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

Deep hypothermic circulatory arrest facilitates repair of congenital cardiac anomalies in infants. It is known empirically that hypothermia protects against central nervous system (CNS) ischemic damage. The Q10O2 is only 2.2 for brain and thus a decrease in metabolic rate does not fully account for protective effects of hypothermia. Since enthalpy of dissociation of H2O is high (approximately 7 kcal/mole), its pH is temperature dependent (7.0 at 25 degrees C, 7.4 at 20 degrees C) and hypothermia may in part protect by its influence on hydrogen ion concentration. A manifestation of CNS susceptibility to ischemia is an obstruction of the microcirculation [no-reflow lesion (NRL)] demonstrated by infusion of carbon black into the cerebral circulation after a period of circulatory arrest. White lesions (NRL) against a gray background on cut section of brain increase in size with increasing time of arrest. The effect of anoxia versus circulatory arrest, brain temperature, and extracellular brain pH on NRL was studied in 45 mongrel dogs, subjected to varying periods of N2-induced anoxia on cardiopulmonary bypass (CPB) at 37 degrees C or 20 degrees C. In some studies jugular venous pH was adjusted by infusion of NaHCO3 or HCl. Control groups included normothermic CPB without anoxic and normothermic CPB, anoxia, and equimolar NaCl infusion. NRL was quantified by planimetry of photographs of cut sections of brain. These results confirm that NRL is abated by hypothermia and suggest that (1) NRL is a function of anoxia and not arrested circulation since perfusion with N2 at 37 degrees C does not protect the brain (i.e., NRL is not solely related to "critical reopening pressure") and (2) NRL is in part a function of extracellular pH.
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PMID:Cerebral anoxia: effect of deep hypothermia and pH. 3 7

Lisuride hydrogen maleate induced stereotyped behaviour in normal as well as in reserpinized mice. It antagonized the motor depression and hypothermia induced by reserpine. On i.p. administration the compound was about as effective as apomorphine and D-amphetamine. As with apomorphine and in contrast to D-amphetamine the effects of lisuride hydrogen maleate in reserpinized mice were not impaired by additional treatment with alpha-methyl-p-tyrosine methylester. In untreated mice, the substance was very potent in lowering body temperature with significant hypothermia measured after dosages as low as 0.10 mg/kg i.p. Occurrence of stereotyped behaviour and hypothermia could be prevented by the dopaminergic antagonist haloperidol. From these data it is concluded that lisuride hydrogen maleate in addition to its interaction with serotoninergic systems is a potent dopaminergic agonist with a probably direct action on dopaminergic receptors. Further arguments in support of such an action of lisuride hydrogen maleate are, in addition to biochemical data, its serum prolactin lowering effect in rats, its strong emetic action in dogs and its effects on rat behaviour.
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PMID:Direct dopaminergic action of lisuride hydrogen maleate, an ergot derivative, in mice. 94 66

1 Three salts of 5-hydroxytryptamine, the hydrogen maleinate, the oxalate and the creatinine sulphate were infused into the hypothalamus of 10-18 day old chickens at ambient temperatures in and below the thermoneutral range. Body temperature was recorded and behaviour observed. Electrocortigrams were recorded in experiments in which 5-hydroxytryptamine hydrogen maleinate was used. The effects of a monoamine oxidase inhibitor and methysergide on these responses were similarly studied. 2 At thermoneutrality (31 degrees C) all 3 salts produced behavioural sleep. 5-Hydroxytryptamine oxalate had inconsistent effects on body temperature. 5-Hydroxytryptamine creatinine sulphate produced hypothermia at small doses and mild hyperthermia at higher doses. 5-Hydroxytryptamine hydrogen maleinate produced hypothermia at all doses tested; the falls in temperature induced by this salt were intensified in magnitude and duration by monoamine oxidase inhibition unlike the responses to the other 2 salts. 3 At temperatures below thermoneutrality (16 degrees C) all 3 salts produced behavioural sleep and electrocortical sleep was recorded with 5-hydroxytryptamine hydrogen maleinate. All 3 salts produced hypothermia, which was intensified in magnitude and duration by monoamine oxidase inhibition. 4 The hypothermia produced by 5-hydroxytryptamine hydrogen maleinate was prevented by equimolar doses of methysergide. 5 The position of the cannula in the hypothalamus was found to be crucial. 6 The results contrast with those found in the adult fowl. No conclusion is drawn as to the relationships of the actions of these salts when infused compared with the effects of endogenous 5-hydroxytryptamine release.
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PMID:Some central effects of 5-hydroxytryptamine in young chickens at and below thermoneutrality. 112 91

