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

Cultured fetal mouse hearts deprived of oxygen and glucose were used to examine the effect of temperature on the mechanical, biochemical, and ultrastructural responses of the deprived myocardium to assess the utility of this in vitro model for studying myocardial necrosis, preservation, and repair. After 4 h of deprivation at 4, 24, 37, or 42 degrees C, 1) beating had ceased;2) ATP levels were decreased by 22% for 4 degrees C insults, 69% for 24 degrees C, 89% for 37 degrees C, and 97% for 42 degrees C; 3) CPK and LDH levels were unchanged; and 4) ultrastructural changes were observed. After 24 h of recovery from deprivation, 1) beating resumed, except for 42 degrees C;2) ATP levels were 102% of control for 4 degrees C; 99% for 24 degrees C; 62% for 37 degrees C; and 4% for 42 degrees C; 3) LDH content was decreased by 0% at 4 degrees C; 6% at 24 degrees C; 35% at 7 degrees C; and 70% at 42 degrees C; and 4) CPK content decreased similarly. Hypothermia protected deprived myocytes while hyperthermia accelerated cell necrosis. Combining deprivation with thermal insult in this in vitro model provides a spectrum of myocardial damage for studying the effect of interventions on repair processes and on metabolic changes in jeopardized myocardium.
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PMID:Thermally induced myocardial preservation and necrosis in deprived fetal mouse hearts. 84 85

In surface-induced deep hypothermia, metabolic acidosis resulting from lactacidemia was observed. In the aspect of myocardial metabolism, the rate of reduction in coronary A-V difference ratio of lactate, pyruvate and NEFA was less than that of coronary flow and myocardial oxygen consumption in the hypothermic heart. Namely, it seems that lactate, pyruvate and NEFA play an important role as energy fuel in the hypothermic heart. On the other hand, myocardial metabolism of glucose was reduced in the hypothermic heart. Moreover, it seems that exogenous corticosteroid and ATP do not influence on the myocardial metabolism of carbohydrate and lipid in the hypothermic heart.
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PMID:Experimental studies on myocardial metabolism of carbohydrate and lipid in surface-induced deep hypothermia. 91 79

The fine structure and the content in energy-rich phosphate compounds, glycogen, and metabolites of the Embden-Meyerhoff-pathway in rabbits hearts or human papillary muscles arrested by magnesium aspartate-procaine are investigated in normothermia and mild or deep hypothermia. In all experimental conditions the break-down of adenine nucleotides and glycogen was distinctly retarded in cardioplegia compared to ischaemic arrest. While e.g. an ATP-content of 3.6 mumole/g wet weight was found after 40 min. at 32 degrees C in the magnesium asparate-procaine arrested heart, it dropped down to 1.3 mumole/g in the ischaemically arrested heart. In cardioplegia after 60 min at 15 degrees C the in vivo contents of ATP and glycogen were determined. The rate in metabolic changes in the magnesium aspartate-procaine arrested human papillary muscle was in the range of that recorded in the arrested rabbit heart. The ultrastructural appearance of the cardioplegically arrested heart did not differ from that of the controls after 20 min at 32 degrees C or 120 min at 15 degrees C. In hearts arrested by cardioplegia 40 min at 32 degrees C first signs of ischaemic lesions e.g. mild swelling of mitochondria and few rarefications in mitochondrial matrix were observed. Because of the significantly improved preservation of the fine structure of the heart and retardation of ischaemically provoked changes in cardiac metabolism, the method of inducing heart arrest by cardioplegia should also clinically be given preference to methods of arresting the heart by ischaemia.
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PMID:Metabolism and structure of the magnesium aspartate-procaine-arrested ischaemic heart of rabbit and man. 94 73

In surface-induced deep hypothermia, metabolic acidosis resulting from lactacidemia was observed. In the hypothermic heart, the rate of reduction in the coronary arteriovenous (A-V) difference ratio of lactate, pyruvate, and nonesterified fatty acids (NEFA) was proportionately less than that of coronary flow and myocardial oxygen consumption, suggesting that lactate, pyruvate, and NEFA play important roles as energy fuels in the hypothermic heart. Myocardial metabolism of glucose was reduced; exogenous corticosteroids and ATP do not influence the myocardial metabolism of carbohydrates and lipids in the hypothermic heart.
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PMID:Experimental studies on myocardial metabolism of carbohydrates and lipids in surface-induced deep hypothermia. 103 4

