killed at 2, 4, and 8 hr. Liver GSH contents were lowered about 55% by both fasting and T4 while GSH transferase activities were lowered about 20% by fasting and 35% by T4. Only T4 pretreatment lowered alcohol dehydrogenase activities. Liver injury (i.e., serum glutamate pyruvate transaminase, histology) after 1,1-DCE was minimal in fed rats, moderate in fasted rats, and intermediate in T4 rats. Fasted rats showed a more pronounced depletion of liver GSH after 1,1-DCE than T4 rats and only in fasted rats did the toxicant decrease activities of the detoxification enzymes. Hypoglycemia after 1,1-DCE occurred in fed rats, but more rapidly in T4 rats. In contrast, fasted rats unexpectedly became hyperglycemic after the toxicant. Patterns of body temperature change after the toxicant, which might be due to its metabolites, were dissimilar. Hypothermia was not observed in fed rats, was only transiently evident in T4 rats, but occurred rapidly within 1 hr in fasted rats and steadily became more severe. The dissimilar patterns of liver enzyme and body temperature and serum glucose change after the toxicant in the three groups are indicative of different pathways of injury potentiation by fasting and hyperthyroidism.
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PMID:Potentiation of 1,1-dichloroethylene hepatotoxicity: comparative effects of hyperthyroidism and fasting. 341 96

To examine the effects of extracorporeal circulation using an artificial heart and lung machine on hepatic energy metabolism in patients with cardiac operation using hypothermia, the arterial blood ketone body ratio (AKBR) reflecting the hepatic mitochondrial redox state was determined in 12 patients who had undergone cardiac operation using extracorporeal circulation from March to August 1991. Changes in AKBR were compared with those before and after extracorporeal circulation. AKBR decreased significantly after the beginning of extracorporeal circulation (p < 0.001) and remained at a lower level throughout extracorporeal circulation. On termination of extracorporeal circulation, the initial level was immediately resumed. The extent of decrease in ketone body ratio at ten minutes before termination of extracorporeal circulation was correlated with short term postoperative hepatic insufficiency. The patients whose ratio decreased below 0.4 showed increased levels in glutamic-pyruvic transaminase at the end of the first and second week after operation. Changes in AKBR were significantly associated with those in blood pressure (r = 0.433; p < 0.005) and body temperature (r = 0.472; p < 0.005). It was concluded that blood pressure and body temperature influence the blood ketone body ratio during extracorporeal circulation.
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PMID:Effects of extracorporeal circulation on blood ketone body ratio reflecting hepatic energy metabolism during cardiac operation. 821 4