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

The effect of cooling to 25 degrees C on myocardial metabolism was studied during four periods of global ischemia (10 minutes each) followed by 15 minutes of reperfusion in dogs on cardiopulmonary bypass. Systemic and heart temperature at normothermia (group N, 34 degrees C; n = 15) was compared with general hypothermia (group H, 25 degrees C; n = 16). Before and at the end of each aortic crossclamp period in small myocardial biopsy specimens the adenosine triphosphate, creatine phosphate, inorganic phosphate, glycogen, and lactate content was analyzed. Also, lactate and inorganic phosphate were measured in the coronary effluents during the repetitive periods of reperfusion. Hemodynamic function was not different at 60 minutes after cardiopulmonary bypass compared with pre-cardiopulmonary bypass values, and was not different between the groups N and H. The tissue content of adenosine triphosphate and glycogen decreased progressively during the experimental period, resulting in slightly depressed values in both groups at the end of cardiopulmonary bypass. Pronounced effects of ischemia and reperfusion on tissue content of creatine phosphate, inorganic phosphate, and lactate were observed after each period of ischemia. The net decrease in tissue creatine phosphate content was not different between groups N and H (41 +/- 4 versus 38 +/- 4 mumol.gm-1 dry weight; mean +/- standard error of the mean) after 10 minutes of ischemia. However, during ischemia the net inorganic phosphate increase in myocardial tissue was significantly higher in group H (70 +/- 7 mumol.gm-1) than in group N (44 +/- 3 mumol.gm-1). These findings do not support the notion that myocardial protection is improved during hypothermia. Moreover, quantitatively the release of inorganic phosphate and lactate did not correlate with the amount accumulated in the myocardial tissue during the preceding periods of ischemia. The release appeared to be temperature dependent, that is, significantly reduced at 25 degrees C. The present data demonstrate why clinical outcome is satisfactory in both surgical procedures, when in general the periods of aortic crossclamping do not exceed 10 minutes each and the reperfusion periods in between the ischemic episodes last about 15 minutes. Besides, the findings indicate that hypothermia is not strictly necessary under these circumstances.
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PMID:Changes in myocardial high-energy phosphate stores and carbohydrate metabolism during intermittent aortic crossclamping in dogs on cardiopulmonary bypass at 34 degrees and 25 degrees C. 199 53

With changing patient demographics resulting in greater risk of myocardial ischemia, avoidance of low-output states must begin with patient selection. From that point, a variety of well-established surgical techniques can be used to provide myocardial protection. Hypothermia and cardioplegia are fundamental among these; however, it should be recognized that alternate approaches must be considered. The well-documented deleterious effects of overdistension and hypoperfusion must be borne in mind. To this is added the complex formulation of contemporary cardioplegic solutions based on thorough understanding of the pathophysiology of ischemic injury. Specific deleterious consequences of ischemia and/or hypothermia are abnormalities of tissue volume regulation, lack of high-energy substrate availability, reduced capacity for postischemic oxidative metabolism, depressed availability of high-energy phosphate precursors, and the potential damage done by oxygen-induced free-radical-mediated oxidant injury.
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PMID:Myocardial protection: what the surgeon does. 213 52

Both ethanol and neurotensin produce sedation and hypothermia. When administered in combination the behavioral effects of these two substances are potentiated. In order to better understand the biochemical nature of this interaction, the direct effects of ethanol on neurotensin receptors and an associated signal transduction process were determined in NIE-115 neuroblastoma cells. Ethanol in physiologically relevant concentrations (50mM) significantly reduced neurotensin stimulated [3H]inositol phosphate production while having no effect on the specific binding of [3H]neurotensin. In addition, ethanol up to 200 mM had no effect on GTPYS mediated [3H]inositol phosphate production. The results indicate that acute exposure to ethanol partially disrupts the normal coupling of activated neurotensin receptors to the guanine nucleotide binding protein associated with phospholipase C.
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PMID:The effects of acute exposure to ethanol on neurotensin and guanine nucleotide-stimulation of phospholipase C activity in intact NIE-115 neuroblastoma cells. 217 77

