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 ability of transient temperature variations for up to 120-min duration to affect myocardial protein synthesis (MPS) with return to normal temperatures was evaluated using 14C-phenylalanine incorporation into total protein of isolated rabbit right ventricular papillary muscles as in vitro model. Muscles were incubated in oxygenated Krebs-Ringer bicarbonate buffer containing tracer amino acid at temperatures of 28-43 degrees C or incubated without tracer at the same temperatures for up to 120 min and then incubated at 37 degrees C for an additional 2 hr with the tracer amino acid present for the final hour of incubation. Higher as well as lower than physiological temperatures depressed MPS. Recovery from thermal injury to MPS was significantly incomplete when the experimental temperature deviated by 6 degrees C or more from the control (28 and 43 degrees C, respectively) and exposure exceeded 60-min duration. Specific activity of the intracellular amino acid pool was directly measured, and variations in specific activity of the tracer pool were not responsible for the observed effects on MPS. Methylprednisolone (10(-5)M), chloroquine phosphate (10(-5) M), and glucose (15 mM) if present during hyperthermia did not ameliorate thermal damage. It is concluded that hypothermia causes inhibition as well as a degree of irreversible inactivation of the protein synthetic mechanism whereas hyperthermia causes predominant denaturation and irreversibile damage to MPS.
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PMID:Reversibility of thermal injury to myocardial protein synthesis. 121 32

In a pilot-study (n = 66) and subsequent controlled experiment (n = 32) the ischemic tolerance of dog liver is examined by means of various clinical and laboratory parameters. During normothermia and without venous decompression the time of ischemic tolerance amounts to 60 minutes. Hypothermia and systemic administration of Aprotinin (Trasylol) and Methylprednisolone (Urbason) do not prolong the tolerance time of ischemia. This time is significantly extended by pre-operative administration of a thiourea-derivate (Propycil). Basing on this decisive improvement of the ischemic tolerance of dog liver, new advances in increasing the ischemic tolerance of human liver are offered.
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PMID:[Efficacy of various treatment methods to extend the ischemia tolerance time of the liver. Experimental studies in dogs]. 170 Aug 71

With methylprednisolone as a chemical inhibitor of leukocytes, extended preservation was conducted with an isolated rabbit lung model. The heart-lung blocks of 39 New Zealand white rabbits were flushed in situ with 100 ml of Euro-Collins' solution, harvested, inflated (70%), and preserved at 4 degrees C. Lungs immediately reperfused with whole blood (control lungs, group 1) were compared with lungs preserved without methylprednisolone for 5, 12, and 24 hours (groups 2 to 4) and those preserved with methylprednisolone for 12 and 24 hours (groups 5 and 6, respectively). Methylprednisolone (30 mg/kg) was administered before harvest and was used as an additive to the flush and in the blood reperfusate. Hypothermia and Euro-Collins' flush alone provided adequate preservation for up to 5 hours; however, lung edema was evident by 12 hours of cold ischemia and became severe by 24 hours. By all measured parameters, the lungs in group 5 (treated with methylprednisolone) demonstrated values equal to or better than control lungs. By 24 hours of preservation the beneficial effects of the steroid treatment were no longer evident. Histologic evaluation revealed mild to moderate injury after 5 hours of cold ischemia; progressive edema and hemorrhage were found after 12 and 24 hours of preservation. This injury was significantly ameliorated by methylprednisolone treatment at 12 hours but not at 24 hours. This study suggests that static preservation for up to 5 hours is possible with hypothermia and a Euro-Collins' flush and that extended preservation to 12 hours is possible with pharmacologic dosages of methylprednisolone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Improved static lung preservation with corticosteroids and hypothermia. 319 47

Anoxic cardiac arrest was studied for one hour in five groups of dogs. Groups I-III were given methylprednisolone (30 mg/kg b.w.) before aortic cross-clamping. Normothermia was used with electrically induced ventricular fibrillation in group I, and without such fibrillation in group II, while group III was studied in local hypothermia. Propranolol (10 micrograms/kg) was given to group IV and verapamil (0.2 mg/kg) to group V before the anoxic arrest in local hypothermia. Judged from the ability of the heart to take over the circulation after anoxic arrest, local cooling preceded by propranolol or verapamil gave working performance comparable with the pre-arrest values. In the cooled, steroid-pretreated hearts the work capacity was depressed to the same degree as in locally cooled hearts without steroid premedication. Methylprednisolone prevented ischemic contracture during normothermic arrest with induced fibrillation, but not in the absence of such fibrillation. As adjuvant to local cooling, pretreatment with metabolism-reducing drugs is favorable for cardiac performance after arrest. Steroid premedication should be considered when normothermic arrest with electrically induced ventricular fibrillation is planned.
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PMID:Myocardial preservation during anoxic arrest. Premedication with propranolol, verapamil or methylprednisolone. 664 2