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

Hamsters undergo hypothermia when exposed to a mixture of 80% helium and 20% oxygen at low ambient temperatures. The hypothermic hamster, rectal temperature (Tre) 7 degrees C, becomes hypoglycemic, and reversal of hypoglycemia is effected with glucose infusion. Hypothermic hamsters at Tre 7 degrees C showed a fivefold increase in survival times from 20 to 100.5 h when infused with glucose which maintained a blood level at about 45 mg/100 ml. A potential role for osmotic effects of the infusion was tested and eliminated. There was no improvement in survival of 3-O-methylglucose or dextran 40-infused animals. The fact that death eventually occurs even in the glucose-infused animal after about 4 days and that VO2 undergoes a slow decrement in that period suggests that hypothermic survival is not wholly substrate limited. Radioactive tracer, [U-14C]glucose, showed that localization of the 14C, was greatest in brain tissue and diaphragm, intermediate in heart and kidney, and lowest in skeletal muscle and liver. The significance of the label at sites important to respiration and circulation was presented.
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PMID:A role for glucose in hypothermic hamsters. 99 Jan 11

A short-term cooling of adult rats and gophers up to 30, 25 and 20 degrees C is accompanied by a rise of the glucose level in blood. No dependence is found between lowering the body temperature drop and degree of glycaemia. Prolongation of hypothermia of 30 and 20 degrees C up to 3 h causes (as compared to the control) a decrease in the glucose amount in blood of gophers but not in the rats. The cooling of the eye-opening, month and adult rats up to 20 degrees C is accompanied by a significant increase in the content of glucose in the brain and skeletal muscles. Simultaneously in the eye-opening and adult animals, contrary to the month ones, the level of glucose in the liver and blood rises. The content of glucose in the brain of the normothermal gophers (61.2 mg.) is 3,4 times as high as in the rat brain. At all the studied stages of artificial hypothermia as well as at 15 and 30-day hibernation (5 degrees C) the amount of glucose of the gopher brain remains at a relatively high level (41.6-101.5 mg%).
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PMID:[Glucose content in the tissues of susliks and rats of different ages under hypothermia]. 102 9

In surface-induced deep hypothermia, metabolic acidosis resulting from lactacidemia was observed. In the hypothermic heart, the rate of reduction in the coronary arteriovenous (A-V) difference ratio of lactate, pyruvate, and nonesterified fatty acids (NEFA) was proportionately less than that of coronary flow and myocardial oxygen consumption, suggesting that lactate, pyruvate, and NEFA play important roles as energy fuels in the hypothermic heart. Myocardial metabolism of glucose was reduced; exogenous corticosteroids and ATP do not influence the myocardial metabolism of carbohydrates and lipids in the hypothermic heart.
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PMID:Experimental studies on myocardial metabolism of carbohydrates and lipids in surface-induced deep hypothermia. 103 4

The authors review the intraoperative use of elective hypotension to reduce the probability of hemorrhage, to increase pliability of the aneurysmal sac for ease of clip application, and to control hemorrhage. The optimum agent and techniques for lowering systemic blood pressure remain controversial, but trimethaphan, sodium nitroprusside, and halothane have been found most useful. When cerebral blood flow falls below the brain's capacity to autoregulate, distinct time-related alterations occur biochemically and histologically. The profile of prolonged reduced adenosine triphosphate (ATP), low phosphocreatine, low glucose, and elevated lactate and lactate/pyruvate ratio is associated with swelling of perivascular astrocytes and "blebbing" of vascular endothelial cells with subsequent cerebral damage. To prevent permanent alteration it is desirable to observe time constraints and to employ other means of protection such as hypothermia, although the authors believe the latter unnecessary for short hypotensive periods. It has been proposed, but not substantiated, that anesthetics which depress rate of cerebral oxygen consumption but do not affect cerebral ATP level protect the brain from hypotension. Several investigations suggest that halothane, a vasodiltor, satisfies the safety requirement. The most prominent contraindication to halothane, however, is elevation of intracranial pressure. At present hypotensive surgery for aneurysmorrhapy is usually performed when intracranial pressure has returned to normal. Experimentally the electroencephalogram has been observed to show alterations prior to biochemical parameters for following brain vulnerability, so that it conceivably could be an effective monitoring technique during prolonged profound hypotension.
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PMID:Systemic hypotension in neurosurgery. 110 33

The effect of temperature on myocardial protein synthesis was evaluated using L-[14C]phenylalanine incorporation into total protein of isolated rabbit right ventricular papillary muscles. Muscles were incubated in oxygenated Krebs-Ringer buffer containing tracer amino acid at temperatures of 25-43 degrees C or incubated without tracer at varying temperatures up to 120 min and then incubated at 37 degrees C for an additional 2 h with the tracer present for the final hour of incubation. Higher as well as lower than physiological temperatures depressed tracer amino acid incorporation. Recovery of myocardial protein synthesis from thermal injury was incomplete when the experimental temperature deviated by 6 degrees C or more from the control and exposure exceeded 60 min. In addition, tracer amino acid incorporation on reoxygenation and return to 37 degrees C in muscles exposed to anoxia at 25 degrees C did not differ from that in muscles exposed to anoxia at 37 degrees C. Specific activity of the intracellular amino acid pool was directly measured in appropriate experiments and variation of this parameter could not account for the depressed tracer amino acid incorporation. Likewise methylprednisolone (10-5 M), chloroquine phosphate (10-5 M), and glucose (15 mM), if present during hyperthemia, did not ameliorate thermal damage. It is concluded that hyperthermia as well as hypothermia can cause irreversible alterations rather than reversible inhibition of myocardial protein synthesis.
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PMID:Thermoregulation of myocardial protein synthesis. 111 53

