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

To clarify the impact of hypothermia on the hormonal control of glucose metabolism, rats were rendered hypothermic (25 C) after catheterization of the portal vein. Glucose, insulin, glucagon, and catecholamine concentrations were serially monitored, and the regional blood flows were measured, allowing the estimation of hormone outputs. Hypothermia reduced the portal blood flow by 50% without changing arterial blood pressure, blood gases, or pH. Portal plasma insulin secretion dropped (0.05 +/- 0.01 vs. 0.23 +/- 0.04 mU/min), and glucagon secretion increased (0.81 +/- 0.18 vs. 0.38 +/- 0.10 ng/min). The B cell responses to glucose, arginine, and glucagon were abolished, while the A cell response to arginine was not significantly affected. Glucose intolerance was apparent after iv glucose or arginine loads. Haloperidol and to a lesser extent phentolamine suppressed the cold-induced glucagon rise. Phentolamine and to a lesser extent haloperidol alleviated the cold-induced suppression of insulin release. Propranolol, naloxone, and atropine were relatively inactive. The cold-induced glucose intolerance was not corrected by phentolamine treatment. A marked resistance to iv insulin was apparent in these rats, which is in contrast to a normal sensitivity to iv glucagon.
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PMID:Glucagon and insulin secretion and their biological activities in hypothermic rats. 643 6

The effectiveness of cold exposure on the secretion of insulin and glucagon were examined using five adult sheep. Endocrine responses were studied in a warm environment and after cold exposure (0 C) from 4-19 days. Compared to levels at room temperature, basal plasma glucose levels were elevated during cold exposure, but basal levels of plasma insulin and glucagon were unchanged. Cold exposure significantly decreased the early insulin response to a primed iv infusion of glucose. Plasma glucose and glucagon levels during glucose infusion were unaffected by cold exposure. The decrease in plasma glucose after iv insulin injection (0.2 U/kg BW) was greater during cold exposure than at room temperature. Butyrate injection (0.625 mmol/kg, iv) resulted in a significantly lower secretion of both insulin and glucagon in the cold than in the warm environment. The glucagon response to arginine infusion (0.5 g/kg over 30 min, iv) was elevated by cold exposure, whereas the insulin response to arginine tended to be reduced. Propranolol infusion (20 micrograms/kg . min, iv) caused a slight inhibition of insulin secretion in the cold environment, but did not affect glucagon levels in either the cold or warm environment. Phentolamine infusion (20 micrograms/kg . min, iv) inhibited glucagon secretion, particularly in the cold environment, and caused a markedly greater stimulation of insulin secretion in the cold. It is concluded that cold exposure insufficient to cause hypothermia decreases insulin secretion in response to a variety of stimuli. Effects of cold on glucagon secretion depend upon the stimulating agent used.
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PMID:Effects of cold exposure on insulin and glucagon secretion in sheep. 675 53

Hypothermia in humans during insulin-induced glucopenia has been largely attributed to impaired heat production. To further study the mechanism for hypothermia during glucoprivation six normal males were given 20-min intravenous infusions of 2-deoxy-D-glucose (2-DG), 50 mg/kg, a competitive inhibitor of glucose utilization. Oxygen and carbon dioxide exchange was measured to determine heat production by indirect calorimetry. Decreases in core temperature were initially associated with activation of mechanisms for heat loss such as sweating and hyperpnea 30-120 min after 2-DG infusion. Hypothermia persisted in spite of markedly increased plasma catecholamine, glucose, and free fatty acid levels from 60 to 180 min and increased heat production from 120 to 180 min after 2-DG infusion. Thus in contrast to the proposed mechanism for insulin-induced hypothermia, the hypothermia of 2-DG-induced glucoprivation is a consequence of increased heat loss and not of decreased heat production.
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PMID:Thermoregulatory and related responses to 2-deoxy-D-glucose administration in humans. 677 17

Two series of experiments with the isolated perfused rat pancreas were performed in parallel. The conditions differed only with respect to temperature, which was 37.5 degrees C in one series and 28 degrees C in the other. The lowering of the temperature decreased insulin secretion induced by glucose as well as the insulin response to tolbutamide and acetylcholine. Unlike insulin, glucagon secretion was not significantly modified by hypothermia. Our results suggest that the mechanisms involved in glucagon and insulin secretion are different.
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PMID:Different effects of hypothermia on insulin and glucagon secretion from the isolated perfused rat pancreas. 699 4

