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

A series of 22 cases of fatal accidental or suicidal hypothermia is presented. Necropsy findings on which the diagnosis can be based were analysed. Purple skin and swelling of face, hands and feet, as well as violet patches on elbows or knees were the most frequent external signs (Frequency 54--59%). The most conspicuous internal macroscopic signs were gastric erosions or haemorrhages, which were seen in half of the cases. Other less frequent signs were pulmonary oedema and acute renal and hepatic degeneration. Microscopically the myocardium showed small degenerative foci and/or fuchsinophilic fibres in two thirds of the cases. The myocardium was macroscopically normal. Histamine and serotonin assays from urine did not indicate increased excretion during exposure. Catecholamine concentrations in urine were high (greater than 0.1 mug/ml) in most hypothermia deaths indicating increased excretion due to cold. The best diagnostic signs seem to be purple skin and oedema in face and ears, stomach erosions, degenerative foci in myocardium and high concentration of catecholamines in the urine.
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PMID:Necropsy findings in fatal hypothermia cases. 97 1

The role of neurotensin in radiation-induced hypothermia was examined. Intracerebroventricular (ICV) administration of neurotensin produced dose-dependent hypothermia. Histamine appears to mediate neurotensin-induced hypothermia because the mast cell stabilizer disodium cromoglycate and antihistamines blocked the hypothermic effects of neurotensin. An ICV pretreatment with neurotensin antibody attenuated neurotensin-induced hypothermia, but did not attenuate radiation-induced hypothermia, suggesting that radiation-induced hypothermia was not mediated by neurotensin.
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PMID:Role of neurotensin in radiation-induced hypothermia in rats. 202 92

This review presents our new findings regarding the centrally-induced effects of histamine and clonidine. We have found for the first time that histamine administered intracerebroventricularly (icv) induces a dose-related increase in serum free fatty acids (FFA) in conscious rats. Both H1 and H2 receptors participate in this stimulation. Histamine interacts with central alpha 1 and beta-adrenoceptors and with cholinergic muscarinic receptors when inducing hyperlipemic response in non-stressed rats. Clonidine given icv induces also hyperlipemia which, as shown by us, is elicited by a central alpha 2-adrenergic mechanism. In hypothermia caused in rats by clonidine not only already known central alpha-adrenergic but also an H2-histaminergic mechanism participates to an equal extent. We have found for the first time that in conscious rats both under normal and stress conditions not only central histamine H1- but also H2-receptors mediate the stimulation of the pituitary-adrenocortical response measured indirectly through corticosterone secretion. In our study evidence has for the first time been obtained that in non-stressed rats brain histaminergic mechanism interacts with alpha 1, alpha 2- and beta-adrenoceptors and with cholinergic muscarinic receptors when stimulating the pituitary-adrenocortical response. By contrast, in stressed animals central histamine H1- and H2-receptors interact with alpha 1- and alpha 2- but not beta-adrenergic and cholinergic muscarinic receptors when increasing the corticosterone response. We have also demonstrated that in contrast to a known inhibitory action on adrenocortical secretion in anesthetized dogs, clonidine given icv increases the corticosterone response in both non-stressed and stressed rats by stimulating alpha-adrenoceptors. In stressed animals this effect of clonidine is also mediated, to an equal extent, by H2-receptor mechanism. Our data strongly suggest that in some central effects clonidine affects both alpha 2 and H2 receptor mechanism. This challenges the view that clonidine is a selective alpha-adrenergic agonist.
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PMID:Central metabolic and pituitary-adrenocortical stimulatory action of histamine and clonidine. 608 56

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

The effect of intracerebroventricular (i.c.v.) administration of histamine (H), H1- and H2-receptor agonists and their antagonists, on the cloacal temperature of pigeon has been investigated. Histamine produced a dose-dependent hypothermia at an ambient temperature of 24 degrees C which was significantly blocked by a combination of mepyramine and cimetidine but was only partially antagonized by either of them alone. H1-receptor as well as H2-receptor agonists also produced hypothermic response with a time-course similar to that of H. Their effects were also significantly antagonized by mepyramine and cimetidine respectively. The histamine response was not modified by pretreatment with alpha- or beta-adrenoceptor antagonists. Histamine produced an insignificant hyperthermia at 10 degrees C but the hypothermic effect increased as the ambient temperature was raised up to 40 degrees C. It is concluded that both H1- and H2-histamine receptors are present in the brain of pigeon and are responsible for H-induced hypothermia.
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PMID:Analysis of hypothermic response to centrally administered histamine in pigeons. 666 93

1 The effect of intracerebroventricular (i.c.v.) injection of histamine on the rectal temperature of Mastomys natalensis at ambient temperatures of 10, 24 and 33 degrees C has been studied. 2 Low doses (0.1-1.0 microgram) of histamine produced hypothermia while larger doses (5-20 micrograms) produced dose-dependent hyperthermia. The hypothermic effect was significantly antagonized by mepyramine while the hyperthermia was blocked by cimetidine. 3 Histamine H1-receptor agonists, 2-methyl-histamine and 2-pyridyl-ethylamine, also produced hypothermia which could be blocked by mepyramine. 4 Histamine H2-receptor agonists, impromidine and dimaprit, produced hyperthermia which was antagonized by cimetidine. 5 Pretreatment of the animals with a beta-adrenoceptor antagonist, MJ1999, did not affect the response to histamine. 6 The hyperthermic effect of histamine (10 micrograms) was most marked at 10 degrees C and was attenuated at 33 degrees C. 7 It is concluded that both H1 and H2-histamine receptors are present in the brain of Mastomys. The H1-receptors mediate hypothermia and H2-receptors hyperthermia.
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PMID:Analysis of histamine receptors in the central thermoregulatory mechanism of Mastomys natalensis. 707 79

