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

Hypothermic protection of myocardia during E.C.C. has been estimated on a 35 dogs experimental series and on a clinical series of 700 acquired cardiopathies of adult, including 400 valvular replacements and 300 aorto-coronary by-pass. Experimental results have been estimated by biochemic and morphologic controls done on myocardic samples took up by drillbiopsy. The biochemical study includes among others a dosing of the high-energy phosphorus compounds (P.C. and A.T.P.). Morphological study was done by optic and electronic microscopy. Results made clear the superiority of the hypothermic ischemia at 10 degrees C on the continued perfusion at 32 degrees C with fibrillative heart. An hypothermic protection method with successively cold perfusion of the coronary system and a heart immersion in a salted solution at 4 degrees C has been utilized during valvular and coronary surgery on human in 700 cases. The total mortality was of 5,8 p. 100. The rate of post-operative infarcts was 2,4 p. 100. Incidence of intra-ventricular conduction troubles has been 1,1 p. 100. There was no relation between mortality and morbidity of myocardic origin and the lasting of the ischemic clamp, which were of 21 mn up to 165 mn. The low incidence of complications of myocardic origin is due to the hypothermic protection of the myocardia.
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PMID:[Protection of the myocardium by hypothermia during extracorporeal circulation. Experimental and clinical study]. 1 26

3-Alkyl(phenyl)aminoaphtho[2,1-b]pyran-1-ones (III) were prepared from N-alkyl or N-phenylethoxycarbonylacetamides and 2-naphthol in the presence of phosphorus oxychloride, in order to evaluate their pharmacological activity on the CNS in comparison with previously described 3-dialkylaminoaphtho[2,1-b]pyran-1-ones. Compounds (III) gave 2-morpholinomethyl derivatives as well as N-acetyl and N-ethtoxycarbonyl derivatives. The reaction of (III) in which R = alkyl and N,N-dimethylformamide-POCl3 afforded 2-formyl derivatives and in some cases also 8-alkyl-9,10-bisdimethylaminoaphtho[1',2':5,6]pyrano[2,3-b]pyrrol-11(8H)-ones; when R = phenyl, only naphtho[1',2':5,6]pyrano[2,3-b]quinolin-14-one was obtained from the same reaction. Pharmacological evaluation showed that compounds (III) had a weak CNS depressant activity. Some of them also exhibited antagonist effect on reserpine-induced blepharospasm and hypothermia and on metrazole-induced seizures in the mouse. Within the limits of these activities a special behavior was found for the compound 3-ethylaminoaphtho[2,1-b]pyran-1-one [(III b) - K 12479].
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PMID:[Chemical and pharmacological research on pyran derivatives. XIV. 3-alkylaminoaphtho/2,1-b/pyran-1-ones and derivatives]. 47 69

Rats were kept in barochamber for 2 hours at the pressure of 240 mm Hg after subcutaneous administration of (1)14C-acetate. Hypobaric hypoxia caused depression in the incorporation of labeled acetate similar in both phospholipid (PL) components. But the dependence of depression in the metabolic rate upon hypothermia which accompanied hypoxia was more pronounced for hydrophobic portion of PB (carbon skeleton of fatty acids) than for hydrophilic one. Similarity in the degree of the hypoxia induced depression of incorporation of the precursors containing labeled phosphorus and carbon allows one to suggest that the carbon-containing parts of PL hydrophilic components (glycerol and nitrogen bases) and residues of ortho-phosphoric acid respond to hypoxia as a whole.
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PMID:[Effect of hypobaric hypoxia on the acetate-1-14C incorporation rate in hydrophilic and hydrophobic brain phospholipid components]. 51 97

Barbiturates have been used as a method of cerebral protection in patients undergoing open heart operations. Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess barbiturate-induced alterations in the cerebral tissue energy state during cardiopulmonary bypass, hypothermic circulatory arrest, and subsequent reperfusion. Sheep were positioned in a 4.7-T magnet with a radiofrequency coil over the skull. Nuclear magnetic resonance spectra were obtained at 37 degrees C, during cardiopulmonary bypass before and after drug administration at 37 degrees C and 15 degrees C, throughout a 1-hour period of hypothermic circulatory arrest, and during a 2-hour reperfusion period. A group of animals (n = 8) was administered a bolus of sodium thiopental (40 mg/kg) during bypass at 37 degrees C followed by an infusion of 3.3 mg.kg-1 x min-1 until hypothermic arrest. A control group of animals (n = 8) received no barbiturate. The phosphocreatine/adenosine triphosphate ratio, reflecting tissue energy state, was lower during cardiopulmonary bypass at 15 degrees C in the treated animals compared with controls (1.06 +/- 0.08 versus 1.36 +/- 0.17; p < 0.001). Lower phosphocreatine/adenosine triphosphate ratios were observed throughout all periods of arrest and reperfusion in the barbiturate-treated animals compared with controls (p < or = 0.01). Thiopental prevented the increase in cerebral energy state normally observed with hypothermia and resulted in a decrease in the energy state of the brain during hypothermic circulatory arrest and subsequent reperfusion. These results suggest that thiopental administration before a period of hypothermic circulatory arrest may prove detrimental to the preservation of the energy state of the brain.
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PMID:Barbiturates impair cerebral metabolism during hypothermic circulatory arrest. 144 98

