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 current study was undertaken so that the effects of both ischemia and ischemia + hypothermia could be examined in mammalian liver. Particular reference was made to the function of glycolysis, which is the only mechanism for energy production under these conditions. The response of adenylate pools reflected the energy imbalance created during warm ischemia within minutes of organ isolation. ATP levels and energy charge values for control (freshly isolated) livers were 1.20 +/- 0.07 and 0.49 +/- 0.02 mumol/g. Within 5 min of warm ischemia, ATP levels had dropped well below control values and by 30 min warm ischemia, ATP, AMP, and E.C. values were 0.21, 2.01, and 0.17 mumol/g, respectively. Cold ischemic livers (flushed with Marshall's citrate solution and stored on ice) exhibited similar, but more protracted, patterns of adenylate depletion (ATP and ADP) and accumulation (AMP). In both warm and cold ischemic livers, levels of fructose-6-phosphate (F6P) and fructose-1,6-bisphosphate (F1,6P2) indicated a marked activation of glycolysis at the phosphofructokinase (PFK) locus after a certain time of ischemia. Although the activations occurred at different times (30 min and 10 h for warm and cold ischemic livers, respectively), the patterns of change in levels of glycolytic metabolites associated with the PFK-catalyzed reaction were similar; levels of F6P dropped and F1,6P2 increased. Changes in metabolite levels (phosphoenol pyruvate and pyruvate) associated with another key suspect regulatory enzyme, pyruvate kinase, indicated no role in regulatory control of glycolysis during warm or cold ischemia. The activation of PFK at 30 min and 10 h of warm and cold ischemia, respectively, may reflect the accumulating effects of loss of intracellular homeostasis, which leads to impending irreversible damage.
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PMID:Glycolysis and energy metabolism in rat liver during warm and cold ischemia: evidence of an activation of the regulatory enzyme phosphofructokinase. 798 53

The present study was carried out to investigate mechanism of adaptogenic activity of seabuckthorn dry leaves aqueous lyophilized extract, administered in rats at a dose of 100 mg/kg body weight prior to cold (5 degrees C)-hypoxia (428 mmHg)-restraint (C-H-R) exposure up to fall of T(rec) 23 degrees C and recovery (T(rec) 37 degrees C) from C-H-R induced hypothermia. The effect of extract treatment was studied on key metabolic regulatory enzymes in blood, liver and muscle and tissue glycogen in rats on attaining T(rec) 23 degrees C and post stress recovery of T(rec) 37 degrees C. In control rats during C-H-R exposure on attaining T(rec) 23 degrees C there was significant decrease in enzyme activities of blood hexokinase (HK), citrate synthase (CS) and glucose-6-phosphate dehydrogenase (G-6-PD); liver CS; and in muscle glycogen, and CS and G-6-PD activities. In control rats on recovery of T(rec) 37 degrees C there was also a significant decrease in liver and muscle glycogen levels along with decreased enzyme activities of blood G-6-PD; liver CS; and liver and muscle G-6-PD. This suggested that during severe stressful exposure to C-H-R and post stress recovery the aerobic metabolism as well as hexose monophosphate (HMP) pathway is suppressed. The single and five doses extract treatment restricted the decrease or better maintained tissue glycogen and enzyme activities, viz. HK, phosphofructokinase (PFK), CS and G-6-PD, in blood, liver and muscle, during C-H-R exposure (T(rec) 23 degrees C) and recovery of T(rec) 37 degrees C. The results suggest that seabuckthorn extract treatment caused a trend for shifting anaerobic metabolism to aerobic during C-H-R exposure and post stress recovery.
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PMID:Possible mechanism of adaptogenic activity of seabuckthorn (Hippophae rhamnoides) during exposure to cold, hypoxia and restraint (C-H-R) stress induced hypothermia and post stress recovery in rats. 1767 45

Mechanism of rhodiola root extract adaptogenic activity was studied in rats. The extract was orally administered in rats (100mg/kg body weight), 30 min prior to cold (5 degrees C)-hypoxia (428 mmHg)-restraint (C-H-R) exposure up to fall of T(rec)23 degrees C and recovery (T(rec)37 degrees C) from hypothermia. In untreated control rats serum lactate and non-esterified fatty acids (NEFA) increased on attaining T(rec)23 degrees C with decreased blood enzyme activities hexokinase (HK), phosphofructokinase (PFK), citrate synthase (CS) and glucose-6-phosphate dehydrogenase (G-6-PD), on attaining T(rec)23 degrees C and T(rec)37 degrees C. Decreases were also observed in liver and muscle tissues HK and G-6-PD enzyme activities and liver glycogen and CS on attaining T(rec)23 degrees C and recovery; muscle PFK during recovery; muscle CS on attaining T(rec)23 degrees C. Single and five doses of extract administration restricted increase in serum lactate values of rats on attaining T(rec)23 degrees C and maintained blood NEFA in single dose extract treated animals, indicating improved utilization of NEFA as energy fuel. The single and five doses extract treatment decreased or better maintained tissue glycogen and enzyme activities, viz. HK, PFK, CS and G-6-PD, in blood, liver and muscle, on attaining T(rec)23 degrees C and recovery. The results suggest that rhodiola extract treatment in rats shifted anaerobic metabolism to aerobic, during C-H-R exposure and post stress recovery.
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PMID:Mechanism of action of Rhodiola imbricata Edgew during exposure to cold, hypoxia and restraint (C-H-R) stress induced hypothermia and post stress recovery in rats. 1924 14