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

I assessed the effect of therapeutic hypothermia on the activity in cerebrospinal fluid of creatine kinase (EC 2.7.3.2) and its brain isoenzyme (CK-BB), lactate dehydrogenase (EC 1.1.1.27), and aspartate aminotransferase (EC 2.6.1.1.) as markers of cerebral damage in patients with transient anoxic-ischemic brain injury. Moderate hypothermia (30-32 degrees C) lasting more than 24 h resulted in disproportionately greater activity of creatine kinase during the post-insult period than in patients not treated with hypothermia but having similar insults and outcome (p less than .01 for survivors, and p less than .005 for nonsurvivors). No differences were observed for the thermostable enzymes lactate dehydrogenase and aspartate aminotransferase, which demonstrates that the effect of hypothermia must be taken into account when thermolabile enzymes are used as sole markers of brain damage in such patients.
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PMID:Effects of therapeutic hypothermia on activity of some enzymes in cerebrospinal fluid of patients with anoxic-ischemic brain injury. 371 42

New 2-site labeled monoclonal antibody techniques were used to measure serially plasma levels of brain-type creatine kinase (CK-BB), heart-type creatine kinase (CK-MB) and muscle-type creatine kinase (CK-MM) during a 20-hour postoperative period in 24 infants after deep hypothermia and total circulatory arrest used in pediatric cardiac surgery. A control group of 7 children undergoing cardiovascular procedures without extracorporeal circulation or circulatory arrest also were studied. There were marked increases in CK-MB and CK-BB levels in the circulatory arrest group but not in the closed group. CK-BB increased from 3.2 +/- 0.5 to 27 +/- 10 ng/ml and CK-MB from 5.9 +/- 2.1 to 137 +/- 12 ng/ml. The CK-MM concentrations increased from 299 +/- 91 and 194 +/- 49 ng/ml to 1,220 +/- 274 and 1,322 +/- 142 ng/ml in the closed and circulatory arrest groups, respectively. Peak levels of CK-MB and CK-BB occurred an average of 133 and 127 minutes, respectively, after reperfusion. The half-time of CK-BB differed significantly from that of CK-MB (149 +/- 15 vs 359 +/- 20 minutes). The arrest time had a more marked effect on CK-BB concentration than on CK-MB and CK-MM concentrations. Arteriointernal jugular venous concentration differences were consistently negative for CK-BB in the circulatory arrest group, but not for CK-MM and CK-MB.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Detection of cerebral injury after total circulatory arrest and profound hypothermia by estimation of specific creatine kinase isoenzyme levels using monoclonal antibody techniques. 378 13

A 74-year-old man with myxedema and hypothermia had increased activities in plasma of creatine kinase (CK; EC 2.7.3.2), aspartate aminotransferase (AST; EC 2.6.1.1), and lactate dehydrogenase (LD; EC 1.1.1.27) and increased proportions of CK-MB (up to 20% of total CK) and LD1 isoenzymes, but no clinical or investigational evidence of associated myocardial infarction. This case illustrates that plasma enzyme activity and isoenzyme profiles in such clinical settings should be interpreted with caution, because increases in CK-MB and LD1 may relate to myxedema coma or hypothermia (or both) rather than to myocardial infarction.
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PMID:Cardiac enzyme changes in myxedema coma. 382 11

The immature myocardium has a greater tolerance for ischemia than does the mature heart. The effect of ischemia when combined with hypothermia on the newborn heart is poorly understood but has important clinical applications. This study examined the metabolic and functional recovery after 90 minutes of global ischemia at 20 degrees C in neonatal (1 week), immature (1 month), and mature (4 month) isolated working rabbit hearts. Following ischemia, aortic flow, cardiac output, heart rate, and stroke work remained at baseline values for neonatal hearts. Only coronary flow was significantly reduced from a control level of 4.5 +/- 1.4 (standard error of the mean) to 3.3 +/- 1.1 ml/min, p less than 0.05. In the immature group, hemodynamic parameters were below baseline, although no statistical differences were noted. Among mature hearts, however, all hemodynamic values were significantly below preischemic control. Water content was significantly higher in immature (73.2% +/- 1.4%) and mature (75.3% +/- 2.5%) hearts when compared with the neonatal group (46.8% +/- 4.6%), p less than 0.001. Coronary sinus creatine kinase was unchanged from baseline at 10 and 30 minutes following ischemia in the neonatal group. Although demonstrating substantial increases from baseline, statistical significance was not seen in the immature group because of the wide variation about the mean. In the mature group, creatine kinase rose significantly from preischemic levels of 15.4 +/- 4.3 IU/L/gm to 184.2 +/- 51.6 IU/L/gm at 10 minutes (p less than 0.01) and 123.7 +/- 31.9 IU/L/gm at 30 minutes (p less than 0.05). This study demonstrated improved tolerance to prolonged hypothermic ischemia in neonatal rabbit hearts when compared with older hearts subjected to the same conditions. The role of cardioplegic solutions in protecting the neonatal heart during cardiac operations when deep hypothermia is used may be of lesser importance than in the older patient.
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PMID:Recovery of left ventricular function after hypothermic global ischemia. Age-related differences in the isolated working rabbit heart. 394 54

