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

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

In order to analyze factors of importance for the efficiency of myocardial protection during open-heart surgery, a study was made of 144 patients undergoing isolated aortic valve replacement with various cardioplegic techniques. The cardioplegia was of Bretschneider type in 54 cases, St Thomas in 31 and Ringer-potassium type in 11 cases. Single or multi-dose blood cardioplegia was used in 11 cases and continuous blood cardioplegia in 30 cases. Local cardiac hypothermia was additionally employed in all patients. The efficiency of myocardial protection was assessed mainly from the incidence of postoperative conduction disturbances, myocardial enzyme release and need for inotropic support. All patients survived the operation. In 20% surgery was followed by transient or persistent disturbance of conduction, in 9% by abnormally increased CK-MB release and in 5% by requirement for inotropic support. Preoperative risk factors such as high age or severe left ventricular (LV) hypertrophy or dysfunction had little influence on the results. Patients in whom aortic stenosis (AS) was dominant in the complex with aortic insufficiency (AS + AI) showed 20-hour postoperative CK-MB enzyme activity twice as high as those with pure aortic insufficiency. The most important factors in myocardial protection were the duration of aortic occlusion and the myocardial temperature during cardioplegia. When the aortic occlusion lasted more than 80 min there was a 32% incidence of conduction disturbances and 20-hour CK-MB activity thrice as high as after shorter occlusion. Patients with mean myocardial temperature below 18 degrees C during cardioplegia invariably had low enzyme activities, which indicated good myocardial protection. The best overall results were obtained in patients operated on during hypothermia at 25-27 degrees C, with single or multi-dose blood cardioplegia and with efficient local cooling of the heart.
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PMID:Multicentre investigation of myocardial protection with cold cardioplegia. 686 39

An isolated rat heart preparation was used to characterize the temperature dependence of the calcium paradox and also to assess the validity of various indices of hypothermic protection. Hearts were subjected to 10-min periods of calcium depletion at various degrees of hypothermia followed by 20 min of normothermic calcium repletion. Using enzyme or protein leakage during calcium repletion as an index of hypothermic protection during calcium depletion, paradox injury was reduced extensively by relatively moderate hypothermia. Thus, depletion at 29 degrees C reduced total creatine kinase leakage by 57 +/- 4% from 1585 +/- 24 IU/g dry wt to 677 +/- 63 IU/g dry wt and at 25 degrees C leakage was reduced by 85 +/- 4% from 1585 +/- 24 IU/g dry wt to 237 +/- 71 IU/g dry wt. However, upon calcium repletion there was no recovery of contractile function. It was not until the myocardial depletion temperature was reduced to 20 degrees C that some functional recovery occurred. Under these circumstances cumulative creatine kinase leakage was reduced to below 88 IU/g dry wt, 6% of its normothermic value and protein leakage was undetectable. Functional recovery was not complete until the temperature was reduced to 15 degrees C or below. Correlation of cumulative enzyme leakage with functional recovery suggested a narrow release threshold (50 to 100 IU/g dry wt) above which no recovery occurred and below which a full recovery could be confidently predicted. Morphological assessments an all-or-none phenomenon; thus although increasingly severe hypothermia progressively reduced the percent of cells that sustained damage (as opposed to the degree of damage in all cells), it was not until 100% of cells appeared ultrastructurally undamaged that functional recovery was observed. Calcium-free perfusion at 4 degrees C protected the intercalated discs from gross lesions and prevented the separation of the external lamina from the surface coat. Our results also stress the heterogeneity of tissue injury and hypothermic protection and in addition shed further light upon the component mechanisms contributing to calcium injury.
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PMID:The temperature dependence of the calcium paradox: enzymatic, functional and morphological correlates of cellular injury. 687 88

