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

This retrospective analysis tests the hypothesis that topical cardiac hypothermia is an unnecessary adjunct to intraoperative myocardial protection and an avoidable cause of pulmonary morbidity in patients with coronary disease receiving blood cardioplegia. The hospital records of 150 nonrandomized consecutive patients undergoing elective and emergency isolated coronary revascularization were reviewed. All patients received multidose cold blood cardioplegia followed by warm blood cardioplegic reperfusion distributed through grafts. Fifty patients received iced slush, 50 received topical 4 degrees C saline, and no topical cooling was used in 50 others. Patients groups were comparable in number of grafts (3.7 versus 3.5 versus 3.5) and crossclamp time (61 versus 62 versus 61 minutes). More emergency operations were performed in the patients receiving no topical hypothermia (12/50 versus 8/50 versus 7/50). Postoperative x-ray films were reviewed by a radiologist who did not know of patient grouping. Postoperative results were comparable in hemodynamics, inotropic requirements (10/50 ice versus 8/50 saline versus 5/50 no cooling), myocardial infarction (1/50 versus 2/50 versus 2/50), and enzymes (aspartate aminotransferase myocardial band creatine kinase). No patient died. Ice topical hypothermia (versus no topical cooling) was associated with more left pleural effusions (25/50 versus 9/50; p less than 0.05), atelectasis (33/50 versus 18/50; p less than 0.05), elevated left hemidiaphragms (13/50 versus 0/50; p less than 0.05), and longer postoperative hospitalization (11.2 versus 8.5 days; p less than 0.05). Topical 4 degrees C saline reduced diaphragmatic elevation and pleural effusion (versus topical ice) but was associated with more atelectasis (34/50 versus 18/50; p less than 0.05) than no topical cooling. These data suggest that routine topical hypothermia is an unnecessary adjunct to blood cardioplegic protection in patients with coronary disease, since supplemental topical cooling does not improve postoperative hemodynamics or reduce inotropic requirements, enzyme release, or prevalence of postoperative myocardial infarction, and it increases pulmonary morbidity, which can be reduced by its avoidance.
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PMID:Topical cardiac hypothermia in patients with coronary disease. An unnecessary adjunct to cardioplegic protection and cause of pulmonary morbidity. 151 52

We examined the effects of two degrees of hypothermia on hepatic oxygen delivery and uptake, hepatic lactate uptake as a marker of hepatic function, and the effect of hypothermia on ischemia-reperfusion injury in the liver in miniature pigs (n = 18, 21-30 kg body wt). Hepatic arterial and portal venous blood flows were measured while hepatic oxygen delivery was progressively decreased without venous congestion in the preportal area. With decreases in hepatic blood and oxygen supply, oxygen extraction gradually increased from 50 to 90% in the normothermic group and from 25 to 70 and 84% in the hypothermic (30. and 34 degrees C, respectively) groups. The values of critical hepatic oxygen delivery were between 7.3 and 11.9 ml O2.min-1.100 g-1 without significant differences among the groups. During reperfusion after ischemic insult, hepatic oxygen uptake returned to base-line values in both hypothermic groups but remained substantially below base-line values in normothermic groups of animals. Hepatic enzyme concentrations (lactate dehydrogenase, alanine aminotransferase, aspartate aminotransferase, and alcohol dehydrogenase) were substantially increased (up to 30-fold) in normothermic animals, but the concentrations did not increase in either of the hypothermic groups. These results demonstrated that hypothermia per se does not affect hepatic oxygen delivery but decreases hepatic oxygen demand and uptake, provides an effective protection from hepatic oxygen deprivation, and lessens reperfusion injury.
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PMID:Hypothermia, hepatic oxygen supply-demand, and ischemia-reperfusion injury in pigs. 236 Jun 37

We assessed the release of creatine kinase MB as both mass and activity during the postoperative period following cardiac surgery. CK-MB mass was determined by enzyme immunoassay using reagents obtained from Hybritech. CK-MB activity was determined both by agarose electrophoresis and by an immunochemical method. Fifty-five patients who underwent coronary artery bypass surgery and 52 control subjects who had orthopedic surgery were selected for study. Serial serum samples were collected following surgery and total LD, CK, AST, LD-1, CK-MB mass, and CK-MB activity determined. Results were compared to each other and to surgical parameters. All patients exhibited significant CK-MB mass and activity after surgery and peak serum levels were 6-94 micrograms/L and 12-84 U/L, respectively. CK-MB mass correlated with CK-MB activity on paired samples (r = 0.94). Total AST and CK activities correlated with CK-MB mass (r = 0.60, and 0.63, respectively). Peak levels of CK-MB mass correlated significantly with peak MB activity (r = 0.88), peak LD-1 (r = 0.62), peak AST (r = 0.71), and time on pump (r = 0.54). Similar correlations were also seen between peak CK-MB activity and these parameters. No relationship could be identified between extent of CK-MB mass release and number of grafts, degree of hypothermia, or minimum PaO2. The time course of CK-MB mass release exhibited 85% concordance with CK-MB activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in serum CK-MB mass after coronary artery bypass surgery. 350 Aug 9

