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

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.
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PMID:Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression. 181 84

Little is known about adrenocortical function after coronary bypass surgery in which moderate to deep hypothermia and cardiopulmonary bypass are used particularly with intraoperative steroid administration. Therefore, we performed a pilot study in which immediately preoperative and 18-hour postoperative serum cortisol levels were determined in eight patients who received 1.0 to 1.5 gm of methylprednisolone intravenously during surgery; postoperative serum cortisol (3 +/- 1 microgram%) levels were lower than preoperative levels (15 +/- 3 microgram%, p less than 0.05). To determine the possible cause of these striking findings, the effects of moderate to profound hypothermia and cardiopulmonary bypass upon adrenocortical functioning were investigated without the influence of intraoperative steroid administration. Serum cortisol and aldosterone levels and their response to adrenocorticotropic hormone (ACTH) (Cortrosyn) were determined before coronary bypass surgery and at various postoperative intervals in seven patients. Postoperative cortisol and aldosterone levels increased markedly over their preoperative values, reaching a maximum at 6 to 12 hours (cortisol 16 +/- 8 vs 63 +/- 23 micrograms%, p less than 0.05, aldosterone 15 +/- 5 vs 51 +/- 22 ng%, p less than 0.05). Adrenal response to ACTH was normal preoperatively, during rewarming from hypothermia, and 18 hours, and 7 days postoperatively. In summary, normal adrenal responsiveness occurs after coronary bypass surgery, in spite of hypothermic cardiopulmonary bypass and the effects of anesthesia, and a single dose of methylprednisolone during surgery is associated with markedly lower serum cortisol levels and prevents the usual adrenal stress response to bypass surgery for at least 18 hours postoperatively.
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PMID:Adrenal function following coronary bypass surgery. 299 Jan 87

Resuscitation of a neonate requires both immediate cardiopulmonary resuscitation and extended intensive care. Initial resuscitation of the neonate, as for adults, must include support of the airway, breathing and circulation. Because of the unique physiology of a newborn infant, some aspects of drug therapy differ significantly from their counterparts in the resuscitation of adults, and hypoglycemia and hypothermia pose special threats to a distressed neonate. Epinephrine and atropine can be administered via an endotracheal tube, but vascular access, which is most easily obtained by cannulating an umbilical vessel, is required for administering other drugs. Initial drug therapy, including glucose, oxygen and bicarbonate, is intended to restore metabolic homeostasis. Bicarbonate administration must be preceded by adequate alveolar ventilation. Drugs used to increase cardiac output early in resuscitation include those that increase heart rate, increase preload or improve myocardial function. Other drugs used in extended intensive care may also improve cardiac output, alter the distribution of the circulation or alter pulmonary function or gas exchange. These agents will be reviewed in a subsequent article.
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PMID:The pharmacology of neonatal resuscitation and cardiopulmonary intensive care. Part I--Immediate resuscitation. 372 30

Concentrations of catecholamines in vitreous fluid and urine in guinea pigs dying of cold and the effects of freezing and autolysis on these parameters were studied. The analysis was performed by high performance liquid chromatography with electrochemical detection. Noradrenaline (NA) concentration in vitreous fluid was more than 20 times higher in the cold exposed animals than in controls (44.2 +/- 9.2 versus 2.0 +/- 1.0 ng/mL). Autolysis alone caused an increase to 33.5 +/- 7.7 ng/mL, and freezing alone to 13.4 +/- 5.3 ng/mL. The highest values were in the group with exposure, freezing, and autolysis. Adrenaline (A) concentration in the vitreous fluid increased fourfold (3.9 +/- 1.5 versus 0.7 +/- 0.5 ng/mL) in cold exposure and twofold as a result of autolysis. Dopamine (DA) concentration in vitreous fluid was elevated only in the group with exposure, freezing, and autolysis. The increase of NA concentration in urine was fivefold during the whole exposure (from 19.4 +/- 6.9 to 109 +/- 57.3 ng/mL), but A was increased by twentyfold (from 10 +/- 5.1 to 213.2 +/- 168.7 ng/mL), whereas DA concentration did not change. The increase of average excretion of NA to urine was eightfold during the first 6 h of exposure, and that of A tenfold. According to the present results, elevated concentrations of catecholamines in the vitreous fluid and urine can be used as a diagnostic aid for hypothermia death. Concerning the values of noradrenaline in the vitreous, the increase as a result of autolysis must be taken in account when interpreting the results.
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PMID:Catecholamines in the vitreous fluid and urine of guinea pigs dying of cold and the effect of postmortem freezing and autolysis. 378 3