Postoperative graft patency and thirteen perioperative variables were evaluated as potential risk factors for perioperative myocardial infarction (MI) in 102 consecutive patients undergoing coronary artery bypass grafting. Also, the incidence of perioperative MI and the amount of CK-MB released in the postoperative period were compared in three groups of patients selected according to the myocardial preservation technique employed: (1) topical hypothermia with and (2) without aortic cross-clamping and (3) cardioplegia. A perioperative MI as detected by electrocardiogram, enzymes, and myocardial scintigraphy with technetium 99 developed in 15 patients. Most important predictors of perioperative MI were found to be (1) left main and triple-vessel coronary artery disease, (2) a left ventricular end-diastolic pressure greater than or equal to 15 mm Hg, (3) a decreased ejection fraction (p < 0.05), and (4) cardiopulmonary bypass time > 120 minutes (p < 0.01). The incidence of perioperative MI was 50% in patients with three or more risk factors and 7% in those with less than three risk factors (p < 0.001). Graft patency was similar in patients with or without perioperative MI. Differing myocardial preservation techniques did not influence CK-MB release or the incidence of perioperative MI. Thus, the severity of ischemic heart disease and the length of the cardiopulmonary bypass time were important predictors of perioperative MI while graft patency and myocardial preservation technique did not appear to be related to its incidence in this study.
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PMID:Predictors of perioperative myocardial infarction in coronary artery operation. 697 16

Fifty patients undergoing isolated coronary artery bypass grafting procedures using a clear, cold cardioplegic solution, topical hypothermia, and reduced systemic flow for intraoperative myocardial protection were evaluated for myocardial injury by serial plasma creatine kinase-MB isoenzyme (CK-MB) measurements and electrocardiograms. Forty-one (82%) of the patients had three-vessel disease. Preoperative left ventricular contractility determined angiographically was normal in 13 patients (26%), mildly abnormal in 26 (52%), and moderately or severely abnormal in 11 (22%). The number of arteries grafted ranged from 2 to 6 (mean, 3.5). The mean duration of aortic clamping was 38.6 +/- 1.6 minutes. There were no hospital deaths. Enzymatic and electrocardiographic (ECG) evidence of myocardial infarction occurred in 1 patient. Nonspecific ECG changes occurred in 16 patients (32%), and th electrocardiograms were unchanged in the remaining 33 patients (66%). In the 49 patients without ECG evidence of infarction, the mean peak plasma CK-MB value, which occurred 6 hours after the onset of cardiopulmonary bypass, was 7.9 +/- 0.8 IU/L (standard error of the mean) and the mean integrated area 158 +/- 19.5 IU/L X hours. There was no correlation between these CK-MB values and the extent of disease, number of arteries grafted, or the duration of myocardial ischemia. These data document a low incidence of perioperative myocardial injury with this technique, and can serve as a baseline for comparison with other techniques for intraoperative myocardial protection in this setting.
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PMID:Detection of myocardial injury after coronary artery bypass grafting using a hypothermic, cardioplegic technique. 697 14

Serum time-activity curves for myoglobin, creatine-kinase (CK) and its isoenzyme MB were determined during and after coronary bypass surgery and aortic valve replacement. Hypothermic potassium cardioplegia was the method employed to initiate cardiac arrest. Cardiac myoglobin and CK-MB release rates were maximal 0.5 to 1.0 h post aortic cross-clamp release (PACR) with maximal concentrations at 1 and 4 h PACR respectively. The cardiac release ceased within 5 h PACR but was followed by a noncardiac release with maximal concentrations from 10 to 35 h PACR. The cardiac myoglobin release was significantly lower in the coronary bypass group, whereas no significant intergroup difference was observed for CK-MB. The cumulative CK-MB release corresponded roughly to about 5 g of myocardium.
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PMID:Myocardial and non-myocardial release of myoglobin and creatine-kinase MB following cardiac operations with hypothermic potassium cardioplegia. 697 88

