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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interrelation between the energy and nitrogenous metabolism of the myocardium during cardioplegia has been studied in patients with congenital valvular heart disease (tetralogy of Fallot--12 patients, ventricular septal defect--5 patients). Whole body hypothermia with repeated heart reperfusion with cold cardioplegic blood perfusate was used for the protection of the myocardium. However, ATP level of the myocardium of some patients decreased by 20% and more of the baseline. This loss was accompanied by a reduction in glutamate and aspartate levels and a rise in ammonium and alanine levels in the myocardium (by 17.7 +/- 3.8; 17.6 +/- 5.9; 61.4 +/- 12.5 and 92.4 +/- 26.3% of the baseline, respectively).
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PMID:[Effect of cardioplegia on nitrogen and energy metabolism of the human heart]. 366 4

Changes in the concentration of amino acids and other metabolites were determined in the perfusate during 24 hr of ex vivo hypothermic perfusion of dog kidneys. There was an increase in concentration of most of the amino acids. Two patterns were identified. One showed an increase in concentrations up to 12 hr, and then a leveling off as exemplified by alanine, serine, and glutamate. The other pattern was one of persistent elevation as exemplified by phenylalanine, threonine, and methionine. Glucose, lactate, pyruvate, sodium, potassium, pH, and pO2 were also measured in the perfusate. The results suggest that a degradation of kidney protein may occur during the first 24 hr of perfusion. The levels of other metabolites measured support the fact that glycolysis is responsible for a considerable portion of the total energy production in the kidney under hypothermia.
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PMID:Changes in concentration of amino acids and other metabolites during hypothermic perfusion of the canine kidney. 374 9

The effects of several analogs of melanotropin-release inhibiting factor (MIF, Pro-Leu-Gly-NH2) on the development of tolerance to the hyperthermic, hypothermic and cataleptic actions of morphine were investigated in male Sprague-Dawley rats. The analogs that were examined included. Pro-Gly-Gly-NH2 (I), Pro-VAl-Gly-NH2 (II), Pro-Leu-beta-Ala-NH2 (III), Pro-Leu-Gly-NHCH3 (IV), Pro-Leu-NH2 (V) and cyclo (Pro-Gly) (VI). Subcutaneous implantation of four morphine pellets (each containing 75 mg of morphine free base) during a 3-day period was used to develop tolerance to the pharmacological effects of morphine. Concurrent daily subcutaneous administration of any of the above peptides (I through VI) at a 10 mu mol/kg dose did not modify the development of tolerance to morphine-induced hyperthermia, hypothermia or catalepsy. The development of tolerance to morphine was, however, inhibited by equivalent doses of MIF. Treatment with these peptides did not alter the distribution of morphine in brain and plasma. It is concluded that the structural requirements for the inhibitory effect of MIF on the development of tolerance to morphine are very strict and that the following modifications in the structure of MIF result in the loss of activity (a) substitution of Gly or Val in place of Leu (b) replacement of Gly-NH2 with Gly-NHCH3 or beta-Ala-NH2 (c) removal of Gly, and (d) removal of Leu followed by cyclization of Pro-Gly.
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PMID:Structure activity relationship studies with hypothalamic peptide hormones III. Effect of melanotropin-release inhibiting factor and analogs on tolerance to morphine in the rat. 612 92

The intracerebroventricular (i.c.v.) injection of taurine produced a fall in core temperature, the extent of which was dependent on the thermal gradient between the body and the environment. Concurrently, a sudden rise in ear skin temperature, which was maximal in the cold and negligible at 30 degrees C, was observed. The fever induced by i.v. injection of Escherichia coli endotoxin was antagonized by taurine. High temperatures produced by i.c.v. injection of prostaglandin E1 were also suppressed by taurine. Intracerebroventricular injections of bicuculline and strychnine, but not those of picrotoxin or pentylentetrazol, were able to reduce hypothermia induced by taurine. Intracerebroventricular injection of the taurine reuptake inhibitor guanidinoethyl sulfonate, on the contrary, did enhance the hypothermic response to taurine. Injection (i.c.v.) of serotonin (5-HT) elicited a fall in core temperature which was not accompanied by a rise in ear skin temperature, but was antagonized by the concurrent injection of the 5-HT antagonist methysergide. Pretreating animals with p-chlorophenyl-alanine caused a significant fall of brain 5-HT contents and a reduction of the hypothermic response to taurine. The latter effect was also observed when the animals were i.c.v. pretreated either the methysergide or with the 5-HT reuptake blockers chlorimipramine and Lilly 110140. These findings give support to the hypothesis that taurine-induced hypothermia in rabbits mediated by some taurine sensitive cells and, at least in part, by serotonergic synaptic mechanisms.
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PMID:Hypothermia induced in rabbits by intracerebroventricular taurine: specificity and relationships with central serotonin (5-HT) systems. 645 8

