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

An isolated rabbit heart preparation was used to characterize the effects of hypothermia on the deterioration in mitochondrial respiratory function and on the calcium overload that occurs during ischemia and reperfusion. Hearts were perfused aerobically with an asanguineous solution for 120 minutes or made totally ischemic for 90 minutes at 37 degrees, 34 degrees, 28 degrees, 22 degrees C, respectively, and reperfused for 30 minutes at 37 degrees C. Mitochondrial function was assessed by measuring calcium content, yield, oxygen consumption, and adenosine triphosphate-producing capacities. In addition, the mechanical function of the hearts was measured together with tissue adenosine triphosphate, creatine phosphate, and calcium content. In a separate series of experiments, the effect of temperature on the initial rate of respiration-supported calcium accumulation of mitochondria from freshly excised, nonperfused rabbit hearts was determined. The hearts made ischemic at 37 degrees C were severely depleted of tissue adenosine triphosphate and creatine phosphate. Their mitochondria accumulated calcium and the oxidative phosphorylating activity was impaired. During reperfusion, tissue and mitochondrial calcium levels were substantially increased, state 3 of mitochondrial respiration was further impaired, and the adenosine triphosphate-generating capacities were severely reduced. Diastolic pressure increased and there was no recovery of developed pressure. Isolated mitochondrial function of hearts made ischemic at 28 degrees and 22 degrees C was protected. There was a less marked increase in tissue and mitochondrial calcium, and the initial rate and total production of adenosine triphosphate were maintained. In these hearts there was an almost complete recovery of mechanical performance at reperfusion, whereas the ischemia-induced depletion of tissue adenosine triphosphate and creatine phosphate was not significantly reduced by hypothermia. The hearts made ischemic at 34 degrees C were only partially protected. These data suggest that a decrease in temperature from 37 degrees to 22 degrees C during ischemia did not significantly prevent depletion of adenosine triphosphate at the end of ischemia but reduced tissue and mitochondrial calcium overload, maintaining mitochondrial function. Thus in our experiments the protective effect of hypothermia might be related to a direct reduction of tissue and mitochondrial calcium accumulation rather than to a slowing in rates of energy utilization. This possibility is supported by the finding that in freshly excised, nonperfused rabbit hearts, hypothermia significantly reduced the initial rate of mitochondrial calcium transport.
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PMID:Effects of temperature on myocardial calcium homeostasis and mitochondrial function during ischemia and reperfusion. 232 31

The cellular response to hypotonic stimulation was studied with videometric methods in 266 proximal renal tubules dissected from Carassius auratus (goldfish). In hypotonic solutions (low NaCl), cells underwent rapid swelling followed by gradual shrinking toward isotonic volume (volume-regulatory decrease phase, VRD). Hypothermia (8 degrees C), increased extracellular potassium (15, 25, and 40 mM), quinine (0.1 mM), barium (0.5 mM), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS; 0.02 mM), acetazolamide (0.1 mM), decrements in extracellular bicarbonate, and increases in extracellular chloride impaired VRD. Ouabain (1.0 mM), furosemide (0.1 mM), and the chloride channel blocker 5-nitro-2-(3-phenylpropylalanine) benzoate (NPPB; 0.001 mM) had no effect. While VRD occurred in the absence of extracellular calcium influx, addition of the calcium ionophore A23187 (0.01 mM) in the presence of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA; 2.0 mM) impaired this process both in acidic and alkaline media. Trifluoroperazine (0.01 mM) reversibly inhibited VRD. The effect of this calmodulin inhibitor could not be overridden with the cationic ionophore gramicidin (0.5 microM). The data suggest that Carassius proximal renal tubular cells volume regulate in hypotonic solutions by the loss of KCl and osmotically obligated water. We postulate that the main efflux of potassium is through a calcium-gated potassium channel with its counter ion extruded through a calmodulin-regulated Cl(-)-HCO3- exchanger.
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PMID:Possible role of basolateral cell membrane in proximal renal tubule osmoregulation. 233 Oct 23

Experiments were performed to determine the ability of verapamil to reverse ethanol-induced hypothermia and behavioral changes. Permanent cannulae for intracerebroventricular (i.c.v.) infusion were implanted bilaterally in rats following standard stereotaxic procedures. Following post-operative recovery, either verapamil or artificial cerebral spinal fluid (ACSF) was infused i.c.v., followed by 4.0 g/kg ethanol in saline administered by intragastric gavage. Changes in body temperature and overall activity were monitored. In another series of experiments, rats were given either i.c.v. verapamil or ACSF followed by 1.5 g/kg intraperitoneal ethanol. Ability to turn over and open-field activity were monitored. In addition, to investigate the action of verapamil alone on body temperature, rats were infused i.c.v. either with verapamil or control ACSF, followed by intragastric administration of a volume of saline equal to 4.0 g/kg ethanol (20% v/v). At an ambient temperature of 22 degrees C, verapamil, infused prior to ethanol administration, significantly and rapidly attenuated the thermolytic action of ethanol. Central administration of verapamil alone did not induce a significant change in body temperature until more than 1.5 hr after injection, at which time temperature began to gradually increase. Pretreatment with verapamil induced significantly faster recovery from ethanol-induced changes in overall activity. Only a non-significant reversal of ethanol's effects on open-field activity and time taken to turn over occurred. These results demonstrate that verapamil can significantly antagonize ethanol-induced hypothermia and possibly motor disturbances in rats, leading us to postulate the possible involvement of neuronal Ca2+ channels in these effects of ethanol.
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PMID:Verapamil effects on physiological and behavioral responses to ethanol in the rat. 233 96

