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

A dramatic decrease in mortality from Hemophilus influenzae meningitis has occurred in recent years. Morbidity and long-term sequellae remain significant problems. A follow-up investigation of 73 cases of H. influenzae meningitis seen over a three-year period revealed: 2 deaths, 6 children with major sequellae (retardation, spastic quadriplegia, blindness, persistent seizure disorder), 10 with minor residua, and 55 with no detectable disability. Statistical analysis of clinical parameters demonstrated a significant risk of death or major morbidity in those patients who, at the time of admission, had seizures, coma, hypothermia, shock, age less than 12 months, hemoglobin less than 11 gm/100 ml, pretreatment symptoms for longer than three days, a spinal fluid white blood cell count less than 1,000/cu mm, or a spinal fluid glucose value less than 20 mg/100 ml. Using these parameters, those patients at highest risk of having lasting major morbidity with H. influenzae meningitis can be predicted, allowing more vigorous intensive care which may reduce the mortality and morbidity further.
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PMID:Prediction of morbidity in Hemophilus influenzae meningitis. 84 May 37

Cultured fetal mouse hearts deprived of oxygen and glucose were used to examine the effect of temperature on the mechanical, biochemical, and ultrastructural responses of the deprived myocardium to assess the utility of this in vitro model for studying myocardial necrosis, preservation, and repair. After 4 h of deprivation at 4, 24, 37, or 42 degrees C, 1) beating had ceased;2) ATP levels were decreased by 22% for 4 degrees C insults, 69% for 24 degrees C, 89% for 37 degrees C, and 97% for 42 degrees C; 3) CPK and LDH levels were unchanged; and 4) ultrastructural changes were observed. After 24 h of recovery from deprivation, 1) beating resumed, except for 42 degrees C;2) ATP levels were 102% of control for 4 degrees C; 99% for 24 degrees C; 62% for 37 degrees C; and 4% for 42 degrees C; 3) LDH content was decreased by 0% at 4 degrees C; 6% at 24 degrees C; 35% at 7 degrees C; and 70% at 42 degrees C; and 4) CPK content decreased similarly. Hypothermia protected deprived myocytes while hyperthermia accelerated cell necrosis. Combining deprivation with thermal insult in this in vitro model provides a spectrum of myocardial damage for studying the effect of interventions on repair processes and on metabolic changes in jeopardized myocardium.
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PMID:Thermally induced myocardial preservation and necrosis in deprived fetal mouse hearts. 84 85

The concentrations of blood glucose, serum insulin, free fatty acids, and triglycerides were examined preoperatively, during anesthesia, during extracorporeal circulation, and during the following 3 postoperative days in 29 patients. The patients were divided into three groups according to the duration of extracorporeal circulation and the use of hypothermia: short perfusion group (SPG, bypass time shorter than 60 minutes, 15 patients), long perfusion group in normothermia (LPGN, bypass time longer than 60 minutes, 8 patients), and long perfusion group in hypothermia (LPGH, temperature during bypass below 33 degrees C., 6 patients). In all three groups, the concentrations of free fatty acids and blood glucose rose significantly because of anesthesia (p less than 0.001). After cardiopulmonary bypass, the concentrations of free fatty acids diminished significantly. The blood glucose remained at high level until the second postoperative day and was significantly higher in the LPG than in the SPG (p less than 0.05). The serum insulin level remained low during anesthesia and extracorporeal circulation in the SPG and LPGH but rose during the postoperative period; the maximal values were recorded on the first postoperative day. There were no significant differences between the groups with regard to serum insulin during the study. These changes and their metabolic background are discussed.
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PMID:Effects of open-heart surgery on carbohydrate and lipid metabolism. 85 Apr 24

Unanesthetized, male rats were exposed to normal air (NA), or NA and a 4 h-exposure of He-O2 (79% helium, 21% oxygen) at ambient temperature (Ta) of 22 or - 10 degrees C. Blood samples from each individual were taken from a chronically implanted carotid cannula at 1) preexposure, 2) during exposure, 3) 2.5 h after exposure, and 4) 19-20 h after exposure. Exposure to He-O2 at 22 degrees C caused an increase in plasma free fatty acids (FFA) and corticosterone of 45% and 49%, respectively, with little change in plasma glucose and thyroxine. Exposure to He-O2 at 10 degrees C for 3 h invariably induced hypothermia with body temperature (Tb) decreased to 23.7 +- 0.5 degrees C (N = 10). During hypothermia, plasma glucose, FFA, and corticosterone were significantly higher (P LESS THAN 0.05) than those at preexposure and those after exposure to NA at -10 degrees C. During spontaneous recovery from hypothermia, at Ta = 19 degrees C and NA, glucose, corticosterone, and thyroxine returned to normal, but FFA remained significantly higher than at preexposure. The ability of animals to rewarm spontaneously from hypothermia and the quick return of metabolic substrates and hormones to normal after rewarming indicates the preservation of regulatory mechanisms for metabolism at depressed Tb when hypothermia is induced by He-O2 and cold.
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PMID:Changes in plasma glucose, FFA, corticosterone, and thyroxine in He-O2-induced hypothermia. 86 34

The variations of plasma glucose and insulin levels were studied during the course of deep hypothermia with cardiocirculatory arrest of 60 minutes in 3 experimental groups of dogs using a pump mixture of homologous blood and Ringer's lactate solution at 33%, 50%, and 100% hemodilution. Insulin levels decreased in all groups during the cooling period and remained stable throughout the rest of the experiments, showing a slight significant increase only at the end of rewarming after a temperature of 30 degrees C was reached. Glucose levels reacted similarly except during rewarming, where an important increase in glucose concentration greatly preceded the rise in insulin. We stress the importance of this dissociation in view of the possible clinical implications that may exist.
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PMID:Plasma levels of glucose and insulin during deep hypothermia with varying degrees of hemodilution in dogs. 86 70

