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

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

Anatomic lesions associated with hypothermia are variable and nonspecific. Only a few gross lesions and no microscopic pathology were noted in the acute deaths of this series. An interesting anatomic observation was the low weight of the lungs in 45% of the hypothermic deaths. Hypothermia is recognized as frequently producing hyperglycemia and 80% of a group of such patients clinically treated at the Hennepin County Medical Center had elevated blood sugar values. This correlates with an average vitreous glucose of 82.6 mg/dL in the hypothermic deaths. By contrast, the average vitreous glucose value found in each of two separate control groups was 37 mg/dL. Establishing hypothermia as the cause of death requires a proper history of exposure and the absence of any other clear-cut lethal factor. Certain biochemical tests may provide supporting evidence. Among these is an elevated vitreous glucose in a nondiabetic individual.
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PMID:Hypothermia: autopsy findings and vitreous glucose. 672 52

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
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PMID:A study of profound hypothermia by surface cooling. 677 40

This study was designed to sequence the earliest metabolic abnormalities associated with the development of obesity in the obese hyperglycemic mouse (C57BL/6J ob/ob). In situ lipogenesis was measured with 3H2O in fetuses at day 19 of gestation and in 5-, 10-, 15-, and 35-day-old mice. Preobese 15-day-old animals were identified on the basis of rectal hypothermia. The earliest increased accumulation of fatty acids was observed in the carcass of 15-day-old preobese animals (ob/ob) compared to their lean littermates (+/?) and known lean controls (+/+). The increased carcass lipogenesis in these animals was accompanied by an increase in plasma insulin concentration. Weaned 35-day-old obese animals showed a significant increase in hepatic and subcutaneous adipose tissue lipogenesis, plasma insulin, and glucose values when compared to their littermates (+/?). The results indicate that increased carcass lipogenesis, hyperinsulinemia, and hypothermia appear between days 10 and 15 and that these abnormalities precede the hyperglycemia and increased hepatic lipogenesis observed in the mature ob/ob mice.
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PMID:Early development of lipogenesis in genetically obese (ob/ob) mice. 699 15

Hypoglycemia is but one of a number of causes of hypothermia, but is important to keep in mind as a possible precipitating or concurrent event even in those cases in which there are other obvious explanations for decreased body temperature (exposure, alcoholism, starvation, sepsis or hypothyroidism). Hypoglycemia may occur in as many as 40 percent of very cold patients, and be clinically unrecognized because symptoms are masked by the hypothermia itself. Although serum glucose levels are depressed, a cold-induced renal tubular glycosuria may occur. Glucose in the urine, therefore, cannot be used as assurance of hyperglycemia in a hypothermic patient. And, although cold protects against serious end organ damage from hypoglycemia by decreasing tissue metabolic need for glucose, a serum specimen should be drawn for glucose determination in all hypothermic patients and a 50 percent glucose solution immediately given intravenously. If this is not done, serum glucose levels may plummet as the patient is rewarmed and begins to shiver.
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PMID:Hypoglycemia and accidental hypothermia in an alcoholic population. 723 90

The effects of 1.0, 3.0 and 5.0 g/kg of ethanol on blood glucose levels and body temperature were examined in rats submitted to either acute food deprivation (24 or 48 hr), chronic starvation, or to both chronic plus acute food deprivation. The results show that: (a) 3.0 and 5.0 g/kg produced either an increase or a decrease of glucose levels depending on the state of fasting; (b) rats not deprived of food presented hyperglycemia while being hypothermic; (c) a marked hypothermia was present when no substantial alterations in glycemia were observed; and (d) in cases where hypoglycemia and hypothermia occurred, the fall in body temperature paralleled or preceded the decrease in glucose levels.
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PMID:Blood glucose and body temperature alterations induced by ethanol in rats submitted to different levels of food deprivation. 729 Dec 58

In continuing our studies on the effects of preinduced hypothermia on the endurance capacities, thermoregulatory responses, and clinical chemical indices of heat injury, 10 mg of 5-thio-D-glucose (5-TG) were administered intravenously to restrained rats kept at 4 degrees C. When rectal temperatures (Tre) fell to 29-30 degrees C, the rats were removed to a hot environment (35 degrees C), where they exercised on a level treadmill (9.14 m/min) to hyperthermic exhaustion (Tre = 41.5-43 degrees C). Preinduced hypothermia was effective in significantly (p < 0.001) prolonging the time to hyperthermic exhaustion. In these hypothermic rats, increments in Tre (degree C/min) while on the treadmill were significantly (p < 0.001) increased while rates of skin temperature (Tsk) heating were significantly (p < 0.001) reduced when compared to normothermic controls. Administration of 5-TG effected significant (p < 0.001) hyperglycemia, which returned to control levels following the exhaustive run in the heat. Prolonged endurance times among the hypothermic rats caused slight increases in the levels of circulating plasma indices of heat/exercise injury. We concluded from these studies that hypothermia induced by 5-TG administration and cold exposure is effective in increasing the endurance capacity of rats exercising in the heat. However, homeostatic mechanisms supercede to increase the heating rate, and thus return Tre to equilibrium levels.
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PMID:Hypothermia induced by 5-thio-D-glucose: Effects on treadmill performance in the heat. 741 40

