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

Previous studies from this laboratory utilized mass spectrometry to measure myocardial oxygen (PO2) and carbon dioxide (PCO2) tensions in isolated feline hearts subjected to periods of global ischemia and reperfusion. Myocardial carbon dioxide tension was found to increase during ischemia, and its rate of increase was found to correlate inversely with subsequent recovery of myocardial function following reflow. The present study utilized phosphorus-31 nuclear magnetic resonance (NMR) to assess whether the severity of intracellular acidosis or the depletion of high energy phosphate stores would show a similar correlation with recovery of function. Hyperkalemic cardioplegia employed as a myocardial preservation technqiue in combination with hypothermia was compared with hypothermia alone as the control intervention. The experimental results demonstrated that intracellular pH fell to 6.09 +/- 0.13 with hypothermia alone and to 6.31 +/- 0.09 with cardioplegia plus hypothermia. Furthermore, myocardial ATP content fell to 22% +/- 2% of control with hypothermia alone, while falling to 36% +/- 4% of control with the combined therapy. Recovery of myocardial performance was found to correlate inversely with the severity of intracellular acidosis and depletion of ATP during ischemia. In contrast, no relationship was observed between preservation of phosphoryl-creatinine levels either during ischemia or after reflow and recovery of ventricular function. These results suggest that, similar to mass spectrometry, which allows monitoring of myocardial PCO2, 31P NMR permits the on-line monitoring of intracellular pH as well as high energy phosphate compounds, and thereby provides useful metabolic indices of the severity of ischemia. Since tight coupling was found between changes in these parameters and subsequent recovery of contractile performance, further development of 31P NMR for evaluation of techniques designed to minimize the severity of ischemic damage would seem indicated.
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PMID:Mass spectrometry and phosphorus-31 nuclear magnetic resonance demonstrate additive myocardial protection by potassium cardioplegia and hypothermia during global ischemia. 677 61

Phosphorus-31 nuclear magnetic resonance (31P NMR) can estimate tissue intracellular pH as well as the content of high-energy phosphate metabolites in isolated perfused hearts. We used 31P NMR to examine mechanisms associated with the recovery of ventricular function in hearts subjected to global ischemia and reperfusion, with special emphasis on intracellular pH, a previously unreported variable. Single-dose and multiple-dose administration of a hyperkalemic cardioplegic solution were compared with hypothermia alone in 18 isolated perfused rabbit hearts. Hearts in group 1 were subjected to 24 degrees C hypothermia during 60 minutes of global ischemia; group 2 hearts received a single injection of 37-mM KCL cardioplegic solution at 10 degrees C at the onset of ischemia; and group 3 hearts received a similar initial cardioplegic injection followed by two subsequent 24 degrees C injections at 20-minute intervals during the ischemic period. Using an intraventricular balloon, maximal dP/dt provided a quantitative index of left ventricular performance before and after ischemia. Return of ventricular function expressed as a percentage of control was 54 +/- 11% for group 1, 84 +/- 6% for group 2, and 101 +/- 18% for group 3. Differences in the rate of development of intracellular acidosis were noted during the 60-minute ischemic period. Intracellular pH fell to 6.09 +/- 0.12 in group 1, 6.31 +/- 0.09 in group 2, an 6.79 +/- 0.03 in group 3. In all three groups intracellular pH returned to control (pH 7.20) within 10 minutes of reflow. The metabolic correlates of functional recovery appeared to be the tissue content of ATP at the end of ischemia and after reflow. ATP content at the end of ischemia was 22 +/- 2% of control in group 1 hearts, 31 +/- 4% in group 2 and 64 +/- 2% in group 3. After 45 minutes of reperfusion, ATP levels recovered to 33 +/- 9% of control in group 1, to 71 +/- 9% in group 2 and to 86 +/- 6% in group 3. Although there were no differences between groups in the content of creatine phosphate after 60 minutes of ischemia, the rates of creatine phosphate decline were dissimilar. Further, during the early reflow period, a marked overshoot in tissue creatine phosphate was detected, especially in groups 1 and 2. Histologic damage assessed by light microscopy correlated with the metabolic data, confirming that multidose cardioplegia provided the best preservation of cellular morphology. These results demonstrate that the magnitude of intracellular acidosis and the associated increase in inorganic phosphate correlate inversely with recovery of postischemic ventricular structure and function. ATP, but not creatine phosphate, content correlates with return of contractile performance after reperfusion. The overshoot in creatine phosphate during early reperfusion might impede optimal restoration of ATP content and, as a result, optimal recovery of cell functions.
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PMID:Mechanisms of ischemic myocardial cell damage assessed by phosphorus-31 nuclear magnetic resonance. 679 21