Nonshivering thermogenesis (NST) was examined during cold exposure (30 degrees C) in 5-day-old rats, during food deprivation. NST in the fed state doubled the O2 consumption observed at neutral temperatures. With fasting, the additional O2 consumption stimulated by cold dropped to that observed at thermoneutrality within 6 h, and colonic temperature (Tco) dropped concomitantly. Blood glucose (BG) concentration was halved. Oxygen consumption and Tco in the cold varied linearly with BG changes during food deprivation. 6-Hydroxydopamine transiently stimulated norepinephrine release and elevated metabolism nonadditively with cold stimulation in fed animals, and also stimulated O2 consumption. The drug also partially restored BG concentration, after it had declined during fasting. NST and BG were also restored by gastric infusion of glucose. These data suggest that the decline of NST, and the subsequent hypothermia during food deprivation, is in large part a sympathetically mediated reflex response to low cerebral BG concentration. However, glucose injection in doses sufficient to restore BG after fasting did not restore NST, nor was NST abolished by intracellular glucoprivation with 2-deoxy-D-glucose in fed rats. Thus, it is not argued that BG concentration is in itself an adequate signal for controlling NST.
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PMID:Sympathetic inhibition of thermogenesis in the infant rat: possible glucostatic control. 87 42

1 Intracerebroventricular injection of prostanglandin F2alpha (10-40 microgram) decreases food intake in a dose-dependent manner in rats trained to consume their daily total food intake in a 2 h period. 2 This anorexia is also observed in satiated rats, which had ad libitum access to food. 3 The anorectic activity of prostaglandin F2alpha is not modified by changes in the internal environment of the body after food intake, such as increased blood glucose and insulin levels and decreased fatty acid levels, or by the presence or absence of food in the stomach, as is evident from the anorectic activity of prostaglandin F2alpha in partially satiated rats. 4 The anorexia is not due to pain or irritative properties of prostaglandin F2alpha since induction of comparable pain with 3% acetic acid does not affect food intake in rats deprived of food for 22 hours. 5 Anorectic doses of prostaglandin F2alpha when injected intraperitoneally cause hypothermia. 6 The results suggest that the inhibitory activity of prostaglandin F2alpha on food intake is at both peripheral and central sites. 7 Prostaglandin F2alpha-induced anorexia is associated with the behavioural tranquilization that is seen after the ingestion of food.
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PMID:Some observations on the anorectic activity of prostaglandin F2alpha. 89 Feb 8

In surface-induced deep hypothermia, metabolic acidosis resulting from lactacidemia was observed. In the aspect of myocardial metabolism, the rate of reduction in coronary A-V difference ratio of lactate, pyruvate and NEFA was less than that of coronary flow and myocardial oxygen consumption in the hypothermic heart. Namely, it seems that lactate, pyruvate and NEFA play an important role as energy fuel in the hypothermic heart. On the other hand, myocardial metabolism of glucose was reduced in the hypothermic heart. Moreover, it seems that exogenous corticosteroid and ATP do not influence on the myocardial metabolism of carbohydrate and lipid in the hypothermic heart.
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PMID:Experimental studies on myocardial metabolism of carbohydrate and lipid in surface-induced deep hypothermia. 91 79

On the basis of the above discussion, a number of useful guidelines appear for the anesthetic management of alcohol and drug abusers. 1. Because of the decreased ability of intoxicated patients to withstand hemorrhage, blood replacement therapy should probably be instituted earlier than in the nonintoxicated patient. 2. Because the chronic alcoholic may actually be iso-osmotically overhydrated, fluid therapy must be planned with care. 3. Because of the tendency to hypoglycemia, glucose should be added to the fluid management regimen. 4. Because of the enzyme induction effect of chronic ETOH ingestion, anesthetic agents that are in part metabolized (methoxyflurane, halothane, fluroxene) are perhaps best avoided. Increased ability to metabolize anesthetic agents appears to be associated with toxicity. 5. Because ETOH is a CNS depressant and has been shown to have amnesia-inducing properties, supplementation of nitrous oxide-relaxant technique with narcotics or other depressant drugs should be reduced, if not eliminated. 6. Because acutely intoxicated individuals are more prone to hypothermia, their core temperature should be monitored intraoperatively. All intravenous fluids should be warmed and a warming blanket should be employed, if necessary, to maintain body temperature. 7. Because of the sympathomimetic effect of many of the drugs, pulse and blood pressure can be misleading in the assessment of blood loss.
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PMID:Preanesthetic care. Intoxication and trauma. 96 73

2-Deoxy-D-glucose (2-DG), insulin, or norepinephrine (NE), when injected into the cerebral ventricles of conscious mice, produce decreased rates of O2 consumption and hypothermia. These changes are accompanied by hyperglycemia with 2-DG, hypoglycemia with insulin, and normoglycemia with NE. Desipramine blocks the reduction in body temperature and O2 consumption produced by each of these agents, but does not modify significantly their effects on plasma glucose. The latter suggests that the thermal and oxidative responses to central glucopenia can be dissociated from concurrent alterations in circulating glucose. Propranolol enhances the hypothermic response produced by administered 2-DG, insulin, or NE. Phentolamine, however, antagonizes the hypothermia only with NE, indicating the 2-DG and insulin are probably not acting through the release of endogenous NE.
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PMID:Drug modification of hypothermia induced by CNS glucopenia in the mouse. 98 1


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