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

1 Unilateral intrahypothalamic injection of either dopamine (10 mug) or amphetamine (10 mug) caused a fall in core temperature in the rat. Pimozide (0.5 mg/kg, i.p.) significantly reduced the hypothermic response, whereas pretreatment with phentolamine (1 mg/kg, i.p.) or methysergide (5 mg/kg, i.p.) was ineffective.2 Systemic pretreatment with cocaine (20 mg/kg) abolished the hypothermic effect of amphetamine, but slightly enhanced the hypothermic response to dopamine.3 Systemic pretreatment with tranylcypromine (10 mg/kg) had no significant effect on the fall in core temperature induced by either amphetamine or dopamine.4 Intraperitoneal injection of cocaine and tranylcypromine, on their own, caused a fall in core temperature in the rat, which was significantly antagonized by either systemic or central pretreatment with pimozide. Phentolamine and methysergide failed to block the hypothermia.5 Unilateral intrahypothalamic injection of cocaine (20 mug) or tranylcypromine (10 mug) also caused a significant fall in core temperature, which was reduced by intrahypothalamic pretreatment with pimozide (0.5 mug), but not significantly changed by pretreatment with phentolamine (25 mug) or methysergide (5 mug).6 These results provide evidence for the presence of a dopaminergic system within the preoptic region, which mediates a lowering of core temperature in the rat.
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PMID:Evidence for an endogenous dopamine-mediated hypothermia in the rat. 51 9

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

Corticotropin-releasing factor (CRF) has been shown to reverse effect of pentobarbital (PbNa) within the central nervous system. In this study, the mechanism of the antagonistic effect of CRF on PbNa-induced anesthesia and hypothermia in rats was examined. Intraventricular administration of CRF significantly shortened sleeping time and antagonized hypothermia induced by PbNa. Propranolol (148 micrograms, 0.5 mumol), a beta-blocker, completely reversed the CRF effect, although propranolol alone affected neither sleeping time nor rectal temperature. Phentolamine, an alpha-blocker, reversed the antagonistic effect of CRF on PbNa, though the same dose of phentolamine alone increased the sleeping time in the absence of CRF. Atropine, an anticholinergic agent, did not affect the ability of CRF to reverse the effects of PbNa. These results suggest that the ability of CRF to reduce some of the effects of PbNa may be mediated at least in part by brain beta-noradrenergic receptors.
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PMID:Corticotropin-releasing factor reverses the effect of pentobarbital through a beta-noradrenergic mechanism in rats. 284 61

Chlorpromazine, given either subcutaneously (0.375 mg/kg) or unilaterally into the preoptic/anterior hypothalamic area through a chronically implanted cannula (20 micrograms), was found to enhance the hypothermic response to delta-9-tetrahydrocannabinol (THC; 5 mg/kg i.p.) in unrestrained adult male MF1 mice, kept at 22 degrees C. In mg/kg terms, chlorpromazine was no more potent when injected into the preoptic/anterior hypothalamic area than when given subcutaneously. Phentolamine (54 micrograms) had no significant effect on hypothermia induced by THC when injected into the hypothalamus although it did enhance this response when given subcutaneously (15 mg/kg). Hypothermia induced by THC was also enhanced by flupentixol (0.375 mg/kg s.c.), piflutixol (23.4 micrograms/kg s.c.), pentolinium (5 mg/kg s.c.), prazosin (0.1875 mg/kg s.c.) and indoramin (6 mg/kg s.c.) but not by SCH 23390 (6 mg/kg s.c.) or sulpiride (40 mg/kg s.c.). When taken together with the results from a previous study, these data support the hypothesis that chlorpromazine enhances hypothermia induced in mice by THC by antagonizing alpha-adrenoceptors so as to decrease the capacity of the animals to minimise peripheral blood flow by vasoconstriction. The present data also support the hypothesis that flupentixol and piflutixol interacted with THC not by antagonizing dopamine at D1 or D2 receptors but rather by blocking alpha-adrenoceptors.
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PMID:The hypothermic response of mice to delta-9-tetrahydrocannabinol is enhanced by chlorpromazine, thioxanthenes, alpha-adrenoceptor antagonists and pentolinium but not by SCH 23390 or sulpiride. 289 30

This study assessed the effects of phentolamine on rewarming patterns and metabolic acidosis in 37 patients subjected to hypothermia during cardiopulmonary bypass for the performance of aortocoronary bypass grafting. An additional 16 patients undergoing the same surgery received no phentolamine and served as a control group. In all patients, sodium bicarbonate (44.6 mEq) was administered only when the negative base excess was 3.0 mEq/L or greater. Sixty-eight percent of the patients receiving phentolamine and 56% of the control patients exhibited a uniform rewarming pattern in which the rectal, hand, and foot temperatures increased in parallel. In 32% of the patients receiving phentolamine and in 44% of the control patients, rectal and hand temperatures increased more than foot temperature during rewarming. Analysis of base excess values in the subgroups of patients with similar rewarming patterns indicated that base deficits were significantly decreased in patients receiving phentolamine. Phentolamine administration was also associated with significantly lower blood lactate levels and sodium bicarbonate requirements, as well as improvements in overall appearance and mental status. These data suggest that the routine use of phentolamine in patients undergoing cardiopulmonary bypass may be associated with more uniform body cooling and rewarming and improved tissue perfusion.
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PMID:Effect of phentolamine in controlling temperature and acidosis associated with cardiopulmonary bypass. 298 56