Histamine has been shown to possess many neurotransmitter-like properties, and a variety of studies indicate that central histamine may function in modulating behavioral arousal. To examine this possibility further, histamine was administered into the lateral cerebral ventricles of the conscious and pentobarbital-anesthetized rat. In the conscious animal, histamine induced a significant increase in spontaneous motor activity which consisted of increased grooming and exploratory behaviors (sniffing, rearing and locomotion) as compared to saline-treated controls. In the pentobarbital-pretreated rat, histamine caused a dose-related decrease in narcosis duration and hypothermia without altering the disposition of pentobarbital in brain or plasma. Administration of compounds structurally related to histamine did not alter spontaneous activity or shorten narcosis duration. While pretreatment with the H2-histamine antagonist, cimetidine, was no effective, H1-histamine antagonists were found to abolish histamine-induced arousal. Administration of haloperidol in doses that significantly attenuated increased spontaneous motor activity by amphetamine did not alter histamine-induced hyperactivity. Likewise, atropine did not significantly alter histamine-induced arousal. These data support the hypothesis that histamine may function in modulating behavioral arousal.
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PMID:Histamine-induced arousal in the conscious and pentobarbital-pretreated rat. 708 7

Tumor necrosis factor-alpha production and products of mast cell, basophil, and eosinophil degranulation (prostaglandin D2, histamine, and eosinophil cationic protein) were prospectively studied in 26 children undergoing cardiac operations. The relationship between inflammatory response to cardiopulmonary bypass and transient postoperative arrhythmias was analyzed. Cardiopulmonary bypass was conducted with circulatory arrest and deep hypothermia in 10 patients and with continuous low-flow and moderate hypothermia in 16 patients. Transient postoperative arrhythmias diagnosed on standard or atrial electrocardiograms (or both) were seen in eight of the 26 examined children: accelerated junctional rhythm (n = 3), junctional ectopic tachycardia (n = 3), second-degree atrioventricular block (n = 1), and third-degree atrioventricular block (n = 1). Children with transient postoperative arrhythmias were younger than those without (p < 0.05). Compared with baseline values, there was in all patients a significant release of histamine and eosinophil cationic protein (p < 0.05) related to cardiopulmonary bypass, reaching peak values 4 hours after the operation. In contrast, tumor necrosis factor-alpha production and prostaglandin D2 release were not significant. This suggests that activated basophils but not mast cells are the major sources of histamine liberated during and after cardiopulmonary bypass. Histamine release but not eosinophil cationic protein release correlated with circulatory arrest and deep hypothermia (p < 0.05), suggesting the participation of physicochemical alterations of circulating basophils leading to histamine liberation. Four hours after the operation, patients with transient postoperative arrhythmias had significantly higher blood concentrations of histamine (p < 0.02) and eosinophil cationic protein (p < 0.05) than did those without transient postoperative arrhythmias. On the first postoperative day, four of the eight patients with transient postoperative arrhythmias had persisting elevated histamine levels, whereas in patients without transient postoperative arrhythmias histamine reached baseline values. The multivariate analysis retained histamine release and eosinophil cationic protein variations related to cardiopulmonary bypass for the emerging model to predict transient postoperative arrhythmias. The results of this study show significant histamine release related to cardiopulmonary bypass. Furthermore, they document a possible relationship between circulating histamine and transient postoperative arrhythmias. The latter may therefore be suspected among the consequences of the inflammatory response to cardiopulmonary bypass.
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PMID:Histamine liberation related to cardiopulmonary bypass in children: possible relation to transient postoperative arrhythmias. 862 22

The first indication that histamine might be important in the functioning of the brain was the finding that the centrally penetrating histamine H1 antagonists had marked sedative properties. Subsequently with the development of more specific compounds and drugs for the H1, H2 and H3 receptors a greater understanding of the neurotransmitter/modulator role of histamine in the CNS has been possible. Histamine is now associated with wakefulness, suppression of seizures, hypothermia and emesis. The histamine H1 antagonists have been shown to potentiate opioid-induced analgesia, and modify eating and drinking patterns as well as endocrine secretions from the pituitary gland. Additionally, clinically useful antidepressants have been shown to inhibit histamine-sensitive adenylate cyclase from the mammalian brain. Recently, a possible role for both histamine H1 and H2 receptors in schizophrenia has been reported. As more specific and centrally-penetrating histaminergic compounds are developed, so the roles of histamine as a neurotransmitter/modulator in the brain will be better understood.
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PMID:Histaminergic drugs as modulators of CNS function. 873 45

Effects of intracerebroventricular injection of histamine and its related compounds on rectal temperature were studied in mice. Histamine (0.1-1.0 mu g) and histidine (500-1,000 mg/kg) caused a dose-related hypothermia. H1 agonist, 2-methylhistamine and 2-thiazolylethylamine also displayed a dose-dependent hypothermia. In addition, H2 agonists, 4-methylhistamine and dimaprit elicited a decrease in body temperature. Preinjection of not only H1-antagonists (diphenhydramine and chlorpheniramine) but also H2 antagonists (cimetidine and ranitidine) abolished histamine-induced hypothermia. Either intracerebroventricular or intraperitoneal injection of thioperamide, a histamine H3 antagonist, showed hypothermia. The hypothermic effect produced by intracerebroventricular injection of thioperamide was significantly blocked by (R)-alpha-methylhistamine, a selective H3 agonist. In addition, the effect induced by thioperamide was inhibited by H1 and H2 antagonists, indicating that the H3 receptor also participates in histamine-induced hypothermia.
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PMID:Effects of intracerebroventricular injection of histamine and its related compounds on rectal temperature in mice. 905 87


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