Retrograde cerebral perfusion through a superior vena caval cannula is a new technique for protecting the brain during aortic arch operations. In mongrel dogs (n = 10; 13 to 15 kg) we have performed retrograde cerebral perfusion (300 mL/min) by infusing blood through a superior vena caval cannula with aortic and inferior vena caval drainage. We have measured the cerebral tissue blood flow, oxygen consumption, and carbon dioxide exudation during retrograde cerebral perfusion at normothermia (NT, 37 degrees C) and hypothermia (HT, 20 degrees C) and have compared these values with values obtained in dogs during cardiopulmonary bypass (1,200 mL/min). Cerebral tissue blood flow was measured by the hydrogen clearance method. During retrograde cerebral perfusion about 20% of the superior vena caval perfusate was returned through the aorta and the rest drained from the inferior vena cava. Cerebral vascular resistance during retrograde cerebral perfusion was lower than that during cardiopulmonary bypass (NT, 63.8 +/- 52.5 versus 126.9 +/- 58.4; HT, 28.4 +/- 32.8 versus 69.5 +/- 28.7 x 10(3) dynes.s.cm(-5). Retrograde cerebral perfusion provided half the cerebral tissue blood flow of cardiopulmonary bypass (NT, 14.7 +/- 6.4 versus 34.3 +/- 7.8; HT, 17.6 +/- 5.6 versus 37.2 +/- 10.6 mL/min). Retrograde cerebral perfusion also provided a third of the oxygen (NT, 4.4 +/- 2.1 versus 12.3 +/- 7.1; HT, 1.4 +/- 0.8 versus 4.2 +/- 1.3 mL/min) and discharged 20% of the carbon dioxide (NT, 0.24 +/- 0.08 versus 1.19 +/- 0.58; HT, 0.15 +/- 0.06 versus 0.51 +/- 0.17 mmol/min) when compared with cardiopulmonary bypass. Retrograde cerebral perfusion may reduce ischemic damage during interruption of cerebral blood flow.
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PMID:Retrograde cerebral perfusion through a superior vena caval cannula protects the brain. 172 41

Downregulation of cholinergic receptors is a consequence of subchronic exposure to an organophosphate anticholinesterase. The purpose of this investigation was to determine if there was a downregulation of the cholinergic receptors in mice following administration of a single dose of soman (pinacolyl methylphosphonofluoridate) or physostigmine. The change in the temporal response (mean minimum temperature and area under the curve) of core temperature following administration of either a muscarinic or nicotinic agonist such as oxotremorine (156 micrograms/kg, IP) or nicotine hydrogen tartrate (15 mg/kg, SC) was used as an indicator of downregulation of muscarinic or nicotinic receptors, respectively. Twenty-four h following soman (100 micrograms/kg, SC) administration, there was a significant decrease (p less than 0.05) in oxotremorine- but not nicotine-induced hypothermia. The significant differences in the mean minimum temperature and AUC were still present 4 days after exposure to the soman. Neither lower doses of the organophosphate anticholinesterase, soman (50 and 70 micrograms/kg), nor the carbamate anticholinesterase, physostigmine (500 micrograms/kg), produced a significant change in either oxotremorine- or nicotine-induced hypothermia. The results of this study suggest that receptor downregulation observed after subchronic administration of soman is also evident following administration of a single, sublethal dose of an organophosphate anticholinesterase, soman, but not after administration of a carbamate anticholinesterase, physostigmine. The in vivo assessment of the muscarinic receptor using oxotremorine hypothermia may be a sensitive indicator of the functionality of the drug-receptor coupling and indicate a physiological consequence of receptor downregulation.
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PMID:Effect of a single dose of an acetylcholinesterase inhibitor on oxotremorine- and nicotine-induced hypothermia in mice. 176 13