An isolated working rat heart preparation was used to characterise the temperature-dependency of the anti-ischaemic properties of nifedipine. In this study hearts were subjected to pre-ischaemic infusion with the St Thomas' cardioplegic solution with or without added nifedipine (0.075 mumol X litre-1). Hearts were then rendered globally ischaemic for various periods, (35, 42, 48, 56, 55, 65, 80, 105 or 130 min) at various temperatures (37.0, 35.5, 34.0, 32.5, 31.0, 29.0, 27.0, 24.0 or 20.0 degrees C, respectively). The duration of ischaemia at each temperature was selected to produce a post-ischaemic (37 degrees C) recovery of aortic flow that was approximately 50% of its pre-ischaemic (37 degrees C) control. In addition to functional indices (aortic flow, cardiac output, coronary flow, aortic pressure and heart rate) creatine kinase leakage during reperfusion was measured. At all temperatures at or above 31 degrees C the addition of nifedipine enhanced significantly (maximal value = 43%) the post-ischaemic recovery of aortic flow and other indices of pump function, while at the same time reducing significantly (by up to 56%) enzyme leakage. At ischaemic temperatures below 31 degrees C nifedipine failed to afford any significant additional protection when assessed functionally or enzymatically. It would therefore appear that hypothermia either blocks the action of nifedipine or, by acting on some common mechanism, renders the actions of the drug redundant.
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PMID:Temperature-dependency of nifedipine as a protective agent during cardioplegia in the rat. 397 70

The effect of diltiazem on creatine kinase release and tissue adenosine triphosphate content was investigated during calcium paradox in the isolated perfused rat heart. Creatine kinase loss was minimal during the calcium-free phase, but there was a 100-fold increase in creatine kinase release after reperfusion with normal calcium-containing medium. Diltiazem reduced creatine kinase loss by 35 percent when added to calcium-free medium and by approximately 80 percent when added to both calcium-free and reperfusion media. Adenosine triphosphate content was significantly increased from 2.98 mumol in untreated calcium paradox hearts to 5 mumol/g dry weight in diltiazem-treated hearts. With hypothermia the calcium paradox injury was completely inhibited if the temperature of calcium-free perfusion was maintained at 15 degrees C. Diltiazem appears to exert its protective effect through its ability to prevent the cellular separation and alterations in the gap junctions during calcium deprivation of cells and to limit calcium entry into the cells after reperfusion with calcium-containing medium.
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PMID:Prevention of calcium paradox-related myocardial cell injury with diltiazem, a calcium channel blocking agent. 628 3

Six patients undergoing aortic arch replacement during deep hypothermia and circulatory arrest were subjected to studies including serial determinations of total creatine kinase (CK) activity in the cerebrospinal fluid (CSF), monitoring of the intracranial epidural pressure and the cerebral perfusion pressure and clinical neurological evaluation. In two of four patients with postoperative pressure monitoring, a marked increase in pressure was seen. In one case this pressure rise terminated in brain tamponade six days postoperatively, despite aggressive treatment with steroids, mannitol and barbiturate. In comparison with patients undergoing surgery for valve replacement or aorto-coronary by-pass, some of the patients with aortic arch replacement clearly sustained more severe cerebral damage, as judged by clinical examination and autopsy findings as well as by assessment of the degree or extent of the neuronal damage from CK activity in CSF. Patients of this type are obvious candidates for postoperative neuro-intensive monitoring and care. Repeated pulsed Doppler flow velocity determinations in precerebral arteries, performed bedside, combined with monitoring of the cerebral perfusion pressure, provide a useful indication of the cerebral circulatory state in such situations.
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PMID:Cerebral damage following open-heart surgery in deep hypothermia and circulatory arrest. 664 99