1. Changes in temperature were determined following injection of noradrenaline, adrenaline, isoprenaline, dopamine and 5-hydroxytryptamine (5-HT) into the cerebral ventricles of the conscious mouse.2. Noradrenaline (1-20 mug) and dopamine (10-160 mug) caused falls in body temperature. Adrenaline (1-20 mug) caused a slight and transient rise in body temperature followed by a fall. Isoprenaline (5-20 mug) caused a rise in body temperature, hypothermia only occurring after very high doses (200 mug) of this catecholamine.3. alpha- and beta-adrenergic blocking agents, phentolamine (> 2 mug) and propranolol (> 5 mug) respectively, caused falls in body temperature when injected into the cerebral ventricles of the mouse.4. Specific drug antagonism studies were limited owing to the intrinsic effects of the alpha- and beta-adrenergic blocking agents. However, some evidence was obtained to indicate that noradrenaline mediated its effects through a central alpha-type adrenergic receptor.5. 5-HT (10-160 mug) caused a fall in body temperature. The action of this indoleamine and the catecholamines in regard to thermoregulatory function is discussed.
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PMID:Temperature changes produced by the injection of catecholamines and 5-hydroxytryptamine into the cerebral ventricles of the conscious mouse. 605 3

Noradrenaline (NA), adrenaline (ADR), isoprenaline (ISO) and dopamine (DA) were given through a chronically implanted cannula in the lateral cerebral ventricle of Mastomys natalensis. Low doses of NA (0.05-0.25 microgram) reduced rectal temperature while larger doses (0.35 microgram upwards) produced dose-dependent hyperthermia. The hypothermic effect was antagonised by alpha-adrenoceptor and the hyperthermia by beta-adrenoceptor antagonists. alpha-Methyl noradrenaline produced less hyperthermia but it antagonised the hyperthermic effect of NA. Adrenaline (0.1-10 microgram) was ineffective per se but when given after tolazoline it produced hyperthermia and after propranolol it produced hypothermia. The dose-dependent hyperthermia with isoprenaline (0.1-10 microgram) was blocked by propranolol and MJ-1999. Dopamine (0.5-20 microgram) and its agonists apomorphine, amantadine and BS 9641 produced hyperthermia which was antagonised by haloperidol and pimozide but not by alpha- or beta adrenoceptor antagonists. Noradrenaline (1.0 microgram) produced hypothermia at ambient temperature of 10 degrees C and 16 degrees C. It had no effect at 20 degrees C which seems to be the thermoneutral zone for mastomys. The hyperthermic effect at 33 degrees C was less than at 24 degrees C. Dopamine (10 micrograms) response was attenuated at 33 degrees C and unaffected at other ambient temperatures. It is concluded that alpha- and beta-adrenoceptors and DA-receptors exist in the central thermoregulatory mechanism in mastomys. The alpha-receptors are concerned with lowering the body temperature whereas the beta-receptors and DA-receptors are involved in raising it.
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PMID:The effect of intracerebroventricular administration of catecholamines and their antagonists on rectal temperature of Mastomys natalensis. 612 Apr 69