Techniques for organ preservation generally use hypothermia to retard metabolic requirements. However, excessive hypothermia may also produce injury. Using a canine left lung allotransplantation procedure, we compared two preservation temperatures (4 degrees and 10 degrees C) in terms of subsequent lung function measured by temporary occlusion of the right pulmonary artery after implantation of the preserved left donor lung. The lungs were flushed with low-potassium dextran electrolyte solution, inflated with 100% oxygen, and preserved for 18 hours. To investigate possible changes of energy stores at different temperatures, we performed phosphorus 31-nuclear magnetic resonance analyses of lung samples. Sequential determinations of adenosine triphosphate levels in lung tissue preserved at 4 degrees, 10 degrees, and 22 degrees C were studied. After transplantation, lungs preserved at 10 degrees C (n = 6) provided significantly better arterial oxygen tension than those preserved at 4 degrees C (n = 6), 451 +/- 46 mm Hg versus 243 +/- 86 mm Hg (p less than 0.05), and lower pulmonary vascular resistance, 581 +/- 68 dynes.sec.cm-5 versus 1006 +/- 157 dynes.sec.cm-5 (p less than 0.05). Adenosine triphosphate levels at 4 degrees and 10 degrees C were stable and did not differ from each other at the end of the 18-hour preservation period: 0.86 +/- 0.04 mumol/gm wet weight for control versus 0.86 +/- 0.07 mumol/gm wet weight for 4 degrees C and 0.93 +/- 0.06 mumol/gm wet weight for 10 degrees C after 18 hours of preservation. Preservation at 22 degrees C caused a 28% depression of adenosine triphosphate after 18 hours of preservation. These results lead us to conclude the following: (1) Optimal temperature for lung preservation is in the vicinity of 10 degrees C, and (2) lung dysfunction caused by excessive hypothermia is not due to a failure to maintain adenosine triphosphate levels. We suspect that adenosine triphosphate is generated by oxidative phosphorylation during lung preservation.
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PMID:In a canine model, lung preservation at 10 degrees C is superior to that at 4 degrees C. A comparison of two preservation temperatures on lung function and on adenosine triphosphate level measured by phosphorus 31-nuclear magnetic resonance. 154 20

31-Phosphorus magnetic resonance spectroscopy was used in a rat model of 10 min severe incomplete forebrain ischaemia (2-vessel occlusion with hypotension) to assess the effect of mild brain hypo- and hyperthermia (+/- 2 degrees C) on intracellular pH and high energy phosphates. In three experimental groups intracerebral temperature was maintained at levels of 34, 36 and 38 degrees C during ischaemia and early reperfusion. The steady level of intracellular pH during ischaemia was 6.63, 6.58 and 6.53 in the 34, 36, and 38 degrees C groups, respectively. The rate of initial recovery of intracellular pH in reperfusion was 0.046 +/- 0.012 pH units per min (+/- s.d.) in the 36 degrees C group compared to 0.056 +/- 0.010 (+/- s.d., P less than 0.05) in the 34 degrees C group and 0.032 +/- 0.009 (+/- s.d., P less than 0.01) in the 38 degrees C group. The recovery in early reperfusion of phosphocreatine and ATP was slower in the 38 degrees C group compared to the other groups. The findings were consistent with recent studies, suggesting that even mild hypothermia may afford protection to the ischaemic brain, and furthermore indicate that mild hyperthermia as fever or even subfebricity may be deleterious for the outcome in stroke patients.
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PMID:The effects of brain temperature on temporary global ischaemia in rat brain. A 31-phosphorous NMR spectroscopy study. 163 61

