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

We have observed an association between hypothermia and hypokalemia in a number of postoperative patients. In order to analyze the incidence and consequences of this correlation, 108 patients undergoing major operations were prospectively studied. Rectal temperature, serum and urinary potassium, arterial blood gases, blood glucose, and routine monitoring were analyzed. Hypothermia occurred in 35 (32%) patients, of whom 20 (57%) suffered from hypokalemia. Hypothermia was accompanied by an undercompensated metabolic acidosis in 15 (75%) and hyperglycemia in 18 (89%), while nine (45%) patients had cardiac dysrhythmias. Urinary potassium excretion was lower in hypothermic patients and therefore cannot explain the finding of hypokalemia. Administration of NaHCO3, insulin, digitalis, and calcium in patients suffering from hypothermia must be done with caution because hypokalemia may coexist with low body temperature and predispose the patients to lethal dysrhythmias.
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PMID:Correlations of serum potassium fluctuations with body temperature after major surgery. 381 76

We studied perinatal care and causes of death in 182 newborn infants who died during the first 28 days of life in the children's hospitals of Bochum, Datteln, and Essen in 1981-1983. Birth weight was below 2 500 g in 73%, cerebral hemorrhage was found in 15% of the infants. Most common causes of death were cardiorespiratory maladaptation (60%), congenital malformation (27%), and severe infection (12%). 90 infants died on the first day, 138 within the first week of life. A matched pair analysis comparing 153 deaths above 750 g with survivors of similar birth weight demonstrated preventable factors in half of the neonatal deaths: hypothermia, acidosis, blindbuffer and volume therapy, and hyperglycemia. More infants survived when born during the daylight hours and when a pediatrician was present at birth. Mortality and incidence of hypothermia were higher in small maternity units. In order to reduce neonatal mortality further, regional perinatal centres for high risk deliveries should be developed in Nordrhein-Westfalen.
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PMID:[Causes of neonatal mortality 1981-1983: a regional analysis]. 387 59

Plasma vasopressin (AVP) increases after endotoxin administration in freely behaving unanesthetized rats. The present experiments sought to determine the factors that mediate this vasopressin response. Endotoxin (150 micrograms/kg iv) elicited a significant increase in plasma AVP concentration. This response was accompanied by unchanged plasma osmolality, hypotension, increased hematocrit (reflecting decreased plasma volume), hypothermia, and hyperglycemia. Pretreatment with the prostaglandin synthesis inhibitor, indomethacin (5 mg/kg sc), had no effect on the vasopressin response to endotoxin but abolished or significantly attenuated the changes in blood pressure, hematocrit, temperature, and plasma glucose while leaving plasma osmolality unaltered. These investigations indicate that endotoxin stimulates vasopressin secretion into plasma independently of changes in plasma osmolality, systemic blood pressure, plasma volume, body temperature, or plasma glucose. The results also suggest that vasopressin responses to endotoxin are not mediated by prostaglandins, whereas prostaglandins do play a role in endotoxin's effects on blood pressure, plasma volume, temperature, and plasma glucose.
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PMID:Endotoxin increases vasopressin release independently of known physiological stimuli. 388 54

Ethanol, administered i.p., produced a dose-dependent increase in plasma norepinephrine and epinephrine concentrations in LS/Ibg (LS) but not in SS/Ibg (SS) lines of mice. Ethanol-induced elevations of plasma epinephrine in LS mice were approximately 10-fold greater than those observed in SS mice. Plasma epinephrine and norepinephrine attained peak concentrations at 20-min post-ethanol administration at doses ranging from 2.8 to 4.1 g/kg. Plasma catecholamines remained elevated for approximately 1 hr and returned to basal values 2 hr after ethanol administration. Significant correlations were obtained between blood ethanol (r = 0.99), plasma epinephrine (r = 0.92) and plasma glucose (r = 0.98) as a function of ethanol dose in LS mice. Chlorisondamine (3 mg/kg), a ganglionic blocker, abolished completely the ethanol-induced increase in plasma catecholamines. These results confirm previous suggestions that the response is centrally mediated through an increased sympathetic outflow rather than by a direct effect on the adrenal medulla. The increase in plasma epinephrine and associated hyperglycemia produced by ethanol was not observed with pentobarbital or halothane anesthesia. Ethanol-induced hypothermia was diminished markedly (47%) by an elevated ambient temperature (28 degrees C) without reducing the hyperglycemic response to ethanol. These results suggest that ethanol-induced hypothermia does not mediate ethanol-induced adrenomedullary catecholamine secretion and concomitant hyperglycemia. It is proposed that the differential ethanol-induced secretion of adrenomedullary catecholamines in LS and SS mice is due to differential central nervous system sensitivities to ethanol.
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PMID:Ethanol-induced adrenomedullary catecholamine secretion in LS/Ibg and SS/Ibg mice. 395 Aug 66

Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
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PMID:Water intoxication with seizures. 396 5

