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

Various modalities have been proposed to protect the liver from injury during the ischemic period or after reperfusion. Most of the drugs were administered before the onset of ischemia, but a beneficial effect of post-treatment was reported for MP, dopamine and ATP-MgCl2. Previous studies were mainly performed upon experimental animals, but hypothermia and steroids were used to protect the liver from ischemic injury in patients as well. However, no controlled clinical trials exist demonstrating the efficacy of any type of prevention or treatment in ischemia of the human liver.
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PMID:Prevention and treatment of ischemia of the liver. 354 77

Mitochondrial function of the liver is one of the limiting factors in liver preservation. Nowadays, prostaglandin I2 (PGI2) is used as a cytoprotective agent in liver preservation without full understanding its mechanism involved. It is the objective of the present study to evaluate the protective effect of PGI2 on mitochondrial function of the rat liver during hypothermic preservation. Collins' solution was used as a preservation solution and PGI2 was added to it in some experimental groups. Both ischemic and non-ischemic livers were perfused with the preservation solution and preserved under simple hypothermia for 8 hr. Parameters of the mitochondrial function such as respiratory control, oxygen consumption rate in state 3 respiration, ADP/O ratio and the rate of ATP synthesis were decreased significantly after 8 hr hypothermic preservation, even if ischemic injury was not induced prior to preservation. ADP/O ratio, which represents the efficiency of oxidative phosphorylation in mitochondria, was improved significantly (p less than 0.01) when PGI2 was used as a cytoprotective agent. The rate of ATP synthesis, a parameter of energy producing reaction, showed a tendency to be increased by PGI2, but was not significant. It was concluded that hypothermic preservation of the rat liver is associated with the deterioration of the mitochondrial function and PGI2 has a favorable effect on the impaired ADP/O ratio of oxidative phosphorylation in mitochondria.
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PMID:Protective effect of prostaglandin I2 on hepatic mitochondrial function of the preserved rat liver. 355 Nov 89

The high-dose effects of chlorocitrate [(-)-threo-chlorocitric acid] were compared in vivo to another halogenated citrate analog, and a well-known inhibitor of the tricarboxylic acid (TCA) cycle, fluorocitrate. The compounds were given iv to two dogs per sex per group, and a control group received an equimolar amount of citric acid. Chlorocitrate (100 mg/kg) showed TCA cycle inhibition as did fluorocitrate (8 mg/kg) in that both caused depletion of ATP and accumulation of citrate in the liver. Chlorocitrate was a significantly weaker inhibitor of citrate metabolism than fluorocitrate as evidenced by a substantially lower accumulation of serum citrate despite a much higher dose. Both halocitrates produced a similar diabetes-like syndrome (hyperglycemia, glycosuria) mediated by a significant hyperglucagonemia and slight hypoinsulinemia. Chlorocitrate was more potent in this effect and a much greater buildup of plasma lactate ensued (18- versus 3.7-fold increase), enough to explain lethality observed in earlier studies. In contrast, fluorocitrate produced a severe life-threatening hypocalcemia (-30%), and hypercalcuria was observed. This effect on calcium distribution was only minimal with chlorocitrate. Both halocitrates had a similar depressive effect on circulation as evidenced by hypothermia, bradycardia, and elongation of the QT-interval. These changes were considered to be the result of lactic acidosis and the ongoing ion imbalance since heart ATP levels were not depleted.
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PMID:Comparative acute toxicity of chlorocitrate and fluorocitrate in dogs. 359 Jan 93

Anaerobic metabolism in heart muscle plays a role in maintenance of myocardial preservation only during ischemia or hypoxia. In an ischemic state, such as during a heart attack or even during the induced ischemia of open heart surgery, there is impairment of blood flow to the myocardium. The major energy-yielding process in the heart is through the metabolism of glucose and lipids by oxidative reactions. Under anaerobic conditions, oxygen is not available to accept the electrons in the metabolic degradation of substrates and anaerobic glycolysis becomes important in the preservation of myocardial viability during the ischemic process. Unfortunately, the accumulated products of glycolysis, namely protons and lactate, work to inhibit glycolysis, ultimately resulting in a depression of anaerobic metabolism. Cardioplegia, as utilized during open heart surgery, has the effect of inducing instantaneous induction of myocardial mechanical and electrical arrest with a maximal inhibition of the energy utilizing metabolic processes. This effectively reduces substrate utilization and prevents the deleterious consequences of the ischemic process. Cardioplegia is most effective when combined with the additive properties of hypothermia, which plays a significant role in decreasing myocardial metabolism. However, during prolonged hypothermic cardioplegic arrest, sufficient ATP cannot be maintained for cellular integrity and anaerobic glycolysis becomes of increasing importance for maintenance of myocardial preservation. This presentation deals with the mechanics of aerobic versus anaerobic metabolism during the ischemic process of open heart surgery.
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PMID:Aerobic vs anaerobic metabolism during ischemia in heart muscle. 359 61