There are few data concerning the effects of hormones on opiate actions. Consequently, we have studied the influences of peripheral endocrine systems upon sensitivity and tolerance to three major morphine effects: antinociception, hypothermia and catalepsy. It was found that in opiate naive animals adrenalectomy increased morphine-induced antinociception, hypothermia and catalepsy, whereas dexamethasone treatment decreased all three opiate effects. Thyroidectomy decreased the antinociceptive and cataleptic actions of morphine, but had no effect on the hypothermic response. Thyroxine treatment markedly altered the temperature response to morphine without affecting the other two actions. Control animals showed both hyperthermia and hypothermia after morphine, but animals treated chronically with thyroxine showed only hyperthermia. Alterations of the gonadal axis in males had no pronounced effects upon the actions of morphine. Further investigations demonstrated that morphine, when administered i.c.v. to thyroidectomized animals, produced responses similar to those seen after s.c. administration. During chronic studies, the only notable effects of endocrine alterations on the development of tolerance to morphine were trends toward suppression with dexamethasone treatment and trends toward augmentation after adrenalectomy. These results indicate that the actions of morphine are influenced by endocrine status. Adrenal hormones exert their effects upon the actions of morphine via peripheral metabolic alterations, whereas the effects of thyroid hormones are mediated at central sites. These results also indicate that the development of tolerance to morphine is not significantly influenced by any of the endocrine systems studied.
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PMID:Endocrine influences on the actions of morphine. I. Alteration of target gland hormones. 668 31

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

Observations are presented on 24 hypothermia deaths, either accidental or suicidal. Most cases occurred in dry, cold circumstances, the air temperature being below 0 degree C. More cases were seen in early winter, suggesting a lack of acclimatization to the cold. Purple skin and swelling of the ears and nose (mild frostbite) were the most frequent external signs of exposure. Frequent internal signs were stomach ulcerations or hemorrhagic gastritis and small degenerative foci in the myocardium. High blood alcohol (about 200 mg/dL) was the most common contributory factor, but psychotropic drugs were detected in a few cases. The total urinary catecholamine content was increased in the hypothermia deaths, with levels of 0.20 +/- 0.16 microgram/mL (mean +/- standard deviation) versus 0.07 +/- 0.07 microgram/mL in sudden natural deaths and 0.02 +/- 0.02 microgram/mL in rapid violent deaths. Adrenaline was more abundant than noradrenaline. It is suggested that urine catecholamine measurements can give useful information for the diagnosis of acute hypothermia.
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PMID:Increased urinary concentration of catecholamines in hypothermia deaths. 709 1

1 Rats and mice given tributyl S,S,S,-phosphorotrithioate (DEF) showed large dose-related falls in body temperature which lasted several hours to several days at environmental temperatures below thermoneutrality (30 to 31 degrees C). 2 DEF produced only mild sedation and a remarkable degree of motor control was retained even when body temperatures fell below 30 degrees C. At the dose producing maximal hypothermia only 2% of rats died within the first 24 h, although prolonged hypothermia was usually lethal. 3 Hypothermia was associated with a complete block of cold-induced thermogenesis, with relatively little effect on basal metabolism at thermoneutrality. 4 Heat conservation mechanisms (peripheral vasoconstriction and piloerection) appeared to be unaffected by DEF and retained their usual temperature thresholds. 5 Adrenal catecholamine secretion in response to handling or acute cold exposure was normal in DEF-treated rats but the fall in body temperature could be markedly reduced by large intraperitoneal injections of noradrenaline, although not atropine. The increase in oxygen consumption produced by injected catecholamines was also unaffected by DEF treatment. 6 It is concluded that the block of cold-induced thermogenesis probably results from a lack of catecholamine release at the tissue level. That this is likely to be mediated at a peripheral site is suggested by the lack of effect of intracerebroventricular DEF.
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PMID:Selective inhibition of thermogenesis by tributyl S,S,S,-phosphorotrithioate (DEF). 743 38


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