Hypothermic potassium cardioplegia is now commonly used to protect the myocardium during surgically induced ischemia. Because the potassium-related membrane depolarization has been shown to increase calcium influx, we undertook this study to define the effects of varying the calcium content in hyperkalemic perfusates and the effects of using magnesium instead of or in addition to potassium as the arresting agent on the ability of hearts to recover normal function after ischemic arrest. We subjected isolated perfused working rat hearts to 60 minutes of cardioplegic arrest followed by 30 minutes of reperfusion, and measured high-energy phosphate levels every 2 1/2 minutes by phosphorus-31 nuclear magnetic resonance spectroscopy. These data were correlated with postischemic recovery of function. Our results show that potassium cardioplegia may be harmful when the calcium concentration is greater than 1 mM. The kalemic injury is significantly reduced when the calcium content is lowered to 0.25 mM and the greatest extent of preservation is provided by a calcium-poor perfusate (0.25 mM) containing 13 mM magnesium. The beneficial effects of magnesium are not enhanced by subsequent addition of potassium. Close correlations were found between all observed metabolic changes during arrest and the degree of recovery of contractile performance after reperfusion. We conclude that the ability of the myocardium to maintain or resynthesize high-energy phosphate after cardioplegic arrest may be an important determinant of postischemic mechanical performance. These results show that phosphorus-31 nuclear magnetic resonance spectroscopy is a valuable method for evaluating interventions to reduce the severity of ischemic damage.
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PMID:Evaluation of high-energy phosphate metabolism during cardioplegic arrest and reperfusion: a phosphorus-31 nuclear magnetic resonance study. 685 Oct 24

Subendocardial ischemia is a common cause of death following ischemic cardiac arrest. We studied relationships among myocardial water content (WC), left ventricular function, coronary blood flow, and myocardial metabolism following ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia, 120 min of aortic occlusion was employed, and myocardial temperature was kept around 20 degrees C in 10 mongrel dogs. Left ventricular function (peak LVP, max dp/dt, LVEDP, LVSWI), coronary blood flow, myocardial enzymes (m-GOT, total CPK, MB-CPK), myocardial ATP and creatine phosphate (CP), and WC of the subendocardium of the left ventricle were measured. Data were obtained in the control state and immediately and 30 and 60 min after aortic unclamping. Significant negative correlations were obtained between WC and max dp/dt (r = -0.8384), coronary blood flow (r = -0.9928), ATP (r = -0.7038), and CP (r = -0.7835). Significant positive correlations were obtained between WC and LVEDP (r = 0.7525), m-GOT (r = 0.7638), and total CPK (r = 0.7079). These data suggest that myocardial edema results in depression of left ventricular function and metabolism.
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PMID:Correlation among water content, left ventricular function, coronary blood flow, and myocardial metabolism after hypothermic ischemic cardiac arrest. 685 73

To determine the myocardial temperature that provides maximal preservation of the heart during global ischemic arrest, five groups of dogs were studied (6 per group). In all animals, the aorta was cross-clamped for 120 minutes. Serial biopsies were done for determination of adenosine triphosphate and creatine phosphate, and study by electron microscopy. Starling curves were derived prior to cardiopulmonary bypass and 60 minutes after bypass. Mitochondrial changes were graded on a scale of 0 to 4. In the control group (Group 1), the aorta was clamped when the rectal temperature reached 25 degrees C (myocardial temperature, 18 degrees to 22 degrees C). In Groups 2, 3, 4, and 5, myocardial temperature was maintained at 6 degrees C, 10 degrees C, 14 degrees C, and 18 degrees C (all +/- 2 degrees C), respectively, by the use of systemic and topical hypothermia and repeated injections of cold cardioplegic solution into the aortic root. All groups showed a depression of left ventricular stroke work index, particularly Group 1 (no survivors), Group 2, and Group 3. The high-energy phosphate stores were well preserved in all groups except Group 1. The mitochondrial ultrastructure showed significant changes in all groups, especially Groups 1 and 5. These data indicate that satisfactory preservation of mitochondrial ultrastructure and high-energy phosphates was achieved at myocardial temperatures lower than 18 degrees C. Extreme hypothermia (Groups 2 and 3) was associated with significant reduction in ventricular function under the experimental conditions employed.
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PMID:The optimal temperature for preservation of the myocardium during global ischemia. 686 4

Preservation of regional myocardial function, high-energy phosphate stores and ultrastructure were assessed in 28 canine hearts subjected to 2 hours of global ischemia at either 12 degrees C or 21 degrees C. The preservation achieved with a potassium arrest solution was simultaneously compared in the same heart with either a nifedipine arrest solution or a potassium plus nifedipine arrest solution. There were no statistically significant differences in regional function recovery between the three arrest solutions at either temperature. At 12 degrees C, slightly better functional preservation was noted for each solution. End-systolic chord length was significantly less elongated after preservation at the lower temperature (p = 0.03). The concentration of ATP and myocardial water content were not significantly better preserved with any solution at either temperature. Myocardial ultrastructure was well preserved regardless of the solution or temperature used. The degree of hypothermia appears to be more important to functional preservation than differences between the three solutions tested. We conclude that with respect to preservation of myocardial function, high-energy phosphate stores, water content and ultrastructure, nifedipine arrest offers no advantages over potassium arrest.
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PMID:Comparison of myocardial preservation with hypothermic potassium and nifedipine arrest. 708 50