Glucocorticoids (GC) are important for thermoregulatory responses to low environmental temperatures. Pretreatment of hamsters, which are capable of natural hibernation, with cortisone acetate has been demonstrated to improve carbohydrate homeostasis during hypothermia. The objectives of the current studies were to evaluate the effects of GC pretreatment of a nonhibernator, the rat, on (i) cooling time, (ii) carbohydrate homeostasis (in terms of liver and cardiac glycogen concentrations and plasma glucose concentration), and (iii) duration of survival in hypothermia. In addition, the effects of liver glycogen depletion on cooling times and survival were examined. Hypothermia was induced in rats by exposure to a helium:oxygen (80:20, Helox) atmosphere at 0 degree C. Pretreatment of rats with triamcinolone acetonide (1.5 mg/kg/day, sc, 48, 24, and 1 hr prior to induction) significantly (P less than 0.05) lengthened induction time, while fasting was associated with a significant decrement (25%). While liver and cardiac glycogen levels in control and GC-treated rats fell approximately 45% during cooling, this reduction occurred over a significantly greater period of time in treated rats and suggests a sparing of glycogen or increased capacity for its production in response to GC. Glycogen utilization was accompanied by a hyperglycemia in control, GC-treated, and fasted groups. Survival in hypothermia at a rectal temperature of 14-15 degrees C in GC-treated (9.5 +/- 1.2 hr) and fasted (10.9 +/- 0.9 hr) rats was not significantly different from control (10.5 +/- 1.1 hr) values. These findings suggest that treatment with GC can increase the thermogenic capacity of the rat (as evidenced by an increased induction time) and promote carbohydrate homeostasis, but does not contribute to an enhancement of survival in the hypothermic nonhibernator.
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PMID:Glucocorticoids and hypothermic induction and survival in the rat. 402 83

Glucoprivic stress induced by 2-DG (2-deoxy-D-glucose) is associated with increased oxygen consumption (thermogenesis) and sympathetic nervous system activity, as well as elevations of circulating levels of various hormones and metabolic substrates. To examine the role of beta-adrenergic stimulation in the thermogenic, hyperglycemic, and lipolytic responses to glucoprivation, we administered intravenous infusions of propranolol or normal saline (placebo) during 2-DG challenges in seven healthy males. 2-DG alone produced large increments in plasma catecholamine levels, hyperglycemia, a 3.5-fold increase in plasma free fatty acid (FFA) levels, a 15 beat/min increase in pulse rate, and hypothermia in spite of a 20% increase in oxygen consumption. When propranolol was given, 2-DG produced only a 50% increase in FFA levels, no change in oxygen consumption, and a 17 beat/min fall in pulse rate associated with a 25% increase in mean arterial blood pressure. Propranolol only slightly attenuated the hyperglycemia and hypothermia associated with 2-DG but potentiated the elevations of plasma epinephrine levels. It is concluded that 2-DG-induced thermogenesis and lipolysis are primarily dependent on beta-adrenergic stimulation.
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PMID:Beta-adrenergic blockade inhibits thermogenesis and lipolysis during glucoprivation in humans. 612 26

In order to clarify the inhibitory mechanism of insulin secretion associated with open-heart surgery, the influence of insulin antagonistic hormones on insulin secretion was studied in 20 patients with congenital heart diseases undergoing open-heart surgery, under simple deep hypothermia. Despite a hyperglycemia, plasma immunoreactive insulin and C-peptide showed no change during the cooling period, while with the exception of plasma human growth hormone, dopamine-beta-hydroxylase, immunoreactive glucagon, cortisol and cyclic AMP in plasma, either showed no change, or a decrease during the cooling period. It is assumed that catecholamine, glucocorticoid and glucagon do not play an important role in the inhibitory mechanism of insulin secretion during hypothermic open-heart surgery, and a transient hypofunction of the pancreas as well as the liver and the adrenal gland is probably involved.
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PMID:Inhibitory mechanisms of insulin secretion associated with hypothermic open-heart surgery. 627 5

Procedures related to profound hypothermia and circulatory arrest have produced a great improvement in the operative results of cardiac repair in neonates and infants. As we already obtained data on the effects of these procedures on cerebral metabolism, we focussed our attention on carbohydrate metabolism to determine whether or not cardiopulmonary bypass with pulsatile flow would improve the results of bypass method for core cooling and rewarming. In 12 mongrel dogs under conditions of hypothermia, plasma levels of glucose, insulin and glucagon as well as cortisol and noradrenaline were monitored in both pulsatile and non-pulsatile bypass groups. The hyperglycemia was significantly depressed and insulin levels increased in cases of pulsatile flow. Thus, even under conditions of hypothermia, pulsatile flow results in an improvement of the blood flow in the pancreas and there is a more extensive utilization of glucose and a greater protective effect on the function of the visceral organs during bypass.
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PMID:Carbohydrate metabolism during pulsatile cardiopulmonary bypass under profound hypothermia. 634 59

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


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