1. Hypothermia induced by infusion of noradrenaline into the hypothalamus of 2-3 week old chicks, within their thermoneutral range, was considerably potentiated by lowering ambient temperature. 2. Noradrenaline-induced hypothermia was associated with reduced carbon dioxide elimination and reduced blood lactate concentrations whereas leg temperature, electromyographic activity, plasma NEFA and plasma glucose concentrations were increased. 3. Mechanisms postulated to explain the phenomenon are inhibitory and facilitatory effects of noradrenaline on some, but not all, heat production and heat loss mechanisms. Increased electromyographic activity after intrahypothalamic noradrenaline is assumed to be due to lack of effect of noradrenaline on spinal thermosensitive centres; increased plasma NEFA concentration may be due to inhibition of NEFA utilization.
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PMID:Effects of noradrenaline infused into the chick hypothalamus on thermoregulation below thermoneutrality. 114 57

Plasma growth hormone (plasma GH) and blood-glucose concentrations were measured in 23 patients undergoing open heart surgery with moderate hypothermia. A significant increase in blood-glucose concentration occurred with sternotomy and increased during bypass, partly as a result of the exogenous glucose load from the perfusate. Following bypass, the blood-glucose remained above the pre-anaesthetic concentration, and this elevation persisted into the period following surgery. Plasma GH also increased with surgery and remained elevated during perfusion. The highest concentrations occurred following bypass when normal temperature had been regained .
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PMID:Growth hormone and blood-glucose concentrations during cardiopulmonary bypass. 114 89

1. The rise in blood glucose and the fall in body temperature which follows the injection of a glucose analogue, 2-deoxy-D-glucose (2-DG) into the lateral cerebral ventricle (I.C.V) of unanaesthetized rats were studied and found to be dose-dependent. These 2-DG induced responses are elicited by the impairment of glucose metabolism within central "glucoreceptors'. 2. 2DG induced hyperglycaemia and hypothermia were completely prevented and even the converse effects occurred when fivefold equimolar amounts of D-fructose were simultaneously injected I.C.V.; fructose, at equimolar doses, did not modify the effects of 2-DG. 3. D-xylose and D-ribose, even at high doses, did not influence 2-DG hyperglycaemia, but increased slightly the 2-DG induced hypothermia. This suggests that the pentose phosphate pathway is unable to support the metabolism within the glucoreceptors. 4. Pyruvate suppressed the 2-DG induced hyperglycaemia with a marked delay, while acetate (as ethyl ester) and a mixture of malate plus oxaloacetate did not prevent 2-DG induced effects. These results may be accounted for by the low dosage used. 5. Acetoacetate and 3-hydroxybutyrate did not prevent 2-DG hypothermia and hyperglycaemia. 6. An effective prevention of the 2-DG induced hyperglycaemia and hypothermia was achieved with fumarate and glutamate, indicating that the stimulation of the Krebs cycle within "glucoreceptors' removes the glucoprivic effects. 7. The results indicate that prevention of 2-DG induced effects occurred only with alternate source of metabolic fuel which can support high respiratory rates in brain tissue. It is concluded that central chemoreceptors are not specifically responsive to glucose, or hexoses, but to the rate of oxidative metabolism.
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PMID:Sensitivity of central chemoreceptors controlling blood glucose and body temperature during glucose deprivation. 115 83

An earlier study reported an increased resistance of chickens to an acute lethal heating episode (43 degrees C. and 45% relative humidity) during aflatoxicosis. This varies from other stresses investigated which interact with aflatoxicosis to make chickens more sensitive to the stress factor. The effects of graded doses of dietary aflatoxin (0, 0.625, 2.5, 5.0, and 10.0 mug./g.) on the body temperature, on body fat, on the serum glucose, and on the effect of varying the severity of the heat stress were measured. Both serum glucose and total body fat were decreased significantly (P less than 0.05) by doses of 2.5 mug./g. and above. Cloacal temperature was decreased slightly but significantly (P less than 0.05) in chickens fed 5 or 10 mug./g. for 12 days or longer. The mean survival time of birds exposed to a heat stress of 40 degrees C. and 45% relative humidity did not vary with the dose of aflatoxin while a milder stress of 37 degrees C. and 45% relative humidity caused chickens fed aflatoxin at 2.5 mug./g. or above to show decreased survival times (P less than 0.05) in comparison to the controls. These data can be rationalized by assuming that the lessened burden of body fat during aflatoxicosis accounts for the increased survival time in a severe (43 degrees C. and 45% relative humidity) heat stress but that other parameters related to physiological stress play a dominant role during a less severe but more prolonged heating episode. It seems likely that the hypoglycemia, hypothermia, and lessened body fat also account for the previously reported increased sensitivity to a lethal cold exposure during aflatoxicosis.
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PMID:Interaction of aflatoxicosis with heat stress. 116 99

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


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