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

Quinine HCl in doses from 10-50 mg/kg lowered the body temperatures of nonfebrile rats in the cold, primarily by suppressing shivering. However, if given an opportunity to turn on a heat lamp the rats worked much more than normal after a quinine injection and were theraby able to counteract the hypothermia to some extent. The effect of quinine is interpreted as an action on effector mechanisms rather than as an alteration of the thermal setpoint.
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PMID:Quinine-induced hypothermia in cold-exposed rats. 89 91

1 Core and tail skin temperature was measured in rats which had guide cannulae implanted into their brains to allow drug injections directly into the preoptic anterior hypothalamus. 2 Apomorphine and dopamine (10 microgram in 1 microliter) injected into the area of the preoptic anterior hypothalamus caused a fall in core temperature which was preceded by a rise in tail skin temperature. 3 The decrease in core temperature following central injection of either apomorphine or dopamine was significantly reduced by pretreating rats for 2 h with pikozide 0.5 mg/kg i.p.). 4 Bilateral intrahypothalamic injection of pimozide (0.5 microgram in 1 microliter) significantly reduced the hypothermic effect of systemic apomorphine (1.25 mg/kg i.p.). 5 Control rats placed 65 cm below a 250 W infrared lamp responded with vasodilation of tail skin blood vessels as indicated by an increase in tail skin temperature. Pimozide pretreatment (0.5 mg/kg i.p.) significantly reduced this response. 6 These results suggest that the preoptic anterior hypothalamus contains dopamine receptors which mediate hypothermia in rodents and raise the possibility that endogenous dopamine has a physiological role in thermoregulation.
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PMID:Do central dopamine receptors have a physiological role in thermoregulation? 91 10

The administration of d-amphetamine (15 mg/kg, i.p.) to rats causes stereotypy, hypothermia among animals placed in a cold environment, and paradoxical behavioral thermoregulation (i.e., animals in a cold environment choose not to place themselves under the beam emitted by a heat lamp). These effects are blocked in animals lesioned unilaterally in the mesolimbic dopaminergic projections to the olfactory tubercule and nucleus accumbens. In contrast, a unilateral lesion destroying the nigro-striatal projections within the caudate nucleus blocks none of these responses, and actually potentiates the induction of stereotypy by d-amphetamine. Both lesions cause the animal to exhibit rotational behavior in response to the subsequent administration of d-amphetamine. These observations suggest that the mesolimbic dopaminergic projections mediate some of the behavioral and visceral effects of d-amphetamine.
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PMID:Dopaminergic neurons in the nigro-striatal and mesolimbic pathways: mediation of specific effects of D-amphetamine. 116 75

A method of measuring thermoregulatory behavior in the rat has been developed, which allows analysis of the mechanism of action of drugs which modify body temperature. The test measures the amount of time a rat will remain exposed to an infrared heat source before making an escape and this evidence has been used to divide drugs into those which act on the central thermostats and those which act on effector systems. A peripherally acting hypothermic drug (N-methyldiphenhydramine) increased the time of exposure to the heat lamp. Tri-iodothyronine increased body temperature and decreased exposure to the heat lamp. Intraventricular oxotremorine caused hypothermia but a decreased exposure to heat suggesting it acts to lower the set-point of the central thermostats. Both effects were blocked by atropine. The possibility that central cholinergic mechanisms in the hypothalamus have a function in determining the setting of the central thermostats is discussed.
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PMID:Behavioral thermoregulation in the study of drugs affecting body temperature. 122 94