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

Two series of experiments were performed in parallel on the isolated perfused rat pancreas. The experimental conditions differed only as pertaining to temperature. In one series the organ and the perfusion liquid were maintained at 37.5 degrees C and in the other at 28 degrees C. The pancreases were perfused from the start of the experiments with a perfusion medium containing 8.3 mmol/l glucose. The effects of various stimulatory agents were studied (glucose 16.6 mmol/l, tolbutamide 0.4 mmol/l, acetylcholine 0.5 micromole/l, glucagon, 2.8 nmol/l, and L-isoprenaline 0.05 micromole/l). At 37.5 degrees C the insulin secretion induced by high glucose or tolbutamide, acetylcholine, and glucagon was biphasic and not statistically different. In all cases the hypothermia (28 degrees C) decreased insulin secretion. However, glucose-induced and tolbutamide-induced insulin secretion was more decreased than the secretion induced by acetylcholine and glucagon. The study of the secretion ratios obtained at 28 degrees C relative to 37.5 degrees C showed that the ratios for the glucose and tolbutamide groups were significantly lower than those obtained for acetylcholine and glucagon groups for both the first and the second phase. The ratios were not significantly different between glucose and tolbutamide on the one hand and acetylcholine and glucagon on the other hand. In all groups the ratios 28 degrees/37.5 degrees for the second phase were lower than those obtained during the first phase. L-isoprenaline induced only a weak increase in insulin secretion and this was not long lasting; this increase was not statistically different at both temperatures.
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PMID:A different action of hypothermia on insulin release from the isolated, perfused rat pancreas, depending on the stimulating agent. 700 May 86

1. Cold exposure caused a marked decrease in insulin response to intravenous injection of glucose, with a sharply declining response over the first 4 days of cold exposure followed by a constant low response up to 13 days of the experimental cold period. 2. The glucose-induced insulin response was unaffected by concomitant infusion of phentolamine in the warm environment. In contrast, the low response of insulin secretion to glucose during cold exposure was so augmented by concomitant infusion of phentolamine as to exceed the response observed in the warm environment. 3. Intravenous infusion of phentolamine caused an increase in the concentration of plasma insulin in the cold but not in the warm environment. 4. Adrenaline completely abolished the insulin response to glucose in the warm environment. 5. Exposure to cold environment brought about an increase in urinary excretion of adrenaline and noradrenaline and in heart rate, but rectal temperature was unchanged. 6. It is concluded that cold exposure insufficient to cause hypothermia produces a marked decrease in insulin secretion by the pancreas of sheep, mediated through adrenergic alpha-receptors stimulated by augmented sympatho-adrenomedullary activity.
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PMID:Insulin secretion in sheep exposed to cold. 700 19

The management of 5 insulin-dependent diabetics following open heart surgery was studied and compared with a group of 5 similar diabetics who had undergone urological or orthopaedic operations. The patients were all treated with a glucose/insulin/potassium infusions regimen, but the cardiac group needed much greater amounts of insulin (1.0 unit/g of glucose) than the non-cardiac group (0.3 units/g) to achieve a similar level of control. The high requirements of the cardiac patients are probably related to trauma, hypothermia and glucose loading when cardiopulmonary bypass begins. Diabetics undergoing such surgery need suitably modified insulin regimens from the outset.
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PMID:Management of diabetes during open heart surgery. 700 93

The dynamics of the content of insulin, somatotropic hormone, glucose and the free fatty acids were studied in 32 male patients with ischaemic heart disease subjected to direct revascularization on the myocardium under neuroleptanalgesia and artificial circulation with moderate hypothermia and haemodilution. It is established that during operations on the coronaries under these conditions insulin secretion is not depressed, despite stable increase of the somatotropic hormone in the blood. High concentrations of glucose and insulin in the blood prevent the rise of the free fatty acids.
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PMID:[Dynamics of the insulin, somatotropic hormone, glucose and free fatty acid content in the blood during a direct myocardial revascularization operation under neuroleptanalgesia]. 703 32

It is well known that deep hypothermia used in open-heart surgery is usually associated with a marked reduction in carbohydrate tolerance, especially dangerous in the diabetic patient, since it might result in severe metabolic complications, namely ketosis and hyperosmolar coma. In order to prevent the occurrence of such complications we treated an insulin-dependent diabetic patient undergoing cardiovascular surgery, with a feed-back insulin infusion operated by an artificial pancreas (GCIIS, Biostator). The Biostator was then used to perform a continuous (minute by minute) blood glucose monitoring in 2 more patients, a type II (non insulin-dependent) diabetic and a non diabetic. Blood samples were drawn sequentially in order to determine plasma free insulin concentration. The glycemic profile observed in the insulin-dependent diabetic under artificial pancreas treatment was similar to that in the non-diabetic. Plasma free insulin levels dropped near to zero during by-pass cooling, returning toward basal level during the rewarming phase. Such results are then discussed by the Authors and given a pathogenetic interpretation.
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PMID:[Use of the endocrine artificial pancreas (GCIIS; Biostator) in heart surgery]. 715


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