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

This study tests the hypothesis that the efficacy of cardioplegic solution depends upon its chemical constituents rather than on its temperature alone. A standard preparation of right heart bypass in the dog was utilized. Left ventricular function curves were inscribed before and after 1 hour of aortic cross-clamping. No deterioration in function was observed in nonischemic control hearts or in hearts protected with cardioplegic solution consisting of potassium chloride (25 mEq. per liter) and mannitol (12.5 Gm. per liter in 5 percent dextrose and 0.2 percent saline at either 4 degrees C or 28 degrees C. Severe myocardial depression was observed in hearts rendered ischemic for 1 hour at 28 degrees C. without protection and also in hearts perfused with 5 percent dextrose and 0.2 percent saline at 28 degrees C. without the potassium chloride and mannitol. The evidence from this study indicates that cardioplegic solution exerts a protective effect beyond that which is afforded by hypothermia.
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PMID:Effect of temperature of cardioplegic solution. 68 67

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. 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

Stress gastritis frequently occurs in association with shock or sepsis. Gastric mucosal ischemia appears to be a key feature in these critically ill patients. The University of Wisconsin cold preservation solution (UWS) is an isoosmolar, nonglucose-based perfusate that minimizes hypothermia-induced cell swelling and prevents intracellular acidosis and oxygen-free radical injury, while providing high energy substrates for donor organs. In a prospective, single-blind study, 18 similar Sprague-Dawley rats were randomly divided to receive only 5 per cent dextrose and water (D5W) (Group 1) or a 50 per cent solution of D5W+UWS (Group 2) for 72 hours. At the end of 72 hours the animals were stressed by the cold-restraint model. The mean number of ulcers for Group 2 was nearly half that of Group 1. Also, Group 2 had a significantly lower mean total ulcer length (P less than 0.005) and ulcer index (P less than 0.05). Most of Group 2 had mild gastritis changes (grade 0 to 1), while more than half of Group 1 had severe gastritis (grade 3). Gastric mucosal pH was similar for both groups. Topically applied UWS appears to reduce the severity and incidence of stress gastritis in this experimental model. Because mucosal pH values were similar, it is thought that UWS may alter the effects of gastric mucosal ischemia at a cellular level.
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PMID:Prevention of stress gastritis with tissue preservation solution. 158 84

Previous research has shown that microinfusion of bombesin into the preoptic area (POA) decreases core body temperature in rats that are food-deprived or made hypoglycemic with insulin. The present study employed 2-deoxy-D-glucose, a competitive inhibitor of glycolysis, to further investigate the importance of a reduction in glucose utilization in the production of bombesin-induced hypothermia. Rats (n = 7) were pretreated with 2-DG (0, 25, 50, 100, 200 mg/kg; IP) followed by bombesin (100 ng/1.0 microliters) microinfusions into the POA. The highest dose of 2-DG (200 mg) was also tested in the absence of bombesin as a control. Pretreatment with 2-DG resulted in a dose-related reduction in Tb following bombesin. Injections of 2-DG alone did not significantly alter Tb. The results provide additional evidence that the production of bombesin-induced hypothermia in fasted rats is linked to a reduction in glucose utilization.
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PMID:Bombesin produces hypothermia in rats pretreated with 2-deoxy-D-glucose. 204 13

The authors retrospectively reviewed the charts of 36 pediatric patients who had undergone cardiac surgery with hypothermic cardiopulmonary bypass (CPB) (n = 24) or profound hypothermia with circulatory arrest (PHCA) (n = 12), none of whom had received dextrose in the clear CPB pump prime, maintenance iv fluids, or cardioplegia solution. The authors studied whether the doses of fentanyl or methylprednisolone, or rates of dextrose infusion from blood products during CPB or from vasoactive infusions in 5% dextrose in water, were correlated with the blood glucose concentrations at the termination of CPB. Because other investigations have indicated that even moderate hyperglycemia during cerebral hypoxia or ischemia may predispose patients to an increased risk of neurologic deficit, the authors wished to determine whether any of these factors might contribute significantly to the elevation in blood glucose commonly seen in these patients. Multiple regression analysis and ANOVA were performed on these data, and a P value of 0.0125 was considered significant. The dose of methylprednisolone, and rates of infusions of dextrose from blood products in the CPB pump prime or from 5% dextrose in water at the termination of CPB did not correlated significantly with the blood glucose level. The dose of fentanyl administered to patients prior to the end of CPB was significantly correlated with the glucose concentration (r2 = 0.416; P = 0.0001). No patient who received greater than or equal to 50 micrograms/kg of fentanyl had a blood glucose concentration of greater than 200 mg/dl.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fentanyl dosage is associated with reduced blood glucose in pediatric patients after hypothermic cardiopulmonary bypass. 233 96