1. The effect on rectal temperature of adrenoceptor blocking agents, injected through a cannula chronically implanted into a lateral cerebral ventricle, was examined in unanaesthetized rabbits, cats and rats, kept at room temperature (19-22 degrees C).2. In rabbits, the alpha-adrenoceptor blocking agent phenoxybenzamine (50 or 100 mug) produced marked hypothermia when injected intraventricularly but not when injected intravenously. In some rabbits as little as 1 mug was effective on intraventricular injection. Phentolamine and ergotamine, the other alpha-adrenoceptor blocking agents examined, had a much weaker hypothermic action when injected intraventricularly, whereas the beta-adrenoceptor blocking agents propranolol, pronethalol and Trasicor had no effect.3. In rabbits in which the noradrenaline stores of the hypothalamus were depleted by intraventricular injections of reserpine, the hypothermic effect of phenoxybenzamine was abolished and remained abolished for a few days.4. In cats, an intraventricular injection of phenoxybenzamine (200 mug) produced long-lasting hyperthermia, but not in all cats, and only with the first, or the first two or three injections. Injected intraperitoneally, this dose had no effect on temperature. Phentolamine (100 or 200 mug) had a very weak hyperthermic effect and phentolamine (500 mug), a hypothermic effect, but only on intraventricular injection, whereas ergotamine (100 and 200 mug) had a weak hyperthermic effect both on intraventricular and intraperitoneal injection. Propranolol and Trasicor had no effect on temperature when injected intraventricularly.5. In rats, phenoxybenzamine (5 or 20 mug) produced long-lasting hypothermia on intraventricular injection.6. Some of the temperature effects produced by intraventricular injections of the alpha-adrenoceptor blocking agents are explained on the assumption that they prevent the effect on temperature produced by a continuous release of noradrenaline from adrenergic neurones innervating the anterior hypothalamus.
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PMID:Effects of adrenoceptor blocking agents on body temperature. 440 May 28

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

Changes in core body temperature and the behavioral activation produced by clonidine were measured in 10-day-old rats at 3 different ambient temperatures (25, 30 and 36 degrees C). Behavioral activation after clonidine is comprised of head raising and rotational movements of the limbs which result in locomotion in open areas and wall climbing if the animal is confronted by a vertical surface. Clonidine enhanced locomotion and wall climbing at all environmental temperatures, but a drug-induced hypothermia was found only in the 25 and 30 degrees C testing conditions. This suggests that the clonidine-induced motor changes are not secondary to a fall in body temperature. In a second experiment the open field responses to clonidine at 25 degrees C were observed in 10-day-old rats pretreated with phentolamine (2 and 15 mg/kg), phenoxybenzamine (2 and 15 mg/kg) or naloxone (0.2 and 2 mg/kg). Phentolamine pretreatment at 15 mg/kg reduced locomotion, wall climbing and attenuated the reduction in core temperature. Phenoxybenzamine at 15 mg/kg only affected the clonidine-induced change in temperature. Thus, it is likely that these behavioral and temperature changes are adrenergically mediated and that the clonidine-induced locomotion and temperature effects may be due to different alpha-adrenergic receptors.
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PMID:Behavioral and temperature changes induced by clonidine in the developing rat. 732 39

The relative importance of different effector mechanisms of thermoregulation may change depending on their availability. Intact rats make only limited use of a learned response on a cold ambient temperature stimulus, and rely almost entirely on autonomic regulatory functions. After destruction of the anterior hypothalamus, rats exhibit a reduced thermoregulatory capacity; i.e. body temperature drops in the cold and rises in the heat. Under this situation a conditioned operant behavior (lever pressing for increasing or decreasing ambient temperature) becomes an important factor to keep body temperature almost constant. Receptor blockers of some putative transmitters in central thermoregulatory pathways influence thermoregulation. Phentolamine induces hypothermia in intact rats in the cold. Hypothalamic lesions are additive in effect with with the drug. Pimozide has no effect neither in the cold nor in the heat intact and lesioned rats. Biperiden in the heat reinforces hyperthermia in intact and lesioned rats as well; in the cold the drug is ineffective. Performance of lesioned rats in an operant pain titration procedure does not differ from intact rats.
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PMID:Operant thermoregulation of rats with anterior hypothalamic lesions. 732 50


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