The catabolism of 5'-adenine nucleotides in the cortex of the rabbit kidney was studied during normothermic and hypothermic ischaemia. Changes were found in the cortical content of ATP, ADP, AMP, and SAN (the sum of 5'-adenine nucleotides) during ischaemia; those changes were delayed by hypothermia. The loss of SAN was found to be significantly correlated to the duration of normothermic as well as hypothermic ischaemia. The oxypurines hypoxanthine and xanthine and the nucleoside inosine were shown to be the final products of the catabolism of 5'-adenine nucleotides. An accumulation of hypoxanthine-xanthine and inosine in the tissue and a corresponding excretion in the perfusion fluid occurred simultaneously with the catabolism of 5'-adenine nucleotides, in equivalent amounts. It is concluded that determination of the amount of oxypurines excreted during kidney preservation is an indirect measure of the loss of SAN in the tissue, and a reflection of the changes in the metabolic state.
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PMID:Breakdown of 5'-adenine nucleotides in ischaemic renal cortex estimated by oxypurine excretion during perfusion. 115 18

Isolated perfused working rat hearts were subjected to elective cardiac arrest for 20 or 30 min. Various methods of arrest were studied, either singly or in combination and with or without coronary perfusion. The functional recovery of the heart following the termination of arrest was found to be related to the concentration of ATP and creatine phosphate in the myocardium at the end of the period of arrest. In turn, these concentrations were dependent upon the method used to induce arrest. Normothermic ischemic arrest led to a marked reduction in high energy phosphates and a poor functional recovery. In contrast, coronary perfusion with hypothermic solutions or solutions containing high concentrations of potassium, induced arrest without depleting ATP or creatine phosphate. These procedures conferred considerable protection on the myocardium and thus permitted good recoveries. The energy status and recovery associated with ischemic arrest could be improved by combining the ischemia with hypothermia or potassium arrest. The latter, while increasing recovery significantly, still failed to afford complete protection to the myocardium. Potassium chloride gave greater protection than potassium citrate. When topical hypothermia was combined with ischemia, a time and temperature relationship was demonstrated but effective protection could only be obtained with severe topical hypothermia over a relatively short time period. The results stress the importance of maintaining high energy phosphates during arrest, and this requires the provision of a continuous supply of oxygen and nutrient, which may perhaps be best achieved by ensuring continuous and adequate coronary perfusion.
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PMID:Ischemic damage and metabolism during elective cardiac arrest. 120 80

Effects of 5 cold storage solution on hepatic high energy phosphate metabolism and metabolic function were examined using the isolated perfused rat liver. University of Wisconsin (UW), Euro-Collins (EC), and 2 cardioplegic solutions, Bretschneider's HTK and St. Thomas Hospital solution, were studied for their protective capacity. Krebs-Henseleit bicarbonate buffer (KHB) was used to point out the effect of simple hypothermia. Liver ATP, total adenine nucleotides and energy charge losses were significantly lower during 21 h of storage in UW-preserved livers. Also, only UW-protected livers were able to complete regeneration of ATP and total adenine nucleotides after 1 h of reperfusion, whereas EC, HTK, St. Thomas and KHB stored livers only showed minimal regeneration. Concerning metabolic function, UW protected livers liberated significantly less LDH and sGOT as well in the 21-hour storage solution as into the perfusate under reperfusion conditions. This study demonstrates the capability of UW solution in liver preservation by its ability to maintain and restore high energy phosphates.
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PMID:Hepatic energy metabolism during hypothermic storage and reperfusion using different protecting solutions. 129 38

