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)

This study investigates the influence of inadequate oxygen supply on CK and CK-MB release rate in congenital cyanotic heart disease in fourteen patients. Eleven patients had Tetralogy of Fallot and 3 Transposition of great vessels. Their age ranged between 10 days and 10 years (mean 50.48 +/- 31.82 months). The corrective repair was carried out under CPB with systemic hypothermia (20 degrees-25 degrees C) and intermittent St. Thomas Cardioplegia perfusion in the aortic root until the septal temperature was below 16 degrees C. Three blood samples were taken before, during and 10 minutes after CPB to quantitate the CK and CK-MB. In 6 cases of Fallot, two simultaneous biopsies, one from the right and another from the left ventricular walls were taken at the end of the 10 first minutes of reperfusion to evaluate the ATP, CP and glycogen contents. CK and CK-MB levels showed an increasing evolution; the CK-MB per cent increased sharply after aortic clamp release and then fell abruptly to low values at the 10th minute after CPB arrest. Comparative evaluation between the 3 values for C K showed significant differences (P less than 0.001) in all, except when the first values were compared to the second (P greater than 0.05) and for CK-MB an overall significant differences were found at P less than 0.025 and P less than 0.001. On the other hand, quantification of ATP, CP and glycogen contents from simultaneous biopsies from the left and the right ventricular walls did not demonstrate significant differences between the two ventricles after the ischemic period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Profile of creatine phosphokinase (CK) and its isoenzyme MB (CK-MB) during corrective procedures of congenital cyanotic heart disease. 274 16

Scimitar horned oryx (Oryx dammah), kept under confined and unconfined conditions were immobilised with etorphine in combination with acepromazine or xylazine or both, and with xylazine alone. Both groups of animals were successfully sedated with etorphine and xylzine, with or without acepromazine, although hypothermia and mild hypoxaemia and a fall in packed cell volume were frequently noted. Xylazine alone produced a dose dependent degree of sedation in semitame subadult animals kept in confinement, but only slight depression in their wild, unconfined counterparts. If xylazine was not included in the immobilising mixture induction was traumatic and full sedation not achieved. Heart rates and arterial pressures (systemic and pulmonary) were also monitored but no remarkable changes were noted. The only abnormalities in blood biochemistry were raised aspartate transminase and creatine kinase. Ruminal regurgitation could be a major problem if endotracheal intubation was not achieved early in the procedure.
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PMID:Physiological effects of etorphine, acepromazine and xylazine in the scimitar horned oryx (Oryx dammah). 277 9

Oxygenation of crystalloid cardioplegic solutions is beneficial, yet bicarbonate-containing solutions equilibrated with 100% oxygen become highly alkaline as carbon dioxide is released. In the isolated perfused rat heart fitted with an intraventricular balloon, we recently observed a sustained contraction related to infusion of cardioplegic solution. In the same model, to record these contractions, we studied myocardial preservation by multidose bicarbonate-containing cardioplegic solutions in which first the calcium content and then the pH was varied. An acalcemic cardioplegic solution (Group 1) and the same solution with calcium provided by adding calcium chloride (Group 2) or blood (Group 3) were equilibrated with 100% oxygen. Ionized calcium concentrations were 0, 0.10 +/- 0.06, and 0.11 +/- 0.07 mmol/L and pH values were 8.74 +/- 0.07, 8.54 +/- 0.08, and 8.40 +/- 0.07, all highly alkaline. Hearts were arrested for 2 hours at 8 degrees +/- 2.5 degrees C and reperfused for 1 hour at 37 degrees C. At end-arrest, myocardial adenosine triphosphate was depleted in all three groups, significantly in Groups 2 and 3. In Group 1 the calcium paradox developed upon reperfusion, with contracture (left ventricular end-diastolic pressure = 60 +/- 7 mm Hg), creatine kinase release up to 620 +/- 134 U/L, a profound further decrease in adenosine triphosphate to 1.9 +/- 1.7 nmol/mg dry weight, and either greatly impaired or no functional recovery (17% +/- 10% of prearrest developed pressure). Three hearts in this group released creatine kinase during arrest and did not resume beating during reperfusion. In Groups 2 and 3, the calcium paradox did not occur; functional recovery was 61% +/- 4% and 71% +/- 9% at 5 minutes of reperfusion. In two additional groups (4 and 5), the pH of the acalcemic cardioplegic solution was decreased by equilibration with 2% and 5% carbon dioxide in oxygen to 7.53 +/- 0.03 and 7.11 +/- 0.02. Contractions during arrest were smaller than in Groups 1, 2, and 3; adenosine triphosphate was maintained during arrest; functional recovery was 101% +/- 3% and 96% +/- 4% at 5 minutes of reperfusion. We conclude that acalcemic solutions with carbon dioxide are superior to highly alkaline calcium-containing solutions. If oxygenation of cardioplegic solutions, of proved value, causes severe alkalinity, then calcium paradox may result even with hypothermia. This hazard is prevented by adding calcium or blood to the solution or carbon dioxide to the oxygen used for equilibration.
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PMID:Oxygenation of cardioplegic solutions. Potential for the calcium paradox. 311 49