Hypothermic total circulatory arrest for repair of congenital heart lesions in neonates requires a period of rapid core cooling on cardiopulmonary bypass during which the myocardium is also exposed to hypothermic perfusion. Myocardial hypothermia in the nonarrested state results in an increase in contractility due to elevation of intracellular calcium levels. This study was designed to test the hypothesis that rapid myocardial cooling before cardioplegic ischemic arrest results in damage, with impaired recovery during reperfusion. Two groups of 10 rabbit hearts were perfused on an isolated Langendorff apparatus. Group N (normothermia) was perfused at 37 degrees C before 2 hours of cardioplegic ischemic arrest at 10 degrees C. Group C (cooling) was perfused at 15 degrees C in the unarrested state for 20 minutes before the same cardioplegic arrest conditions as group N. Left ventricular isovolumic pressure measurements, biochemical measurements from right ventricular biopsy specimens, and ventricular necrosis as defined by tetrazolium staining were used to compare the groups at 30 and 60 minutes of normothermic reperfusion. Developed pressure at a constant volume was preserved in group N at 90.7 +/- 4.5 mm Hg versus 76.9 +/- 6.3 in group C after reperfusion (p less than 0.05). Diastolic compliance showed significant deterioration in group C, with marked elevation of diastolic pressure during reperfusion (group N = 6.8 +/- 2.5 mm Hg versus group C = 38.9 +/- 6.1 after reperfusion; p less than 0.001). Adenosine triphosphate levels were significantly higher in group N both at end-ischemia and after reperfusion versus group C (group N = 17.0 +/- 1.1 nmol/mg protein versus group C = 7.7 +/- 1.0 after reperfusion; p less than 0.001). Group N had 0.4% +/- 0.4% necrosis of ventricular mass versus 19.3% +/- 2.2% with prearrest cooling in group C (p less than 0.0001). These results indicate that, when combined with cardioplegic ischemic arrest, rapid myocardial cooling in the unarrested state results in significant damage. The mechanism may be related to the cytosolic calcium loading effect of hypothermia that is not relieved during the subsequent period of cardioplegic arrest. Although hypothermia is an essential component to ischemic preservation, rapid cooling contracture can adversely influence cardioplegic myocardial protection.
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PMID:Rapid cooling contracture of the myocardium. The adverse effect of prearrest cardiac hypothermia. 239 83

To test the hypothesis that hypothermia prevents myocardial Ca2+ loading during reoxygenation, we examined the effects of 2 h of hypoxia with and without hypothermia on the Ca2+ content of cultured chick embryo ventricular cells. When compared with hypoxic cells at 37 degrees C, hypoxia at 11 degrees C (hypothermia) augmented the 45Ca content of cardiocytes after 30 min of normothermic reoxygenation from 3.85 +/- 0.2 to 4.7 +/- 0.1 nmol/mg protein (P less than 0.001). The Na+ content of hypoxic myocytes was also increased at the end of 2 h of hypoxia from 648 +/- 59 to 1,026 +/- 68 nmol/mg protein in cells exposed to hypoxia at 11 degrees C (P less than 0.001). Hypothermia ameliorated hypoxia-induced depression of cellular ATP content and did not result in significant membrane injury as determined by lactate dehydrogenase release. These data indicate that hypothermia augments rather than decreases the Ca2+ content of hypoxic myocytes during reoxygenation after hypoxia. Ca2+ loading appears to be secondary to an increase in Na+ content, creating a favorable gradient for Ca2+ influx through Na(+)-Ca2+ exchange or an unfavorable gradient for Ca2+ extrusion.
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PMID:Hypothermia increases calcium content of hypoxic myocytes. 238 17

The effect of a change in temperature on net mitochondrial Ca2+ exchange has been investigated in a suspension of adult rat ventricular myocytes. Temperature was varied between 42 degrees C and 15 degrees C. Hypothermia reduced the initial rate of respiration-dependent Ca2+ uptake and reduced the Na+-sensitivity of Ca2+ efflux. The net result of these alterations is that at low temperatures, the Ca2+ level at which a steady-state between mitochondria and sarcoplasm is maintained, will be raised.
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PMID:Effect of temperature on calcium exchange in digitonin-treated rat ventricular myocytes. 241 98