The ability of nifedipine to enhance myocardial protection was assessed using an isolated rat heart model of cardiopulmonary bypass and ischaemic cardiac arrest. With normothermic ischaemic arrest (35 min, 37 degrees C), nifedipine addition improved the protective properties of the St Thomas' cardioplegic solution. Optimal protection was observed with 0.075 mumol nifedipine X litre-1, where post-ischaemic recovery of aortic flow was improved from 47.9 +/- 5.2% to 76.7 +/- 2.9% (P less than 0.001) and creatine kinase leakage was reduced by approximately 50%. Despite the marked additional protection under normothermic conditions the drug was unable to improve contractile recovery after a period of hypothermic ischaemic arrest (150 min, 20 degrees C) although it did allow a significant reduction (22%) in creatine kinase leakage. In other studies, the ability of nifedipine to replace the cardioplegic solution was examined. Under normothermic conditions, it showed a good ability to protect against ischaemia, but this protection did not match that afforded by the St Thomas' cardioplegic solution. Under hypothermic conditions the drug failed to substitute for the cardioplegic solution, suggesting that a common modality between hypothermia and nifedipine-induced protection.
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PMID:Nifedipine and cardioplegia: rat heart studies with the St Thomas' cardioplegic solution. 666 43

To investigate brain changes in induced deep core hypothermia (18 degrees C) with or without circulatory arrest, four groups of dogs were subjected to cardiopulmonary bypass (CPB) under the following conditions: (1) differential head perfusion with pulsatile flow and simultaneous circulatory arrest to the rest of the body; (2) differential perfusion to the head with a nonpulsatile flow; (3) total circulatory arrest; and (4) continuous hypothermic perfusion. Parameters analyzed were: (1) blood flow distribution; (2) creatine kinase isoenzyme (CK-BB) elevation in the cerebrospinal fluid (CSF) and in the brain venous return; and (3) microscopy of the brain in animals killed at 30 minutes, 24 and 48 hours, 1 and 2 weeks, and 1 month. Although minor brain tissue flow differences were found at 37 degrees C among the groups, flows equalized at 18 degrees C. A significant seven-fold brain flow increase followed the period of circulatory arrest in Group III. Rise of CK-BB levels occurred in brain venous return but not in CSF in all groups. Microscopic cellular damage appeared in all groups with an equal degree of severity, regardless of the method of hypothermia and perfusion implemented.
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PMID:Brain damage in profound hypothermia. Perfusion versus circulatory arrest. 670 79

Hypothermia during calcium-free perfusion of hearts protects them from injury caused by subsequent calcium repletion at 37 C (calcium paradox). Injury to calcium-free hearts is also associated with contracture caused by anoxia, 2,4-dinitrophenol (DNP), or caffeine. This study was done for the purpose of determining whether hypothermia during calcium-free perfusions protects hearts from contracture-associated injury. Langendorff-perfused rat hearts were studied in four experimental groups: I) Anoxia: Thirty minutes of anoxic perfusion at 37 C was followed by thirty minutes of anoxic calcium-free perfusion at 37-18 C. II) Calcium paradox: Five minutes of calcium-free perfusion at 37-18 C was followed by calcium repletion at 37 C. III, IVa) Caffeine or DNP: Five minutes of calcium-free perfusion at 37-18 C was followed by addition of 10 mM caffeine or 1 mM DNP in calcium-free medium at 37 C or, IVb) 1 mM DNP in calcium-free medium at 22 C. Injury was assessed by measurement of serial releases of creatine kinase (CK) in effluents and by cellular morphology. The results show that progressive hypothermia to 22 C during calcium-free perfusion periods produced a progressive reduction of CK release and morphologic evidence of injury due to anoxia, caffeine, or DNP, which closely paralleled protection of hearts from the calcium paradox. Protection from injury in all experimental groups was associated with preservation of sarcolemmal membrane integrity and prevention of cell separations at intercalated disk junctions. It is proposed that weakening of intercalated disks occurs during calcium-free perfusions and may be a cause of mechanical fragility of the sarcolemma. Hypothermia may protect hearts from contracture-associated injury by preserving the integrity of intercalated disk junctions during periods of extracellular calcium depletion.
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PMID:Parallel temperature dependence of contracture-associated enzyme release due to anoxia, 2,4-dinitrophenol (DNP), or caffeine and the calcium paradox. 674 11


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