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

Temperature has pronounced and complex effects on cellular physiology. Rates of enzymatic processes display an exponential change with temperature, as expressed by the Q10 relationship. The basis of these effects may be temperature induced phase transitions in membrane lipids and protein associated water, effects on bulk water and effects on the relationship between water and inorganic solutes. Hypothermia may be lead to a collapse in ionic regulation, leading to an uncontrollable and lethal calcium influx. Subfreezing temperatures may cause injury due to cellular freezing with subsequent excessive osmotic swelling, lyotropic effects or excessive osmotic shrinking due to extracellular freezing. Cells may protect themselves by freeze avoidance accomplished by removal of ice nucleators, production of proteinaceous antifreeze agents and accumulation of polyols. Alternatively they may secure extracellular freezing by production of extracellular ice nucleating agents, and counteract lyotropic effects and osmotic shrinking by accumulation of polyols which reduce ice content in a colligative manner.
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PMID:Hypothermia and cellular physiology. 181 67

During hibernation the animals decrease their body temperature down to a few degrees above 0 degree C. This means that when entering into and arousing from hibernation their body temperature passes the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). We found in other experiments that the hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, addition of 0.55 molar CaCl2 to isolated hearts perfused with a potassium free Tyrode solution, addition of procaine to isolated hearts perfused with Tyrode solution after previous administration of adrenaline, ligation of the proximal part of the left anterior descending coronary artery, and electrical stimulation in the vulnerable phase of the heart cycle. Several mechanisms are at work to explain this resistance to VF of the hibernator heart when compared to the nonhibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, different physico-chemical properties with a lower melting point of the lipids in the hibernator, different enzyme temperature activity curves in the hibernator and a different handling of intracellular calcium resulting in a protection against calcium overload in the hibernator heart, when compared with the nonhibernator heart.
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PMID:The hibernator heart--nature's model of resistance to ventricular fibrillation. 181 81

Hypothermia retards cardiac contraction and prolongs the subphases of the cardiac cycle in varying degrees. Six anaesthetized beagle dogs were catheterized and cooled between ice bags until the aortic blood temperature was 25 degrees C and then rewarmed to normothermia. The speed of relaxation decreased to a half from its value in normothermia as indicated by the time constant of exponential isovolumic ventricular pressure fall and by the change in the negative dp/dt. It is suggested that retardation of relaxation is connected with temperature dependent changes in calcium kinetics. Decrease of cardiac output was mediated mainly by decreased stroke volume indicating sympathetic tone in spite of cold narcosis.
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PMID:Cardiac function in hypothermia. 181 82

The synthesis and biological properties of a series of nicotinamide ethers are described. These compounds, structurally novel calcium-independent phosphodiesterase inhibitors, also inhibit the binding of [3H]rolipram to rat brain membranes and reverse reserpine-induced hypothermia in the mouse. Several compounds exhibited potent in vivo activity comparable to the standard agent, rolipram.
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PMID:Nicotinamide ethers: novel inhibitors of calcium-independent phosphodiesterase and [3H]rolipram binding. 182 16

A mathematical formula was derived from an active cross-bridge model to express the changes in the active myocardial force which occurred during systole. Using the formula and the assumption that the energy expenditure for cross-bridge cycling (Um) was a linear function of the force-time integral (FTI), we developed formulae describing the left ventricular Um versus FTI relation, the Um versus force relation, and the Um versus pressure-volume area (PVA) relation. There were strong disagreements between the model predictions and the experimental findings relating oxygen consumption of the heart versus the PVA relation. These differences may have resulted from the oversimplification of important mechanical and/or biochemical properties of the myocardium in the model. However, the model appeared to accurately reproduce the Fenn effect (effect of contraction modes on energy liberation) for the myocardium as well as the effect of catecholamine infusion, hypothermia, and hypothyroidism on the changes in the binding rate of Ca2+ with the regulatory proteins, the myosin ATPase activity, the peak force developed, and the myocardial energy expenditure. We present this work as an intermediate step towards a complete theoretical linkage between the molecular biology, dynamics, and energetics of the human heart.
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PMID:Cross-bridge cycling energy of cardiac muscle estimated from an active cross-bridge model. 182 94

The effects of hypothermic ischemia and reperfusion on sarcolemma and sarcoplasmic reticulum Ca2+ transport were studied in vesicles isolated from rabbit hearts. Hypothermic global ischemia was produced by immersing hearts in saline at 4 degrees C for 3 h. Following hypothermic ischemia, reperfusion was carried out for 40 min using a Langendorff perfusion system for the working heart. Na+,K(+)-ATPase activity of sarcolemmal vesicles (SL), was not depressed by hypothermic ischemia nor by ischemia and reperfusion. The initial rate of Na(+)-Ca2+ exchange in SL vesicles was not depressed, but the maximum amount of Ca2+ uptake was increased both after hypothermic ischemia and after reperfusion. Ca2+ uptake activity of sarcoplasmic reticulum vesicles (SR) isolated from hearts subjected to hypothermic ischemia was slightly lower than that of control, and was further reduced following reperfusion. Ca(2+)-ATPase activity of SR was unaffected by hypothermic ischemia, while it was markedly lowered after reperfusion. Although the phosphoenzyme level in SR vesicles was slightly decreased, the turnover rate was reduced after reperfusion. Reperfusion injury thus took place mainly in SR while SL appeared to be tolerant to ischemia and reperfusion.
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PMID:Effect of hypothermic ischemia and reperfusion on calcium transport by myocardial sarcolemma and sarcoplasmic reticulum. 183 91