The direct effect of hypothermia on the inhibition of insulin secretion may result from inhibition of the availability of energetic substrates and/or the lack of metabolic signals. In order to verify this hypothesis, the insulin secretion and the main metabolic glucose pathways were measured during the incubation of rat islets. In the presence of 16.7 mmol glucose/l and at 37 degrees C, insulin secretion was 925 +/- 119 microU/2 h per ten islets. With the same experimental conditions, glucose utilization, determined as the formation of 3H2O from [5-3H]glucose was 2225 +/- 184 pmol/2 h per ten islets, glucose oxidation measured as the formation of 14CO2 from [U-14C]glucose was 673 +/- 51 pmol/2 h per ten islets, pentose cycle determined as the formation of 14CO2 from either [1-14C]glucose or [6-14C]glucose was 37 +/- 5 pmol/2 h per ten islets; glucose oxidation by the tricarboxilic acid cycle, calculated to be the difference between glucose oxidation and pentose cycle values, was 636 pmol/2 h per ten islets. Hypothermia highly inhibited glucose-induced insulin secretion and glucose utilization. Inhibition of insulin secretion was partial at 27 degrees C since it was 2.5 times lower than that at 37 degrees C, and it was complete at 17 degrees C. Glucose oxidation in the tricarboxilic acid cycle was markedly inhibited by hypothermia since the inhibition coefficient (Q10) between 37 and 27 degrees C was 5. In contrast, glucose oxidation in the pentose phosphate shunt was enhanced at 27 degrees C, reaching 92 +/- 17 pmol/2 h per ten islets, and it was inhibited relatively little at 17 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of low temperatures on glucose-induced insulin secretion and glucose metabolism in isolated pancreatic islets of the rat. 218 49

The myocardial protective effect of intravenous (i.v.) lidoflazine with potassium cardioplegia and hypothermia (28 degrees C) was investigated in 21 greyhounds. Animals were injected a single dose of cardioplegia (30 ml/kg body weight) and subjected to 120 minutes of ischaemia and 60 minutes of reperfusion. Ten dogs served as controls (Group C) and 11 dogs received i.v. lidoflazine (1.25 mg/kg b.w.) (Group L). Myocardial drill biopsies for the adenosine triphosphate (ATP) and the creatine phosphate (CP) levels were obtained. Hemodynamic measurements were made at intervals. In Group C, no dog could be weaned from bypass, whereas all 11 dogs in Group L came off bypass and maintained their circulation for 15 minutes. After a 120 minute ischemic period, the ATP and CP contents diminished significantly in both groups. Following reperfusion, the ATP level was 28% of the control level in Group C (p less than 0.005) and 38% in Group L (p less than 0.01). The CP levels showed an overshoot in both groups. There was no significant difference between the groups. In Group L animals, cardiac output (CO) and mean aortic pressure (MAP) were significantly reduced after bypass; from 5 +/- 1/min to 3.2 +/- 1, from 156 +/- 26 mmHg to 82 +/- 11 mmHg respectively (p less than 0.005). Left ventricular minute work (LVMW) also deteriorated markedly from 9.7 +/- 2 kg-m to 3.2 +/- 1 (p less than 0.005). The use of lidoflazine achieved considerable protection in terms of survival, but did not prevent the severe loss of high-energy phosphates in this experimental model.
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PMID:Myocardial protective effects of lidoflazine during ischemia and reperfusion. 230 23