Physiological and toxicological effects of p.o. methyl parathion (0.375-3.0 mg/kg) or fenvalerate (1000-4000 mg/kg) were examined over a 10-h period in American kestrels (Falco sparverius) maintained in thermoneutral (22 degrees C) and cold (-5 degrees C) environments. Methyl parathion was highly toxic (estimated median lethal dose of 3.08 mg/kg, 95% confidence limits of 2.29-4.14 mg/kg), producing dose-dependent inhibition of brain and plasma cholinesterase activity, hyperglycemia, and elevated plasma corticosterone concentration. Brain and plasma cholinesterase inhibition in excess of 50% was associated with transient but pronounced hypothermia 2 h after intubation, although the magnitude of this response was variable. Fenvalerate, at doses far exceeding those encountered in the environment, caused mild intoxication and elevated plasma alanine amino-transferase activity. Cold intensified methyl parathion toxicity, but did not affect that of fenvalerate. Thus, it would appear that organophosphorus insecticides pose far greater hazard than pyrethroids to raptorial birds.
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PMID:Methyl parathion and fenvalerate toxicity in American kestrels: acute physiological responses and effects of cold. 649 9

Cooling of rats down to the rectal temperature of 20 degrees decreased the alanine- and aspartate transaminase activities in brain tissue. Activity of the enzymes studied was increased after prolongation of the hypothermia within 2 hrs. In adrenalectomized animals hypothermia was responsible for activation of aspartate transaminase and for a decrease in activity of alanine transaminase.
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PMID:[Alteration of activities of alanine- and aspartate transaminases in rat brain under conditions of hypothermia of various duration and in adrenalectomy]. 728 77

The time-courses of liver glycogen, plasma glucose, lactate, alanine and glycerol concentrations in term and preterm rats undergoing hypothermia (30 degrees C) during the first 2 h after delivery have been studied. Hypothermia prevented liver glycogenolysis and the neonatal decrease of plasma glucose concentration in term and preterm rats during the first 2 h after delivery. Hypothermia decreased plasma glucose, lactate and alanine utilization but increased plasma glycerol concentration. These results suggest that hypothermia blunts the utilization of the main metabolic substrates but increases brown adipose tissue lipolysis for thermogenesis.
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PMID:Prematurity in the rat. II. Effect of hypothermia. 736 59

1. Plasma concentrations of glucose, lactate, amino acids, non-esterified fatty acids, glycerol, ketone bodies, insulin and cortisol were measured in 43 elderly patients with hypothermia. In 15 of these patients forearm arteriovenous differences were also measured. Core temperatures ranged from 25.9 to 35.5 degrees C. 2. The metabolic state was of mobilization of glycogen and triacylglycerol stores, with high plasma concentrations of lactate and lipid metabolites. The plasma concentration of glucose was raised in those with hypothermia of a short duration (less than 6 h). In other patients it was low in those with core temperatures around 30 degrees C, but below this temperature it was variable and often high. Concentrations of other metabolites or hormones were not related to core temperature. 3. Plasma concentrations of cortisol were high and positively correlated with those of lactate and glycerol, suggesting active involvement in stimulation of muscle glycogenolysis and of lipolysis. 4. Plasma concentrations of insulin ranged from very low to very high and appeared to depend on the concentrations of both glucose and alanine. 5. Arteriovenous differences were generally small. There was peripheral release of lactate and of amino acids but no overall peripheral uptake of glucose. In nine out of 15 patients there was a significant peripheral release of glucose.
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PMID:Metabolic aspects of hypothermia in the elderly. 747 42

Central administration of exogenous cyclo(His-Pro) (CHP) is known to produce hypothermia in rodents. In the present study, we examined the role of endogenous CHP in cold-induced hypothermia in the desert rat, Mastomys natalensis. The results of these studies show that a rise in hypothalamic CHP content accompanied a decrease in rectal temperature during cold exposure. Immunoneutralization of endogenous CHP resulted in a significant decline in cold-induced hypothermia. In addition, central administration of cyclo(Ala-Gly), a structural analogue of CHP, also led to a decrease in cold-induced hypothermia. The results of these studies show that changes in endogenous CHP levels may affect body temperature regulation.
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PMID:Role of endogenous cyclo(His-Pro) in cold-induced hypothermia in the desert rat (Mastomys natalensis). 770 Aug 49

Myocardial preservation for prolonged ischemia has traditionally centered around deep hypothermia with metabolic arrest. This approach is limited in tolerable ischemic time by the state of energy reserves at the onset of ischemia, because anaerobic glycolysis during ischemia is limited by end-product accumulation (lactate, alanine, and H+). In this study we evaluated a novel preservation solution containing the basic amino acid histidine to buffer H+, glucose as substrate, and low sodium and calcium concentrations to mimic the intracellular ionic environment. Isolated rabbit hearts were subjected to hypothermic ischemia for 8 and 16 hours at 4 degrees and 21 degrees C followed by reperfusion. The buffered solution was compared to University of Wisconsin solution (high potassium). Intracellular pH was maintained at preischemic levels in the buffered solution hearts at 21 degrees C, and this was associated with better preservation of high energy stores and recovery of contractile function. Developed pressure recovered to 90% +/- 3% of preischemic values after 16 hours of 21 degrees C ischemia with the buffered solution as compared with 79% +/- 2% in the University of Wisconsin group at 4 degrees C (contracture occurred in the University of Wisconsin hearts at 21 degrees C). The optimal temperature in the buffered solution hearts was 13 degrees C, and with this temperature acceptable recovery of contractile function was seen after 24 hours of ischemia. On the basis of these results, we conclude that promoting anaerobic glycolysis during ischemia achieves superior prolonged preservation of energetic and contractile function of the heart.
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PMID:Evaluation of highly buffered low-calcium solution for long-term preservation of the heart. Comparison with University of Wisconsin solution. 793 14


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