Aortic and renal vascular reconstruction often involve significant renal ischemia. Profound hypothermia during renal ischemia preserves renal tissue. However, in the clinical setting of vascular reconstruction specific attempts at cooling the kidney are often impractical, and renal ischemia frequently occurs at physiologic temperatures. This study demonstrates that minimal temperature changes during renal ischemia alter the functional and morphologic outcome. Rats anesthetized with halothane underwent a right nephrectomy and placement of a snare around the left renal pedicle for 45 minutes to produce renal ischemia. Seventy-five adult male Sprague-Dawley rats, weighing 250 to 350 gm were divided into three groups based on the body temperature maintained during renal ischemia (35 degrees C, 37 degrees C, 39 degrees C). Body temperature was continuously monitored with a rectal thermistor and maintained by adjustment of a heating pad and lamp. Two postischemic protocols were followed including a creatinine assessment protocol with blood samples collected at 24, 48, and 72 hours and a histologic assessment protocol with biopsy of the kidney at 30 hours. At 24 hours after ischemia plasma creatinine concentrations were increased in rats with elevated body temperatures (35 degrees C vs 37 degrees C; [p = 0.001], 37 degrees C vs 39 degrees C; [p = 0.150]). The 30-hour histologic assessment indicated a difference in morphologic outcome (35 degrees C vs 37 degrees C; [p = 0.063], 37 degrees C vs 39 degrees C; [p = 0.016]), with proximal tubular morphology being better maintained at lower temperatures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Minimal physiologic temperature variations during renal ischemia alter functional and morphologic outcome. 156 May 50

The pathophysiological changes associated with hypothermia were investigated in the rat stomach under anesthetized conditions. The animal was placed in a styrene foam box and the core body temperature was kept between 24 and 36 degrees C using a heat lamp and refrigerant pack. Lowering of body temperature (less than 30 degrees C) produced acid hypersecretion and induced hemorrhagic lesions in the gastric mucosa; these responses reached the maximum at 28 degrees C, and a significant relationship was found between acid output and lesion score. Hypothermia (28 degrees C) also caused a marked increase of gastric contractile activity and mucosal blood flow (MBF), but the ratio of acid output to MBF became greater when compared to that obtained under normothermic conditions. These changes induced by hypothermia (28 degrees C) were completely blocked by vagotomy and were significantly inhibited by atropine, hexamethonium, clonidine, or TRH antiserum. However, lowering body temperature did not significantly affect acid secretory, motility, and ulcerogenic responses induced by carbachol in the vagotomized rat, excluding local mechanisms (suppression of the inhibitory nerves) in the hypothermia-induced changes. We conclude that hypothermia alone stimulates vagally dependent acid secretion and motility, resulting in damage in the gastric mucosa. These changes may be centrally mediated by TRH, which is released in association with the thermogenic response to hypothermia.
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PMID:Vagally mediated acid hypersecretion and lesion formation in anesthetized rat under hypothermic conditions. 167 16

The development of behavioral tolerance to pentobarbital-induced hypothermia, as separable from cellular and metabolic tolerance, was established. Pentobarbital (PB) was administered to 4 groups of rats, 2 groups of which received intermittent (INT) IP PB treatment. One of these groups, INT/EXP, experienced the hypothermic (measured as rectal body temperature) drug effect after PB injection. The other group, INT/NONEXP, was monitored for body temperature functions (room temperature) before receiving PB (vehicle administration) and then prevented from experiencing PB-induced hypothermia by maintenance of body temperature with a towel wrap restraint and a heating lamp. The INT/EXP group also received equivalent exposure to this towel wrap after vehicle administration. Two other groups received chronic PB treatment (IP and in ground chow), one with experience for hypothermia after injections (CHR/EXP) and one prevented from experiencing the hypothermia (CHR/NONEXP). These groups also received equivalent exposure to the body temperature (at room temperature) testing and towel wrap restraint, EXP rats after vehicle injections and NONEXP after drug injections. A postchronic test of all groups compared the extent of PB hypothermia to prechronic test effects to assess the degree of tolerance. The INT/EXP group demonstrated behavioral tolerance for PB-induced hypothermia, as contrasted with the INT/NONEXP group which demonstrated little or no tolerance. Prominent tolerance was noted in both chronic groups for PB hypothermia, without a significant difference between them. After the postchronic test, chronic treatment was discontinued for 9 days (withdrawal) followed by 9 days of extinction training (vehicle behavioral testing). The two intermittent groups demonstrated no change in the hypothermic drug response during the postwithdrawal and postextinction drug tests.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cellular and learned tolerances for pentobarbital hypothermia. 194 65