Spontaneous or induced diabetes, as well as glucose loading, reduce opiate antinociception, presumably through induction of hyperglycemia. While peripheral administration of alloxan is a potent pancreatic beta-cell toxin, intracerebroventricular (ICV) alloxan reduces glucoprivic feeding in the absence of hyperglycemia, presumably through interactions with specific brain glucoreceptors. Our laboratory demonstrated that opioid-mediated 2-deoxy-D-glucose (2DG) antinociception is significantly reduced by central pretreatment with alloxan, and that this deficit is reversed by coadministration with 3M-D-glucose. The present study compared ICV and intravenous (IV) routes of alloxan (200 micrograms) upon morphine (1-10 mg/kg, SC) analgesia on the tail-flick and jump tests in rats, and evaluated these effects in terms of concomitant changes induced by ICV alloxan upon nonopioid-mediated continuous cold-water swim (CCWS: 2 degrees C for 3.5 min) antinociception. Two weeks following central, but not peripheral pretreatment with alloxan, morphine (2.5 and 5.0 mg/kg, SC) antinociception was markedly (30-56%) reduced on both nociceptive tests. In contrast, central pretreatment with alloxan respectively reduced (30 min) and subsequently potentiated (60 and 90 min) CCWS antinociception on the jump test. Alterations in antinociception by central alloxan occurred in the absence of changes in basal nociceptive thresholds, hypothermia or hyperglycemia. These data suggest that central alloxan may be acting upon either specific, but unidentified brain glucoreceptors and/or a glucoprivic control mechanism.
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PMID:Differential actions of central alloxan upon opioid and nonopioid antinociception in rats. 262 9

Since hypothermia is commonly used to lower local and general metabolism during cardiopulmonary bypass, we attempted to identify its specific effects on glucose-insulin interactions. A group of nondiabetic patients undergoing hypothermic (28 degrees C) cardiopulmonary bypass with ischemic (cold) cardiac arrest was compared to a similar group operated on under normothermic conditions with potassium cardioplegia. In the absence of exogenous dextrose administration, hypothermia blocked insulin secretion for the duration of the operation. It also inhibited insulin secretion in response to an exogenous dextrose load (e.g., the priming fluid of the cardiopulmonary bypass circuit) or a glucagon injection, but this inhibition was lifted by rewarming. Blood glucose levels, which during normothermia were mildly elevated even in the absence of dextrose administration, remained normal during the hypothermic phase of cardiopulmonary bypass. By the end of the rewarming period, however, blood glucose levels had reached the same level as observed under normothermic bypass, a fact suggesting that the cold inhibition of hepatic glucose production had been only temporary. Cold inhibition of hepatic glucose production also explains why glucose clearance after a sudden dextrose load was initially faster at low body temperature than at normal temperature. Glucose-clamp studies indicated that insulin resistance was initiated by anesthesia and surgical trauma, and further accentuated by cardiopulmonary bypass, in association with elevated levels of hormones indicative of surgical stress. Regardless of body temperature changes, the assimilation of glucose by nondiabetic subjects during and immediately after bypass called for the infusion of large doses of insulin. A comparison with diabetic subjects showed that insulin-dependent patients (type I diabetes) required no more insulin during cardiopulmonary bypass than normal subjects, whereas patients with type II diabetes exhibited a marked insulin resistance during the operation and in the immediate postoperative period.
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PMID:Glucose-insulin interactions during cardiopulmonary bypass. Hypothermia versus normothermia. 351 20

Comparisons between early daytime and early nighttime effects of 2-deoxy-D-glucose (2DG) injections on food and water intake and rectal temperature were made. Food intake was significantly enhanced by 2DG injections regardless of the phase of the light cycle. In the daytime, water intake was increased by a lower dose of 2DG (200 mg/kg, IP) but there was no further increase at a higher dose (400 mg/kg). At night, the lower dose of 2DG had no effect on water intake but the higher dose suppressed the water intake normally associated with feeding. Administration of 2DG reduced preprandial rectal temperature in a dose dependent fashion in both phases of the light cycle. However, preprandial rectal temperatures were decreased more at night than during the daytime after injection of the higher dose of 2DG. Therefore, 2DG-induced hypothermia is dependent on both the dose of 2DG injected and the phase of the light cycle in which glucoprivation is produced. Furthermore, below a certain level of body temperature, rats markedly reduced drinking behavior while maintaining but not increasing their feeding response to 2DG-induced glucoprivation. These results suggest that behaviors may be directed toward preservations of body temperature in preference to relief of hunger by eating and of thirst by drinking.
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PMID:Effects of 2-deoxy-D-glucose on food and water intake and body temperature in rats. 370 71

The present study assessed in rats the effects of muscarinic receptor antagonism upon analgesia induced by cold-water swims (CWS: 2 degrees C for 3.5 min) and 2-deoxy-D-glucose (2DG: 600 mg/kg). First, CWS analgesia was significantly reduced 30 min after the swim by scopolamine (0.01 and 0.1 mg/kg) and methylscopolamine (10 mg/kg) pretreatment, and was eliminated 60 min after the swim by scopolamine (0.01-10 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment. In contrast, scopolamine potentiated CWS hypothermia. Second, while scopolamine (1 mg/kg) and methylscopolamine (1,10 mg/kg) pretreatment prolonged 2DG analgesia, both antagonists dose-dependently reduced 2DG hyperphagia. Third, the changes in analgesic and hypothermic stress responses were not due to baseline shifts in jump thresholds or body temperatures. However the dose-dependent reductions by scopolamine and methylscopolamine in baseline food intake and 2DG hyperphagia were significantly correlated. Fourth, the dose-dependent reduction by scopolamine and methylscopolamine of pilocarpine analgesia differed in pattern from the other analgesic effects, suggesting heterogeneity in muscarinic receptor modulation of different analgesic responses.
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PMID:Effects of muscarinic receptor antagonism upon two forms of stress-induced analgesia. 374 24


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