The optimal level of hypothermia during myocardial preservation for cardiac transplantation is not known. Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess the effect of different preservation temperatures (15 degrees C in group 1, 4 degrees C in group 2) on the myocardial high-energy phosphate profiles during prolonged global ischemia and subsequent reperfusion of isolated rat hearts. Adenosine triphosphate depletion during ischemia was more gradual in group 2, leading to significant differences in myocardial adenosine triphosphate concentrations between the two groups after 3 hours of ischemia. The fall in intracellular pH during ischemia was significantly less pronounced in hearts preserved at 4 degrees C as compared with those at 15 degrees C. The postischemic recovery of both the left ventricular peak systolic pressure and the maximum rate of increase of left ventricular pressure was enhanced in group 2, although the ischemic period was 3 hours longer than in group 1. Hypothermia at 4 degrees C as compared with 15 degrees C appears to prolong myocardial protection with respect to adenosine triphosphate preservation, prevention of the fall in intracellular pH, and the enhancement of postischemic hemodynamic recovery.
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PMID:Optimal level of hypothermia for prolonged myocardial protection assessed by 31P nuclear magnetic resonance. 163 31

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

The alterations in tissue metabolism induced by hypothermic cardiopulmonary bypass are not completely known. Phosphorus-31 nuclear magnetic resonance spectroscopy was used to determine the effect of hypothermic cardiopulmonary bypass on energy states and intracellular pH of the heart and brain. Sheep were instrumented for cardiopulmonary bypass and had a radiofrequency coil placed over either the heart or skull. The animals were placed in a 4.7-T magnet at 37 degrees C and spectra obtained. The animals were cooled on cardiopulmonary bypass to either 26 degrees C (n = 17) or 18 degrees C (n = 14) for brain studies and to 26 degrees C (n = 12) for heart studies. Hypothermia increased the phosphocreatine/adenosine triphosphate ratio in the heart (2.38 +/- 0.23 versus 3.18 +/- 0.37, 37 degrees versus 26 degrees C, respectively, p = 0.03). The brain phosphocreatine/adenosine triphosphate ratio increased from 1.70 +/- 0.09 at 37 degrees C to 2.00 +/- 0.12 at 26 degrees C (p = 0.009) and 2.10 +/- 0.07 at 18 degrees C (p = 0.0001). Intracellular pH increased during hypothermia (heart: 7.05 +/- 0.02 to 7.18 +/- 0.02, 37 degrees versus 26 degrees C, p = 0.0001; and brain: 7.07 +/- 0.02 versus 7.32 +/- 0.02, 37 degrees versus 18 degrees C, p = 0.0001). The adenosine triphosphate resonance position is known to be sensitive to magnesium binding as well as temperature and was shifted upfield (p less than 0.01) in both the heart and brain. This effect could be totally explained by the temperature dependence of this process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolism of the heart and brain during hypothermic cardiopulmonary bypass. 198 46

The protective effects of hypothermia and potassium-solution cardioplegia on high-energy phosphate levels and intracellular pH were evaluated in the newborn piglet heart by means of in vivo phosphorus nuclear magnetic resonance spectroscopy. All animals underwent cardiopulmonary bypass, cooling to 20 degrees C, 120 minutes of circulatory arrest, rewarming with cardiopulmonary bypass, and 1 hour off extracorporeal support with continuous hemodynamic and nuclear magnetic resonance spectroscopic evaluation. Group I (n = 5) was cooled to 20 degrees C; group II (n = 4) was given a single dose of 20 degrees C cardioplegic solution; group III (n = 7) was given a single dose of 4 degrees C cardioplegic solution; and group IV (n = 4) received 4 degrees C cardioplegic solution every 30 minutes. At end ischemia, adenosine triphosphate, expressed as a percent of control value, was lowest in group I 54% +/- 6.5% but only slightly greater in group II 66% +/- 7.0%. Use of 4 degrees C cardioplegic solution in groups III and IV resulted in a significant decrease in myocardial temperature, 9.9 degrees C versus 17 degrees to 20 degrees C, and significantly higher levels of adenosine triphosphate at end ischemia; with group III levels at 72% +/- 6.0% and group IV levels at 73% +/- 6.0%. Recovery of adenosine triphosphate with reperfusion was not related to the level of adenosine triphosphate at end ischemia and was best in groups I and II, with a recovery level of 95% +/- 4.0%. In group IV, no recovery of adenosine triphosphate occurred with reperfusion, resulting in a significantly lower level of adenosine triphosphate, 74% +/- 6.0%, than in groups I and II. Recovery of ventricular function was good for all groups but was best in hearts receiving a single dose of 4 degrees C cardioplegic solution. In this model, multiple doses of cardioplegic solution were not associated with either improved adenosine triphosphate retention during arrest or improved ventricular function after reperfusion, and in fact resulted in a significantly lower level of adenosine triphosphate with reperfusion. The complete recovery of adenosine triphosphate in groups I and II, despite a nearly 50% adenosine triphosphate loss during ischemia, may result from a decrease in the catabolism of the metabolites of adenosine triphosphate consumption in the newborn heart.
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PMID:Effects of potassium cardioplegia on high-energy phosphate kinetics during circulatory arrest with deep hypothermia in the newborn piglet heart. 199 45


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