Little is known about postnatal changes in myocardial purine metabolism. We therefore studied how ATP catabolism was affected by hypothermia and ischaemia in neonatal and adult hearts. Hypothermia during ischaemia protected isolated adult and newborn hearts against ATP decline. Reperfusion after normothermic ischaemia resulted in higher ATP levels in newborn hearts with less release of ATP-catabolites. During normoxia adult hearts released mainly urate (80% of total purine release), while newborns released mainly hypoxanthine (64%). During early reperfusion adult and newborn hearts released mainly inosine (50-60%). The very low xanthine oxidase activity in the neonatal heart could be an important factor in the observed ATP preservation during reperfusion.
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PMID:Developmental differences in myocardial ATP metabolism. 366 14

The interrelation between the energy and nitrogenous metabolism of the myocardium during cardioplegia has been studied in patients with congenital valvular heart disease (tetralogy of Fallot--12 patients, ventricular septal defect--5 patients). Whole body hypothermia with repeated heart reperfusion with cold cardioplegic blood perfusate was used for the protection of the myocardium. However, ATP level of the myocardium of some patients decreased by 20% and more of the baseline. This loss was accompanied by a reduction in glutamate and aspartate levels and a rise in ammonium and alanine levels in the myocardium (by 17.7 +/- 3.8; 17.6 +/- 5.9; 61.4 +/- 12.5 and 92.4 +/- 26.3% of the baseline, respectively).
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PMID:[Effect of cardioplegia on nitrogen and energy metabolism of the human heart]. 366 4

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.
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PMID:Body temperature: an important determinant of severity of ischemic renal injury. 372 86

Myocardial energy metabolism during hypothermic potassium cardioplegia with blood as the cardioplegia vehicle, given in one or two bolus doses, was studied in eight patients undergoing aortic valve replacement. Myocardial biopsies were taken from the left ventricle 10 min after aortic cross-clamping (a.c.) and immediately before declamping (d.c.) and were analyzed for ATP, creatine phosphate (CP), creatine (C) and lactate. The interindividual range of myocardial temperature was 11-19 degrees C at 10 min a.c. and 11-25 degrees C immediately before d.c. The myocardial ATP concentration fell (17.2 +/- 5.7-12.8 +/- 2.8 mmol X kg-1 dry muscle), the lactate concentration rose (64.7 +/- 35.8-136 +/- 33.8 mmol X kg-1 d.m.) and the total creatine pool (CP + C) was unchanged. Hypothermic blood cardioplegia conferred fairly good initial protection of the myocardium, but the reduction in ATP and the great lactate accumulation towards the end of cardioplegia, especially in patients with myocardial temperature reaching 19-25 degrees C, indicates that such protection is adequate only if the myocardial temperature is maintained between 11 and 18 degrees C.
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PMID:Myocardial metabolism during aortic valve replacement. II. Bolus infusion of cold blood for cardioplegia. 373 44

Cerebral high energy phosphates were studied in the intact rabbit brain using nuclear magnetic resonance spectroscopy. The effect of hypothermia on degradation kinetics in total ischemia due to circulatory arrest was examined, measuring phosphocreatine, adenosine triphosphate, and inorganic phosphate as a function of time at three different temperatures (35, 24, 21 degrees C). Phosphocreatine- and ATP-decays followed single exponential functions at all three temperatures. The half-life times increased by approximately a factor of three upon lowering the temperature from 35 to 21 degrees C with activation energies of 15-20 kcal/mol, which corresponds to values of Q10 between 2.4 and 3.2. In the temperature range studied, no critical temperature was found below which metabolism would stop completely. We conclude that nuclear magnetic resonance spectroscopy allows, in the intact animal, quantitative assessment of the influence of hypothermia on energy metabolism in the brain. This influence is a major concern in the field of cardiac surgery in infants and children who are often operated in total circulatory arrest under deep hypothermia.
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PMID:Cerebral metabolic studies in situ by 31P-nuclear magnetic resonance after hypothermic circulatory arrest. 374 59

The protective effects of cardioplegic solutions (CS) containing creatine phosphate (CP) were studied in a rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. Isolated rat hearts were subjected to a 3-minute coronary infusion with CS containing CP in normothermic (37 degrees C) and hypothermic (4-6 degrees C) regimes. In the normothermia group, the postischemic functional recovery was 70-75% of the preischemic control value, while the cellular ATP and CP content was reduced but insignificantly. By contrast, in the hypothermia group, the postischemic functional recovery was markedly depressed, with the tissue high-energy phosphate content being appreciably lowered. The data obtained confirm high efficacy of CP-containing cardioplegic solutions administered under normothermia conditions.
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PMID:[Effectiveness of protecting the myocardium against ischemia with a normothermic cardioplegic solution and creatine phosphate]. 396 61


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