Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The development of myocardial ischemia is known to elicit the formation and enlargement of collateral vessels. The stimulus for these events is unknown. We have investigated the possibility that cardiac tissue releases a factor that can stimulate endothelial cell proliferation. Hearts from New Zealand rabbits were made progressively ischemic by differential hypothermia. Extracts from these hearts were tested for their growth-stimulating ability and were found to increase the proliferation of fetal bovine aortic endothelial cells as well as DNA synthesis by 3T3 cells. The level of activity in the extracts appears to be related to the degree of ischemia as measured by creatine phosphokinase levels. The liberation of an endothelial cell growth factor by ischemic cardiac tissue may function in the initiation and/or potentiation of coronary collateral formation.
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PMID:Do ischemic hearts stimulate endothelial cell growth? 646 72

Five male rhesus monkeys (Macaca mulatta) were subjected, under ketamine anesthesia, to repeated hypothermia treatments that produced an average rectal temperature of 28.3 degrees C. Following hypothermia induction, the subjects were rewarmed using either a ventrally applied surgical heating pad supplied with 35 degrees C water or a radio-frequency (RF) induction coil operating at 13.56 MHz with an average specific absorption rate (SAR) calculated to be approximately 5.5 W X kg-1. A special temperature probe, nonperturbing to RF, was used in the RF rewarming experiments. Control experiments were also conducted in which only ketamine was administered over a 3-h period. RF rewarming to 35 degrees C typically required only 50 min; whereas, an average of 137 min was required for heating-pad rewarming. Analyses of blood serum collected during and up to 48 h after hypothermia treatments showed elevations at 24 h in creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and glutamic oxaloacetic transaminase (GOT), and these elevations were highest for the ketamine controls and lowest for the RF rewarming experiments. The subjects have been periodically examined since these experiments, and all appear to be in good health. It is concluded that the careful application of RF energy to the central core of the body can successfully be used for rewarming purposes, is more effective than externally applied rewarming techniques, and is potentially useful in remote locations.
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PMID:Hypothermia and electromagnetic rewarming in the rhesus monkey. 651 17

Myocardial protection was evaluated in 2 groups of 5 infants each undergoing correction of either tetralogy of Fallot (TOF) or subcristal ventricular septal defect (VSD). In group A, profound hypothermia and total circulatory arrest (PHTCA) was utilized. In group B, profound hypothermia and total circulatory arrest combined with potassium cardioplegia (PHTCA + K) was the method of protection used. The analysis was carried out by sequential measurements of clinical, electrocardiographic, enzymatic (CK-MB) and ultrastructural parameters. There were no operative deaths. One infant had a second operation for recurrent VSD. The average anoxic time was 35.4 min in group A (PHTCA) and 32.6 min in group B (PHTCA + K). Analysis of our data demonstrated that when potassium cardioplegia was added to PHTCA, there was less intraoperative myocardial damage according to physiological, ultrastructural and biochemical parameters than when profound hypothermia and total circulatory arrest was applied alone.
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PMID:Myocardial protection in infant open heart surgery. 661 54

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


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