Twenty patients having elective coronary artery bypass surgery were randomized for myocardial protection during cardiopulmonary bypass with cold cardioplegia and topical deep hypothermia with the Bretschneider solution in one group and intermittent aortic cross clamping at 30 degrees C in another group. The cardioplegic group showed more consistent results with lower CK-MB elevations both in terms of peak values and areas under the time-enzyme activity curves, although no statistical significance was obtained. There were significantly more infarct suspect time-enzyme activity curves in the intermittent cross clamping group (4 vs. O), and therefore, cold cardioplegia is advocated in preference to intermittent cross clamping in coronary artery bypass surgery.
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PMID:Myocardial protection in coronary artery bypass surgery. A study comparing cold cardioplegia and intermittent aortic cross clamping. 698 70

The purpose of this study was to define further the basis of control of myocardial membrane permeability by further examination of the "calcium paradox." To this end, the protective effect of hypothermia and addition of micromolar amounts of divalent cations during the Ca-free perfusion period were studied. Damage during Ca++ repletion to the isolated arterially perfused, interventricular rabbit septum was assessed by contracture development, loss of developed tension, and loss of 42K and creatine kinase. Progressive hypothermia prolongs the time of Ca-free perfusion needed to cause similar 42K, creatine kinase and developed tension losses upon Ca++ repletion. Complete protection against the Ca-paradox after 30-60 minutes Ca-free perfusion is seen at 18 degree C. The inclusion of 50 microM Ca++ during 30 minutes "Ca-free" perfusion also provides complete protection during Ca++ repletion i.e., there was full mechanical recovery with no 42K or creatine kinase loss. Other divalent cations perfused in 50 microM concentrations during the Ca-free period exhibited variable ability to protect when Ca++ was reperfused. The order of effectiveness (Ca++ greater than Cd++ greater than Mn++ greater than Co++ greater than Mg++) was related to the crystal ionic radius, with those cations whose radii are closest to that of Ca++ (0.99 A) exerting the greatest protective effect. The cation sequence for effectiveness in Ca-paradox protection is the same sequence for potency of excitation-contraction uncoupling. The mechanism of hypothermic protection is likely a phase transition in the membrane lipids (from a more liquid to a less liquid state) which stabilizes membrane structure and preserves Ca++ permeability characteristics during the Ca-free period. The mechanism of protection via cation addition is perhaps a cation's ability to substitute for Ca++ (dependent on unhydrated crystal ionic radius) at critical sarcolemmal binding sites to preserve control of Ca++ permability during the Ca-free period.
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PMID:Calcium depletion in rabbit myocardium. Calcium paradox protection by hypothermia and cation substitution. 709 25

Glutathion (GSH) plays an important role in maintenance of the redox state of the myocardium and acts as the membrane stabilizer. Seventeen patients who underwent cardiac surgery were subjected to cardiopulmonary bypass (CPB) and ischemic cardioplegia. The effect of GSH on ischemic myocardium was evaluated by serum lysosomal enzymes (acid phosphatase, beta-glucuronidase), isoenzymes of creatine phosphokinase (MB-CPK) and aspartate aminotransferase (m-GOT). standard CPB was instituted and systemic hypothermia was employed. GSH was administered to 8 patients in a dose of 200 mg/kg i.v. prior to institution of CPB. Mixed venous blood was sampled before administration of GSH, 10 min after institution of CPB and 0, 1, 6, 24 and 48 hr of reperfusion period following cardioplegia. Activity of acid phosphatase and beta-glucuronidase were significantly suppressed in the GSH-treated group compared to the non-treated group at 24 hours of reperfusion and immediately after aortic unclamping, respectively. Serum MB-CPK levels remained stable during reperfusion, but in the non-treated group, the level increased significantly at 6 hours of reperfusion. Increment of serum m-GOT levels was significantly suppressed at 1, 6 and 24 hours of reperfusion, compared to the non-treated group. These data suggest that pretreatment of GSH can protect the myocardium subjected to CPB from ischemic insult.
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PMID:Effect of glutathion pretreatment on hypothermic ischemic cardioplegia. 710 61


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