Histamine administered intraventricularly or into the anterior hypothalamic preoptic region induced dose-dependent hypothermia in rats with chronic i.c.v. cannula. This hypothermia was almost totally abolished by both the histamine H1- and H2-receptor antagonists, mepyramine or chloropyramine and metiamide or cimetidine, respectively, give i.c.v. prior to histamine. In behavioural thermoregulation studies histamine considerably diminished the mean duration of dwelling of the rat under the heat lamp. This effect was abolished by histamine H1- but not by H2-receptor antagonists. It is concluded that histamine induces hypothermia by lowering the set point of the hypothalamic thermostat by means of H1-receptors. Histamine H2-receptor blockers antagonized the increase in tail skin temperature after histamine administration, suggesting that h2-receptors are involved in a heat loss mechanism.
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PMID:The role of central histamine H1- and H2-receptors in hypothermia induced by histamine in the rat. 612 74

Cats (n = 66) were evaluated in a retrospective clinical study to determine if there were any consistent patterns predisposing them to hypothermia during general anesthesia. There were no differences between any of the anesthetic techniques evaluated, between different body weights, or between different surgical procedures, with regard to the degree of hypothermia developed. Four cats were evaluated with regard to the efficacy of several techniques to maintain or restore body temperature during pentobarbital anesthesia. A circulating warm-water blanket cocooning the subject was most effective. Placing the animal on a circulating warm-water blanket under a 250-W infrared heat lamp, or under a hot-water bottle heat tent was effective, whereas cocooning in hand towels or a space blanket were ineffective.
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PMID:Hypothermia and its prevention during general anesthesia in cats. 725 5

1. Intrahypothalamic injection of either dopamine or 5-hydroxytryptamine (5-HT) in a dose volume of 1 microliters caused a fall in core temperature in lightly restrained rats maintained at an ambient temperature of 17 +/- 1 degree C. 2. Haloperidol (6.5 n-mole), a dopamine antagonist, prevented the hypothermic effect of dopamine (65 n-mole), but was ineffective against the response to either intrahypothalamic 5-HT (114 n-mole) or oxotremorine (6.0 n-mole). 3. Methysergide (14 n-mole) and cryproheptadine (17 n-mole) blocked the effect of both 5-HT and dopamine. However, these same doses failed to antagonise the effect of oxotremorine. 4. Rats placed on 0.65 m below a 250 W infra-red lamp responded to the imposed heat load vasodilation of tail skin blood vessels, as indicated by an increased tail skin temperature. 5. Rats tested 2 weeks after bilateral intrahypothalamic injection of 5,6-dihydroxytryptamine (42 n-mole in 2 microliters) showed a significant reduction in their tail skin temperature response and were less able to withstand the imposed heat load. 6. Three serial sections (0.8 mm thick) were prepared from the preoptic area of the rat brain, one anterior, one posterior and one corresponding to the previously defined dopamine-sensitive site. 7. Pretreatment with 5,6-dihydroxytryptamine significantly reduced the 5-HT concentration in the dopamine sensitive site, but had no effect on the concentration of dopamine. This pretreatment blocked dopamine but not 5-HT-induced hypothermia. 8. The 5-hydroxyindoleacetic acid (5HIAA) concentration in the hypothalamus of the normal rat exposed to a heat load was found to be significantly elevated, whereas there was no change in the 5HIAA concentration in the cortex. 9. Slices of rat preoptic hypothalamus and hippocampus were incubated with [3H]5-HT (0.2-2 microM). These slices accumulated 5-HT with properties characteristic of a neuronal uptake process. 10. Perfusion with either dopamine (greater than 50 microM) or apomorphine (greater than 200 microM) enhanced the release of [3H]5-HT from the prelabelled hypothalamic slices, but failed to stimulate release from hippocampal slices. 11. The release of [3H]5-HT from preoptic slices by dopamine and apomorphine was antagonised by the dopamine antagonists haloperidol (2 microM) and (+) isomer of butaclamol (1 microM), the (-) isomer of butaclamol was inactive. 12. These results support the hypothesis of a dopamine-5HT link in the hypothalamic thermoregulatory pathways of the rat.
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PMID:A dopamine-5-hydroxytryptamine link in the hypothalamic pathways which mediate heat loss in the rat. 743 Dec 48


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