Total energy expenditure (TEE) was measured over two 10-day periods, before and after operation in 16 patients undergoing coronary artery surgery and randomized to have cardiopulmonary bypass with an intraoperative blood temperature of either 28 or 20 degrees C. TEE was measured with doubly labelled water containing stable isotopes of hydrogen and oxygen to allow calculation of TEE over fixed periods from the differential rate of excretion of the two isotopes. Results were available for eight patients in the 28 degrees C group but for only seven in the 20 degrees C group (one patient in this group was excluded as the temperature allocated was not achieved). The groups were similar with respect to body-weight and lean body mass. The 20 degrees C group received more grafts than the 28 degrees C group, resulting in an increase in cross-clamp and bypass times. Mean preoperative TEE was similar in both groups. The mean difference in fractional turnover rates of hydrogen and oxygen was not significantly different in the postoperative period. There was a non-significant increase in the mean 10-day postoperative TEE, calculated in total calories, of 4.7 per cent in the 28 degrees C and 5.1 per cent in the 20 degrees C group. When changes in postoperative TEE were calculated according to lean body mass, the mean increases were respectively 3.7 and 3.2 per cent. Cardiac surgery utilizing cardiopulmonary bypass and intraoperative hypothermia results in only a modest increase in postoperative TEE. In this study a more profound level of intraoperative hypothermia did not influence the change in postoperative TEE.
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PMID:Effects of cardiac surgery and intraoperative hypothermia on energy expenditure as measured by doubly labelled water. 201 84

Cytotoxicity resulting from the interaction of fluorescent light from a flow hood with Hepes-buffered cell culture medium at room temperature was demonstrated. Toxicity was prevented by keeping both cells (V79 Chinese hamster) and medium shielded from direct fluorescent light ("dark conditions") or by supplementing the medium with 10 micrograms/ml catalase; this suggests that extracellular hydrogen peroxide is a major cause of the lethal effect under "lighted conditions." No sensitization resulted from the exposure of cells in a sodium bicarbonate (SBC)-buffered medium to fluorescent light, nor in a catalase supplemented SBC-buffered medium. The Hepes/light reaction during routine cell manipulations presensitized cells to hypothermia damage in the dark with the presensitization being more severe for 5 than for 10 degrees C hypothermic exposure. Presensitization was prevented by performing the complete experiment under dark conditions or by supplementing the medium with 10 micrograms/ml catalase. However, catalase did not improve the hypothermic survival when experiments were performed under dark conditions. Hence, 10 micrograms/ml catalase does not protect cells from hypothermic (5 and 10 degrees C) damage per se, but rather from Hepes/light sublethal damage which interacts with hypothermic sublethal damage to result in lethal lesions. Additionally, under dark conditions, superoxide dismutase (SOD), allopurinol, catalase plus SOD, DMSO, or mannitol did not improve survival when present during hypothermic storage, suggesting that extracellular superoxide anion, hydrogen peroxide, or hydroxyl radicals are not the cause of cell killing under conditions of pure hypothermia uncomplicated by prehypothermic ischemia or hypoxia.
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PMID:Factors influencing survival of mammalian cells exposed to hypothermia. V. Effects of hepes, free radicals, and H2O2 under light and dark conditions. 201 62