We serially measured creatine kinase (CK), lactate dehydrogenase, aspartate aminotransferase (AST) and lactate from the lumbar cerebrospinal fluid in 14 patients with neurologic complications after open heart surgery with cardiopulmonary bypass (CPB). These analyses revealed a correlation between worsening neurologic deficit and the peak CK (r = .87, p less than .001), AST (r = .75, p less than .01), and lactate (r = .93, p less than .001) levels. Lactate increased before enzymes did. In 12 patients without complications, only lactate was significantly (p less than .005) elevated; however, within this group, CK but not lactate could be used to differentiate patients who later developed subtle mental changes. Although CPB appeared to induce metabolic changes in the brain that could possibly disturb function, severe cerebral damage appeared to require additional global or focal anoxic-ischemic factors. Short hypothermia during bypass did not influence CK, but it was falsely elevated after prolonged hypothermic periods. The testing of these enzymes may be a reliable indicator of the degree of brain damage and the prognosis.
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PMID:Temporal pattern of enzyme changes in cerebrospinal fluid in patients with neurologic complications after open heart surgery. 360 28

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

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

Studies have been made on the activity of aspartate and alanine aminotransferase in the brain of 1, 4, 12-14, 16, 22 days, 1, 1 1/2, 3 months and 2 years old rats under hypothermic conditions (20-19 degrees C). It was shown that hypothermia decreases both total and specific activities of the enzymes in the developing brain. Alanine aminotransferase activity in brain homogenates determined at 37 and 20-19 degrees C, exhibits more significant changes than of aspartate aminotransferase.
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PMID:[Aminotransferase activity in the brain of rats of various ages during hypothermia]. 401 66

In a prospective study, 93 patients were observed up to nine months after open-heart surgery using hypothermia, hemodilution and cold cardioplegia. In the first two weeks frequent determinations were made of serum aminotransferase, alkaline phosphatases (ALP), lactic dehydrogenase isoenzymes, gamma glutamyltransferase (GT), total and free bilirubin and bile acids. Plasma hemoglobin was measured at the end of the operation. After the first period, aminotransferases, alkaline phosphatases and bilirubin were determined monthly. On the first postoperative day almost all of the patients showed abnormal aspartate aminotransferase (ASAT) activity and ASAT/ALAT (alanine aminotransferase) greater than 1, and about 25% had hyperbilirubinemia. The findings suggested early postoperative leakage of enzymes not only from the myocardium, but also from the liver. After two weeks the patients presented another pattern of liver dysfunction, with abnormal ALAT in 50%, ASAT/ALAT less than 1, and abnormal ALP and GT in 28 and 45%, respectively. Eight patients were judged to have post-transfusion hepatitis of non-A, non-B type. Six of them had abnormal aminotransferases for more than six months.
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PMID:Hepatic dysfunction after open-heart surgery. 615 78

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

Aspartate aminotransferase (EC 2.6.1.1:AST) is known to have two isoenzymes, one associated with the cytoplasm (c-AST) and the other with the mitochondria (m-AST). We studied the relationships of m-AST activity in the coronary sinus blood to left ventricular function, coronary blood flow, water content and high-energy phosphate stores of the left ventricle following hypothermic ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia of 20 degrees C of myocardial temperature, 120 min of aortic occlusion was employed in 15 mongrel dogs. Left ventricular function (peak left ventricular pressure, left ventricular end-diastolic pressure, max dp/dt, cardiac index, left ventricular stroke work index), coronary blood flow, myocardial oxygen consumption, myocardial enzyme activity (m-AST, CK-MB), myocardial water content and high-energy phosphate stores (adenosine triphosphate, creatine phosphate) of the subendocardium of the left ventricle were measured. Data was obtained in the control state, and after 0, 30 and 60 min of reperfusion. Significant negative correlations were obtained between m-AST activity and peak left ventricular pressure (r = -0.81, p less than 0.001), max dp/dt (r = -0.83, p less than 0.001), cardiac product (r = -0.73, p less than 0.01), coronary blood flow (r = -0.59, p less than 0.05), adenosine triphosphate level (r = 0.72, p less than 0.01) and creatine phosphate level (r = -0.72, p less than 0.02) after 60 min of reperfusion. Significant positive correlations were obtained between m-AST activity and left ventricular end-diastolic pressure (r=0.75, p less than 0.01) and water content (r = 0.78, p less than 0.01) after 60 min of reperfusion. These results led to the assumption that serum m-AST activity in the coronary venous blood is a useful index to evaluate the degree of myocardial injury.
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PMID:Studies on the significance of serum mitochondrial aspartate aminotransferase activity following ischemic cardiac arrest. 714 3


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