Adult male mice were administered several doses of 5-thio-D-glucose (5-TG) at two environmental temperatures, 4 and 22 degrees C. Both intracerebroventricular (icv) and intraperitoneal (ip) administration of 5-TG resulted in significant (P < 0.05 to P < 0.001) decrements in rectal temperature (Tre) that were dose dependent. After 30 min, the hypothermic effects were significantly (P < 0.001, icv, 100 microgram) exacerbated by cold exposure (4 vs. 22 degrees C) and were likewise intensified significantly (P < 0.005, 45 min, fed vs. 18 h fasted) by food deprivation. These reductions in Tre were accompanied by significant (P < 0.001) increases in circulating levels of glucose. The present results indicate that 5-TG may be eliciting both central and peripheral cellular glucopenia concomitant with circulatory hyperglycemia; thus, the resultant hypothermia may be arising from competitive inhibition of glycolysis by 5-TG intermediates as well as reduced availability of tissue glucose.
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PMID:5-Thio-D-glucose: hypothermic responses in mice. 743 91

We present a 66-year-old man with morning fasting hypoglycemia from an unknown cause associated with markedly suppressed levels of insulin. In this patient we examined the diurnal changes of plasma corticotropin-releasing hormone (CRH). ACTH, cortisol, glucose, insulin and body temperature, and the correlations among them. We also discussed an implication of plasma CRH in glucose metabolism by taking these findings together with results from previous studies on plasma CRH in diabetic or hypoglycemic animals and human beings. In this case, the stress induced by severe spontaneous hypoglycemia in the morning fasting state increased CRH in plasma compared to the euglycemia state and simultaneously activated the hypothalamic-pituitary-adrenal system as well as the sympathetic nervous system remarkably. The daily intravenous infusion of glucose brought the fasting hypoglycemia to normal and hypothermia to normothermia in the morning, and improved no or blunt responsiveness of insulin to glucose. On the 50th day of therapy, the i.v. infusion of glucose quickly produced moderate hyperglycemia and an increase in plasma insulin, and inhibited secretions of CRH, ACTH and cortisol. The source of plasma CRH remains obscure. However, the positive correlations of plasma CRH with both plasma ACTH and cortisol and several lines of evidence indicate that CRH in peripheral plasma is derived from both the hypothalamus and extrahypothalamic peripheral tissue and that during stressed conditions, in particular, the CRH increase in plasma is derived mainly from the paraventricular nucleus of the hypothalamus. The role of CRH not only in the systemic circulation but also in the endocrine pancreases for glucose metabolism remains to be clarified.
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PMID:[Peripheral plasma corticotropin-releasing hormone (CRH) in an aged patient with fasting hypoglycemia associated with an insufficient secretion of insulin: an implication of plasma CRH in glucose metabolism]. 755 77

A prospective randomized trial comparing retrograde warm blood cardioplegia with cold oxygenated crystalloid cardioplegia in coronary bypass patients at Emory University revealed an increased risk of adverse neurological events in the warm group (4.5% vs 1.4%, p < 0.005). Multivariant analysis found four variables to be independent predictors of adverse neurological outcome: congestive heart failure (p = 0.002); age (p = 0.002); aortic cross-clamp time (p = 0.02); and randomization to the warm group (p = 0.026). In Toronto, a prospective randomized trial compared antegrade warm blood cardioplegia with antegrade cold blood cardioplegia. Compared to the Emory trial, the Toronto series contained fewer female patients (16% vs 25%), fewer patients older than age 70 (16% vs 30%), and fewer redo operations (4% vs 14%). The other prominent differences between the Emory series and the Toronto series were: extensive use of retrograde cardioplegia in the Emory series; mild hypothermia in the warm group in the Toronto series; and elevated serum glucose in the warm group in the Emory series. The Toronto series showed no difference in adverse neurological events comparing cold versus warm cardioplegia groups. A comparison of these two series suggests that mild hypothermia in the Toronto series, elevated glucose in the Emory series, or the use of retrograde cardioplegia may be operative in the elevated incidence of adverse neurological events seen in the Emory series in addition to a relatively larger number of high-risk patients (female, elderly, and redo) in the Emory series.
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PMID:A critical assessment of neurological risk during warm heart surgery. 757 47


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