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)

Like dibutyryl cyclic AMP, thyrotropin releasing factor (TRF) has potent antianesthetic properties, but only dibutyryl cyclic AMP shortens narcosis dose-relatedly. In contrast, only TRF reverses amobarbital-induced hypothermia (dose-relatedly). In naive rats, dibutyryl cyclic AMP (25-200 mug) induces convulsions while TRF (5-100 mug) produces intermittent hyperactivity and sedation but never convulsions. To determine whether behavioral events may be regulated in the central nervous system through an interaction of the two naturally occurring compounds, TRF (5-100 mug) and dibutyryl cyclic AMP (25-200 mug) were injected simultaneously into the lateral ventricle of the brain of naive rats or rats anesthetized with amobarbital (80 mg/kg). TRF (12.5-50 mug) and dibutyryl cyclic AMP (100-200 MUG) DID NOT SHORTEN NARCOSIS FURTHER THAN DIBUTYRYL CYCLIC AMP alone. Amobarbital protected against the lethal effects of the two compounds injected simultaneously. Long-lasting locomotor disorders and mortality rate increased with increasing doses of TRF (12.5-25 mug) and dibutyryl cyclic AMP (100-200 MUG) GIVEN TO NAIVE RATS. Results did not support the postulate that cyclic AMP is the second messenger of TRF.
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PMID:Regulation of behavioral events by thyrotropin releasing factor and cyclic AMP. 18 23

Calcium-free rat hearts develop separations of fascia adherens junctions of intercalated discs. Such hearts are susceptible to membrane injury and enzyme release during anoxic contracture. Anoxic enzyme release was exacerbated by distention of heart ventricles with a balloon. Dinitrophenol (DNP) and caffeine were used to induce contracture in calcium-free hearts. Both DNP and caffeine caused a massive enzyme release from calcium-free but not from control hearts. Caffeine-induced enzyme release occurred despite Amytal inhibition of mitochondrial respiration. These results demonstrate that in calcium-free hearts with contracture or ventricular distention, enzyme release occurred without calcium repletion, from hearts depleted of ATP and in the absence of mitochondrial function. A relationship between contracture-mediated enzyme release and the calcium paradox was suggested by studies of the effects of hypothermia on enzyme release. Hypothermia to 22 degrees C protects hearts against both the calcium paradox and anoxic, DNP and caffeine injury. The parallel temperature dependence of protection between contracture-mediated enzyme release and the calcium paradox is evidence that contracture may also be a mediator of sarcolemmal membrane injury and enzyme release in the calcium paradox.
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PMID:Mechanism of enzyme release in the calcium paradox. 666 35