The effects of hypothermia and hyperthermia on the cerebral microcirculation were studied using isolated perfused intracerebral (parenchymal) arterioles obtained from rats. In a temperature-dependent manner, hypothermia (20.0 degrees to 35.0 degrees C) dilated the spontaneous tone developed by the arterioles and also diminished their contractile response to potassium and prostaglandin F2 alpha. In contrast, hyperthermia (40.0 degrees to 45.0 degrees C) induced a biphasic response consisting of initial vasoconstriction and secondary vasodilation. Exposure of the vessels to 45.0 degrees C for 30 minutes irreversibly abolished the spontaneous tone and responsiveness of the arterioles when the temperature of the preparation was returned to 37.5 degrees C. In calcium-free solutions, however, the arteriolar diameter was not affected within a temperature range of 20.0 degrees to 45 degrees C. Furthermore, arterioles that had been in a calcium-free solution during exposure to 45 degrees C temperature recovered their viability at 37.5 degrees C. These results suggest that changes in ambient temperature alter calcium-induced contraction in arteriolar smooth muscle, and that the irreversible effects of hyperthermia on the arterioles are dependent upon extracellular calcium. These studies indicate that alterations in brain temperature may affect the pathogenesis of cerebral ischemia by mechanisms that are in part independent of parenchymal metabolism.
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PMID:Effects of hypothermia and hyperthermia on the reactivity of rat intracerebral arterioles in vitro. 186 45

This study was designed to characterize the previously described hypothermic action of norepinephrine (NE) microdialyzed into the medial preoptic area (MPO) of conscious guinea pigs. To this end, the effects on core temperature (Tco) of isotonic pyrogen-free saline (PFS), hypotonic PFS, inactive (oxidized) NE (hypertonic), 5-hydroxytryptamine (5-HT, 10 and 20 micrograms/microliter), PFS with or without 2.4 mM Ca2+, 10 micrograms/microliters NE with Ca2+, and various doses of NE (0.05-60 micrograms/microliters) were compared in a series of studies at an ambient temperature (Ta) of 24 degrees C. The Tco responses to 10 micrograms/microliters NE in a cold (15 +/- 2 degrees C) and a warm (31 +/- 1 degrees C) Ta and during the night in the dark in Ta 24 degrees C were also measured. Bromophenol blue (0.2%) was microdialyzed to assess the extent of diffusion of these dialysates. A stain was found in the MPO, which increased in density but did not spread beyond this region over 3 h of continuous microdialysis. Neither PFS nor the hypotonic and hypertonic solutions had any obvious effect on Tco. Similarly, neither dose of 5-HT evoked a thermal response. Ca2+ added to either PFS or NE did not alter the usual Tco responses to these two solutions. NE induced dose-dependent hypothermia in Ta 24 degrees C. NE microdialyzed in Ta 15 degrees C also produced Tco falls, but these responses were smaller than those in 24 degrees C. NE had no effect in the warm Ta. During the night, NE elicited similar Tco falls, but their recoveries after dialysis ended were slower than during the day.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microdialysis of norepinephrine into preoptic area of guinea pigs: characteristics of hypothermic effect. 190 44

We investigated the contribution of maximal Ca(2+)-activated force to the positive inotropism induced by mild hypothermia. Phosphorus-31 nuclear magnetic resonance spectroscopy revealed that neither energy-related phosphorus compounds in myocardium nor intracellular pH was responsible for the change in contractility. Maximal Ca(2+)-activated pressure (MCAP), the intact-heart correlate of maximal Ca(2+)-activated force, was determined in isolated perfused rabbit hearts by measuring isovolumic left ventricular pressure during tetani at extracellular Ca2+ concentrations greater than or equal to 10 mM. Tetani were elicited by rapid pacing after exposure to ryanodine. MCAP increased by 2.17 +/- 0.28% (mean +/- SE, P less than 0.001, n = 19) for each degree of myocardial cooling between 30 and 38 degrees C. Our results indicate that a primary change in myofilament Ca2+ responsiveness underlies the positive inotropism in hypothermia. The increase in maximal Ca(2+)-activated force may explain the observation of positive inotropism without an upward shift in the relation between oxygen consumption and pressure-volume area, as previously reported for cooled whole hearts.
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PMID:Positive inotropism in hypothermia partially depends on an increase in maximal Ca(2+)-activated force. 192 84

Working rat hearts were perfused for 15 minutes at 37 degrees C before switching to a Langendorff perfusion (60 mm Hg aortic pressure) at 10 degrees C for 40 minutes of hypothermic arrest. Ventricular function was allowed to recover for 15 minutes at 37 degrees C by reestablishing the prehypothermic conditions. The perfusate was Krebs-Henseleit bicarbonate buffer containing 3% bovine serum albumin and either glucose (11 mmol/L) or glucose (11 mmol/L) plus palmitate (1.2 mmol/L) and gassed with 95% O2 and 5% CO2. In hearts receiving glucose alone as substrate, coronary flow was maintained constant during the 40 minutes of hypothermic arrest and returned to prehypothermic rates with rewarming. Ventricular function, as estimated by peak systolic pressure and heart rate, recovered to the prehypothermic level. When palmitate was added, coronary flow decreased continuously throughout the hypothermic perfusion (22% decrease by 40 minutes), and ventricular pressure development was lower throughout the rewarming perfusion. Tissue levels of adenosine triphosphate and creatine phosphate were well maintained and long-chain acyl coenzyme A and acyl carnitine decreased during hypothermia regardless of the substrate provided. With rewarming, tissue levels of adenosine triphosphate and creatine phosphate decreased in those hearts receiving palmitate. Omission of fatty acid either during hypothermia or during the first 5 minutes of rewarming improved recovery of function. Addition of oxfenicine to inhibit fatty acid oxidation, or inhibition of Ca2+ overload by verapamil and low perfusate Ca2+, prevented the effects of palmitate on ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fatty acids suppress recovery of heart function after hypothermic perfusion. 192 62


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