Past studies have not established the optimal myocardial temperature range for hyperkalemic arrest but have generated controversy regarding the safety of exposing the myocardium to more profound levels of hypothermia. We therefore used the isolated working rat heart model of ischemic arrest to study the metabolic and functional effects of cardioplegia at the full range of temperatures pertinent clinically. Experimental conditions were designed to reliably control and maintain myocardial temperature during the 60 minute arrest period. We found that nearly full recovery of function occurred when hearts were arrested at or below 16 degrees C. High-energy phosphate levels measured immediately after arrest were better maintained at 4 degrees and 8 degrees C, despite evidence of decreased anaerobic glycolysis. When measured after the recovery period, high-energy phosphate levels returned to somewhat less than control levels in all groups arrested at or below 24 degrees C. Myocardial glucose utilization was best preserved in hearts arrested at or below 12 degrees C. We found no evidence that greater myocardial edema resulted from arrest at colder temperatures. Severe and permanent damage was observed when hearts were arrested at or above 28 degrees C. In this model, therefore, the best overall metabolic and functional protection occurred when hearts were maintained at 12 degrees C or below potassium-induced cardioplegia. Our results support the idea that cold injury to the heart does not occur and that colder temperatures provide better protection from ischemic myocardial injury.
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PMID:Effect of temperature during potassium arrest on myocardial metabolism and function. 709 10

Aspartate aminotransferase (EC 2.6.1.1:AST) is known to have two isoenzymes, one associated with the cytoplasm (c-AST) and the other with the mitochondria (m-AST). We studied the relationships of m-AST activity in the coronary sinus blood to left ventricular function, coronary blood flow, water content and high-energy phosphate stores of the left ventricle following hypothermic ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia of 20 degrees C of myocardial temperature, 120 min of aortic occlusion was employed in 15 mongrel dogs. Left ventricular function (peak left ventricular pressure, left ventricular end-diastolic pressure, max dp/dt, cardiac index, left ventricular stroke work index), coronary blood flow, myocardial oxygen consumption, myocardial enzyme activity (m-AST, CK-MB), myocardial water content and high-energy phosphate stores (adenosine triphosphate, creatine phosphate) of the subendocardium of the left ventricle were measured. Data was obtained in the control state, and after 0, 30 and 60 min of reperfusion. Significant negative correlations were obtained between m-AST activity and peak left ventricular pressure (r = -0.81, p less than 0.001), max dp/dt (r = -0.83, p less than 0.001), cardiac product (r = -0.73, p less than 0.01), coronary blood flow (r = -0.59, p less than 0.05), adenosine triphosphate level (r = 0.72, p less than 0.01) and creatine phosphate level (r = -0.72, p less than 0.02) after 60 min of reperfusion. Significant positive correlations were obtained between m-AST activity and left ventricular end-diastolic pressure (r=0.75, p less than 0.01) and water content (r = 0.78, p less than 0.01) after 60 min of reperfusion. These results led to the assumption that serum m-AST activity in the coronary venous blood is a useful index to evaluate the degree of myocardial injury.
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PMID:Studies on the significance of serum mitochondrial aspartate aminotransferase activity following ischemic cardiac arrest. 714 3

During short-lasting hypothermia in rats the activity of isocitrate dehydrogenase (E.C.1.1.1.42) and malic dehydrogenase (E.C.1.1.1.37) was determined in the mitochondrial fraction of liver cells, myocardial cells and skeletal muscle fibres of the femoral muscle and no statistically significant differences were found between the obtained values and those in a control group. On the other hand, the activity of glucose-6-phosphate dehydrogenase (E.C.1.1.1.49) in the cytoplasmic fraction of these tissues was decreased in the hypothermic rats by 46% in the liver, by 50% in the myocardium and by 59% in the skeletal muscle of the thigh. A possible cause of this reduced activity of this enzyme in hypothermia could be changes in the structure of the enzymatic protein, deficiency of the hormone activating the enzyme, that is insulin, and/or inhibition of the pentose-phosphate cycle by fatty acids released in excess.
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PMID:Activity of certain enzymes in the mitochondrial and cytoplasmic fractions of liver cells, myocardium and skeletal muscle of the rat during short-lasting hypothermia. 718 57

A week hypothermia (2-4 degrees C) does not cause a considerable decrease in content of glycogen in the liver, muscles, brain tissues of Lacerta strigata, Natrix tessellata and Rana ridibunda. In Eremias arguta pangolins the level of glycogen in the liver and muscles under these conditions is twice as low. Prolongation of hypothermia till three weeks causes a 4-fold decrease in the polysaccharide level in the liver of Eremias arguta and Lacerta strigata. The content of nonesterified fatty acids in blood under hypothermia (especially of three-week one) considerably exceeds the normal level. The content of lactic acid in tissues is two-three times as high under prolonged hypothermia, in the reptile muscles creatine phosphate accumulates in high amounts.
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PMID:[Characteristics of energy metabolism in the tissues of lake frogs and certain reptiles during prolonged deep hypothermia]. 721 Feb 19


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