The objective of this study was to assess the influence of temperature on the coupling among energy failure, depolarization, and ionic fluxes during anoxia. To that end, we induced anoxia by cardiac arrest in anesthetized rats maintained at a body temperature of either 34 degrees C or 40 degrees C, measured extracellular K+ concentration (K+e), and froze the neocortex through the exposed dura for measurements of phosphocreatine (PCr), creatine (Cr), ATP, ADP, and AMP, glucose, glycogen, pyruvate and lactate content after ischemic intervals of maximally 130 s. Free ADP (ADPf) concentrations were derived from the creatine kinase equilibrium. Hypothermia reduced the initial rate of rise in K+e, and delayed the terminal depolarization; however, both hypo- and hyperthermic animals showed massive loss of ion homeostasis at a K+e of 10-15 mM. The initial rate of rise in K+e did not correlate to changes in ATP, or ATP/ADPf ratio, suggesting that temperature changes per se may control the degree of activation of K+ conductances. The results clearly showed that, in both hyper- and hypothermic subjects, energy failure preceded the sudden activation of membrane conductances for ions. The results indicate that temperature primarily influences membrane permeability to ions like K+e (and Na+), and that cerebral energy state is secondarily affected. It is proposed that the higher rate of rise of K+e at high temperatures accelerates ATP hydrolysis primarily by enhancing metabolic rate in glial cells.
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PMID:Changes of labile metabolites during anoxia in moderately hypo- and hyperthermic rats: correlation to membrane fluxes of K+. 142 48

Myocardial cell vulnerability to phospholipase C (PC-PLC) attack was investigated in three different preparations of rat myocardial cells: triacylglycerol (TG)-loaded, hypothermic/rewarmed and energy depleted myocytes. The attack by PC-PLC was evaluated as PC-PLC induced glycerol output due to the combined action of phospholipase C and intracellular lipases. PC-PLC induced glycerol output was significantly higher (p < 0.05) in all three myocyte preparations, compared to their respective controls. Cell morphology (% rod shaped myocytes) of TG-loaded or hypothermic/rewarmed myocytes was not different from their controls, whereas energy depleted myocytes almost exclusively were rounded up, due to hypercontraction of the myofilaments. Hypothermic/rewarmed and energy depleted myocytes showed a significantly higher release of lactate dehydrogenase (LDH), compared to their controls although the difference was much more pronounced in the latter. Finally, the cellular contents of ATP were maintained both in TG-loaded and hypothermic rewarmed myocytes, while energy depleted myocytes contained only about 25% of the normal ATP level. These results demonstrate that attack from exogenously added phospholipases can occur, not only in seriously damaged cardiac myocytes, but in myocytes with a more subtle damage as well.
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PMID:Myocardial cell vulnerability to exogenous phospholipase attack. 148 Jan 54

To ascertain the alterations in cerebral oxidative and energy metabolism that occur during hypothermic circulatory arrest, nitrous oxide-anesthetized, paralyzed, and artificially ventilated newborn dogs were surface cooled to 18-20 degrees C, after which their hearts were arrested with KCl. At 10, 30, 60, and 105 min of circulatory arrest, their brains were prepared by in situ freezing for the regional analysis of glycolytic intermediates and high-energy phosphate reserves. Hypothermia alone was associated with optimal preservation of labile metabolites in brain, even in caudal brainstem and cerebellum, compared with barbiturate-anesthetized littermates. After onset of hypothermic circulatory arrest, glucose decreased progressively in cerebral cortex, caudate nucleus, hippocampus, and subcortical white matter to negligible levels by 30 min. Pyruvate increased transiently (+50%) at 10 min, whereas lactate increased and plateaued (10-11 mmol/kg) at 30 min. The disproportionate increases in pyruvate and lactate resulted in a progressive rise in the lactate/pyruvate ratio. Phosphocreatine fell precipitously to < 0.5 mmol/kg in all structures, with a preservation of ATP for the first 10 min of cerebral ischemia. Thereafter, ATP decreased to < 0.1 mmol/kg in cerebral cortex and between 0.1 and 0.2 mmol/kg in caudate nucleus, hippocampus, and white matter. Total adenine nucleotides (ATP+ADP+AMP) were partially depleted by 30 min in the gray matter structures but were unchanged from control for 60 min in white matter. The findings showed a direct correlation between preservation of cerebral energy stores during hypothermic circulatory arrest and the selective resistance of subcortical white matter to ischemic damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral oxidative metabolism during hypothermia and circulatory arrest in newborn dogs. 148 Apr 56


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