The response of regional-cerebral blood flow (rCBF) to change in the tissue temperature was studied using normal and tumour-bearing monkeys. The local brain was selectively heated by the external microwave irradiation, while the body was kept hypothermic (30.1 +/- 0.1 degrees C, mean +/- standard error) by immersion in a cold water bath. The rCBF in brain and/or tumour tissues was sequentially measured by inhalation hydrogen clearance method. In the normal animal study (n = 7), rCBF changed in response to the tissue temperatures over a range of 29.4-40.7 degrees C with a constant rate 15.2% per degree Celsius change. Similarly, rCBF in the tumour-bearing animals (n = 7) changed proportionately with change in the tissue temperatures over a range of 28.4-42.5 degrees C in tumour and 27.6-41.8 degrees C in brain tissue. The rate in rCBF change per degree Celsius was 6.5% for tumour, which was significantly smaller than that for brain tissue (13.5%) (P less than 0.01). These results indicated that rCBF can be controlled by the defined application of selective heating with temperatures ranging from shallow hypothermia to modest hyperthermia. Vascular response to temperatures in the tumour and brain tissues may play a significant role in the application of heat to brain tumour treatment.
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PMID:Cerebral blood flow response to the tissue temperature in tumour and brain tissues. 255 83

In the feline intestine studies have implicated superoxide (O.-) and other oxygen derived free radicals as initiators of injury as measured by increased capillary permeability during the reperfusion period. Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Pathological consequences of these events include inflammatory neutrophil infiltration, damage to the collagen and mucosal basement membrane, increased capillary permeability, edema, cell degeneration and necrosis. Animal models of neonatal necrotizing enterocolitis (NNEC) indicate that intestinal injury occurs after the etiologic factors (hypothermia, hypoxia) are removed. In order to determine the role of active oxygen species in the pathogenesis of NNEC, weanling hamsters and neonatal piglets were cold stressed and activities of pro/antioxidant enzymes were determined, and histopathologic and ultrastructural studies were performed. Cold stressed weanling hamsters showed a 55.7% (P less than 0.05) decrease in xanthine dehydrogenase/xanthine oxidase activity ratio. Light microscopy revealed scattered colonic mucosal erosions and submucosal edema in 50% of cold stressed animals. Transmission electron microscopy demonstrated degeneration of colonic mucosal epithelial cells, enlarged intracellular spaces, cytoplasmic vacuolization, and nuclear membrane swelling. The colonic serosa was also edematous and infiltrated with bacteria. Large intestinal tissue from cold stressed neonatal piglets showed a significant increase (P less than 0.05) in Mn and Cu, Zn, SOD, CAT, GSH-Red, total GSH, and Glc6-PD at 0 and 12 hrs. post stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal post-ischemic reperfusion injury: studies with neonatal necrotizing enterocolitis. 259 24

The purpose of this work was to study the effects of warm (37 degrees C) and cold (4 degrees C) ischemia on different mitochondrial functions in rat brain, liver and kidney. After 10 to 60 minutes of ischemia at 37 degrees C the energy coupled respiration as well as the ADP-induced malate-aspartate shuttle activity in brain and liver mitochondria or the rate of mitochondrial ATP synthesis in kidney were significantly decreased. However, the respiratory rates and the shuttle activity in the absence of ADP remained unchanged. These data suggest that ischemia primarily affects electron transport in the respiratory chain rather than the hydrogen shuttle and the energy coupling system. When the temperature during the indicated ischemic periods was decreased to 4 degrees C, in brain and liver no significant alterations of these mitochondrial functions were found in comparison with the non-ischemic controls. When rat kidneys were stored for 36 hours at 4 degrees C according to Collins mimicking transplantation conditions, the mitochondrial respiration and ATP synthesis were only slightly decreased. It therefore appears that hypothermia can prevent effectively mitochondrial dysfunction due to ischemia.
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PMID:Effects of warm and cold ischemia on mitochondrial functions in brain, liver and kidney. 277 Jul 17


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