The possible myocardial protective effect of oral propranolol in combination with potassium cardioplegia and hypothermia was investigated in 30 greyhounds, divided into 2 sub-groups, by determining the changes in myocardial ATP and CP levels, ultrastructural changes and the changes in hemodynamics after a 2-hour period of myocardial ischemia. In group 1, in animals with multiple doses of cardioplegia during the 2-hour ischemic period, preoperative treatment with propranolol did not have a significant myocardial protective effect. In group 2, in animals with a single dose of cardioplegia, during the 2-hour ischemic period, propranolol resulted in a trend of improved survival, although the myocardial ATP and CP levels were the same in both sub-groups. In addition, the multiple doses of cardioplegia in group 1 caused increased subcellular edema in the myocardium. This study suggests that oral propranolol treatment may provide additional myocardial protection during ischemic periods when used with potassium cardioplegia and hypothermia. The mechanism of this effect is not established, but could relate to reduced transmembrane calcium influx.
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PMID:Oral beta-blockade with hypothermic potassium cardioplegia in cardiac surgery: is there an additive protective effect? 242 43

The effect of variation in temperature (37-32 and 27 degrees C) on electrical and mechanical activity of depolarized and isoprenaline- or barium-reactivated guinea pig ventricular strips was studied. Lowering the temperature brings a marked prolongation of isoprenaline-induced slow action potentials. In addition the maximal rate of depolarization was strongly reduced at lower temperatures. These effects were observed at an extracellular Ca2+ concentration of either 0.9 or 2.5 mM. The accompanying mechanical activities was significantly increased by reduction in temperature. Barium-induced slow action potentials were similarly affected by temperature variations. These observations suggest that hypothermia exert a sort of calcium antagonistic action probably coupled to a reduction of repolarizing outward potassium currents.
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PMID:Effect of temperature on isoprenaline- and barium-induced slow action potentials in guinea-pig ventricular strips. 243 Aug 55

The effects of nicardipine, a calcium channel blocking agent, injected into the cerebral ventricles, (i.c.v.), on the body temperature of unanaesthetized cats have been investigated. Nicardipine produced a biphasic effect on body temperature: a transient dose-dependent decline followed by a longlasting elevation. The fall, but not the rise, of body temperature was associated with a dose-dependent increase in respiration. Yohimbine, in small doses, but not prazosin and propranolol, when injected into the cerebral ventricles, attenuated the hypothermia evoked by i.c.v. nicardipine. However, all the antagonists, except yohimbine in large doses, depressed the hyperventilation induced by nicardipine. Calcium chloride (i.c.v.) reversed, while i.c.v. methysergide virtually had no effect on hyperthermia caused by i.c.v. nicardipine. Nicardipine virtually had no effect on body temperature of intracerebroventricular reserpine- and alpha-methyl-p-tyrosine-treated cats. It appears, therefore, that nicardipine at least in part evoked hypothermia through alpha-2 adrenoceptors located presynaptically, while nicardipine-induced respiratory changes are mediated also partly via alpha-adrenoceptors having mixed alpha 1 and alpha 2 properties. The hyperthermic effect of nicardipine, on the contrary, is mainly due to an action on voltage-dependent calcium ion channels. The contribution of the hyperventilation to the hypothermic effect of nicardipine cannot be of great importance, since the hypothermia was accompanied with hypoventilation when alpha- and beta-adrenoceptor blocking agents were used.
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PMID:Nature of hypo- and hyperthermia induced by the calcium antagonist nicardipine. 245 79

Developmental differences in ischemic and potassium cardioplegic arrest were evaluated in newborn (birth to 7 day old) and adult (6 to 12 month old) New Zealand white rabbit hearts isolated and perfused by Langendorff's method. An extracellular space washout technique was used to measure intracellular sodium and calcium in the two age groups after ischemia alone, after normothermic and hypothermic cardioplegia, and after cardioplegia with reperfusion. Although the intracellular ionic contents of nonreperfused adult hearts after 30 and 40 minutes of ischemia were identical, there was a twofold elevation in intracellular sodium level after 40 minutes of ischemia in the newborn hearts. Adult hearts arrested by normothermic potassium cardioplegia demonstrated no alteration in the intracellular ionic content, whereas in the newborn hearts, potassium cardioplegia produced excess intracellular calcium loading before reperfusion, which was greater than that occurring with ischemia alone. When hypothermia (12 degrees C) was combined with cardioplegic arrest, a prereperfusion influx of sodium and calcium was not observed in the newborn hearts, and ionic reperfusion injury was blunted in both newborn and adult hearts. These studies demonstrate that the newborn heart is more susceptible than the adult to both ischemia and cardioplegia. This may be due to age-dependent differences in transmembrane passive diffusion, sodium/calcium exchange, or calcium slow channel properties and suggests alternative myocardial protective strategies for the newborn infant.
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PMID:Developmental changes in reperfusion injury. Comparison of intracellular ion accumulation in ischemic and cardioplegic arrest. 245 61


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