A system has been developed for the nuclear magnetic resonance spectroscopic evaluation of cerebral high-energy phosphate levels during hypothermic total circulatory arrest and reperfusion by means of cardiopulmonary bypass in large animals. The use of intermittent hypothermic asanguineous cerebral perfusion, termed cerebroplegia, for the preservation of cerebral high-energy phosphates during a 2-hour period of hypothermic total circulatory arrest and reperfusion has been evaluated. Cardiopulmonary bypass was used to achieve deep hypothermia (12 degrees to 15 degrees C) during 2 hours of circulatory arrest and reperfusion. Juvenile sheep were divided into two groups. Group 1 animals (n = 8) (no cerebroplegia) served as the control group. In group 2 animals (n = 7), cerebroplegia was established by intermittent bilateral carotid artery infusion of a hypothermic oxygenated asanguineous cardioplegic solution. Nuclear magnetic resonance spectroscopy recorded changes in cerebral adenosine triphosphate, creatine phosphate, and intracellular pH. Adenosine triphosphate, creatine phosphate, and pH were higher in the group 2 animals for all points during the arrest period and until 60 minutes after reperfusion (p less than 0.05). Electroencephalographic activity returned after 36 minutes of reperfusion in group 2, but it did not return until 117 minutes in group 1 (p less than 0.05). In summary, cerebral high-energy phosphates and pH were maintained and the electroencephalographic signal returned more rapidly during circulatory arrest with the institution of cerebroplegia. These studies suggest that cerebroplegia is protective of the brain during circulatory arrest.
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PMID:Intermittent hypothermic asanguineous cerebral perfusion (cerebroplegia) protects the brain during prolonged circulatory arrest. A phosphorus 31 nuclear magnetic resonance study. 232 27

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

Functional and structural safety of the myocardium following 6-hour preservation at 4-6 degrees C in ion-balanced cardioplegic solution alone or in combination with pharmacological corrective was evaluated in rats. Langendorff and Neely model of isolated heart perfusion was used. The addition of creatine phosphate in a conservation of 10 mM/l to the solution or donor pretreatment with 70 mg/kg vitamin E was found to potentiate the protective properties of the solution under deep hypothermia. The combined use of the agents proved to warrant the initial intact structural and functional status of the rat myocardium.
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PMID:[Optimal conditions for preservation of isolated heart using creatine phosphate and vitamin E (an experimental study)]. 237 58

To elucidate the metabolic changes during a relatively short ischemic period, papillary muscle excisions were investigated in 38 patients operated for mitral valve replacement. The overall mean age was 62 years, in 27 women and 11 men. Two excisions were made during ischemia, the first after 13 minutes and the second after 48 minutes of aortic occlusion. These excisions were analyzed for adenine nucleotide, creatine phosphate, lactate and pyruvate contents. The results indicated an ongoing metabolism with an accumulation of lactate, and also influences on the energy charge. For example, although the content of ATP was unchanged between the excisions, the relation to creatine phosphate, as a source for ATP level maintenance, was altered. This is of clinical importance since cardioplegia and hypothermia (myocardial temperature below 20 degrees C) were employed and the interval between the excisions was only 35 minutes on average. Although no significant decrease in myocardial ATP took place, 31 of 38 patients needed inotropic support to wean them off bypass. On the basis of the present results further efforts seem necessary to improve myocardial preservation techniques.
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PMID:Myocardial energy metabolism during mitral valve replacement. 243 93

Effect of the derivative of 1,4-dihydropyridine-glutapyron on the activity of Ca2(+)-ATPase, lipid peroxidation and formation of the high-energy phosphate in the myocardium under deep hypothermia was investigated. Analysis of chemiluminescence parameters and changes of malondialdehyde production as a measure of peroxidation has shown high antioxidant activity of glutapyron under deep hypothermia. The inhibition of peroxidation by glutapyron takes place in the lipids of erythrocyte and heart mitochondrial membranes. Due to antioxidant activity glutapyron is able to inhibit initiation of free radical lipid oxidation, to stabilize membrane structure and to preserve function of membrane integrated proteins. In the aggregate these actins promote activity maintenance of high-energy phosphate production and transport reactions in heart under deep hypothermia.
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PMID:[Cardioprotective properties of a 1,4-dihydropyridine derivative, glutapyrone, in deep hypothermia]. 253 73


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