The etiology and clinical course of acute nontraumatic rhabdomyolysis and ensuing renal failure was surveyed in a series of 40 consecutive patients. In 28 cases the muscle damage occurred after excessive consumption of ethyl alcohol and/or other intoxications. Prolonged lying immobilized was the reason or contributing factor for rhabdomyolysis in 22 cases. The other evident etiologies were convulsions, vigorous physical exercise, arterial occlusion and hypothermia. Typical local signs of rhabdomyolysis--pain, swelling and weakness of the affected muscles--were absent in one fourth of the patients. In these cases the diagnosis was based on transient elevation of serum creatine kinase enzyme activity. Dialyses were required to manage acute renal failure in 24 subjects. All 36 survivors recovered normal renal function. Neurological defects in the extremities still persisted in 16 patients at three months' follow-up.
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PMID:Acute renal failure following nontraumatic rhabdomyolysis. 323 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

The effect of two different myocardial preservation techniques on perioperative myocardial necrosis during coronary artery bypass surgery was assessed by serial myocardial creatine kinase determinations in 100 consecutive patients operated on by the same surgeon. Topical hypothermia with cold potassium cardioplegia was used randomly in 50 patients (group 1), and topical hypothermia with local interruption of the coronary circulation was used in the other 50 patients (group 2). Myocardial creatine kinase was measured by column chromatography every 6 hours for 36 hours after surgery. There was no significant difference between the two groups in terms of age, sex, functional class, extent of coronary artery disease, number of bypassed arteries, ejection fraction, or cardiopulmonary bypass time. Myocardial creatine kinase release (mean +/- standard error of the mean) was 193 +/- 33 IU/L X hours in group 1 patients operated on with cardioplegia and 210 +/- 31 IU/L X hours in group 2 patients operated on with topical hypothermia (p greater than 0.5). Myocardial creatine kinase peaks were 9.2 +/- 1.9 IU/L and 10.0 +/- 1.6 IU/L, respectively (p greater than 0.5). Perioperative myocardial infarction, as defined by serum enzyme activity and electrocardiographic criteria, occurred in 4 patients in group 1 and 3 patients in group 2. Thus, the addition of cardioplegia to topical hypothermia, although perhaps offering technical advantages, does not appear to improve myocardial protection over topical hypothermia with local interruption of the coronary circulation during coronary artery bypass surgery.
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PMID:Cold potassium cardioplegia versus topical hypothermia and intermittent aortic occlusion for myocardial protection during coronary artery surgery: a randomized clinical study. 351 46

The protective effect of cardioplegia upon neonatal myocardium during ischemia has not been clearly established. This study evaluated the effects of cardioplegia on left ventricular function in isolated working neonatal rabbit hearts (aged 1 week) subjected to 120 minutes of global ischemia at 28 degrees C. Four groups were studied: Group 1, hypothermia alone; Group 2, intermittent washout with an oxygenated noncardioplegic solution; Group 3, multidose cardioplegia; Group 4, single-dose cardioplegia. After ischemia, cardiac output was reduced to 72% +/- 5% (mean +/- standard error of the mean) of control (p less than 0.02) in Group 1 and to 56% +/- 4% in Group 2 (p less than 0.001). In contrast, there was no significant reduction from baseline cardiac output in those animals receiving cardioplegic solution (Group 3, 93% +/- 6%, and Group 4, 97% +/- 4%). Group 2 hearts demonstrated significantly worse recovery of cardiac output and stroke volume than all other groups. After ischemia, the first derivative of left ventricular pressure fell to 73% +/- 13% of control in Group 1 (p less than 0.1) and to 89% +/- 5% in Group 2 (p less than 0.05). However, the first derivative of left ventricular pressure was restored to control values in Group 3 (118% +/- 11%) and Group 4 (114% +/- 9%). When compared to baseline, creatine kinase was higher 30 minutes after reperfusion in Group 1 (40 +/- 8 versus 143 +/- 32 IU/L/gm, p less than 0.05) and in Group 2 (39 +/- 7 versus 163 +/- 33 IU/L/gm, p less than 0.05). Creatine kinase remained unchanged from baseline in Groups 3 and 4. This study demonstrates excellent preservation of left ventricular function in the neonatal rabbit heart protected with cardioplegic solution. In contrast, neither hypothermia alone nor intermittent washout with an oxygenated noncardioplegic solution was effective in preventing myocardial dysfunction. As in adults, the administration of cardioplegic solution preserves ventricular function during ischemia in neonatal hearts.
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PMID:Protection of the neonatal myocardium during hypothermic ischemia. Effect of cardioplegia on left ventricular function in the rabbit. 359 97

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

The pathogenesis of the calcium paradox has not been established. In calcium-free perfused hearts, caffeine, which releases calcium from the sarcoplasmic reticulum, causes severe myocardial injury, with creatine kinase (CK) release and contraction band necrosis similar in many respects to the calcium paradox. It has been postulated that contracture, initiated by a small rise in intracellular calcium, may cause sarcolemmal injury in both the calcium paradox and caffeine-induced myocardial injury. The present study was initiated to determine whether interventions which modulate caffeine-induced contracture will also correspondingly alter cellular injury. The effects of caffeine dose, procaine, extended calcium-free perfusion, elevated potassium, temperature, and increasing intracellular sodium on caffeine-induced contracture were examined in Langendorff-perfused adult rat hearts. Caffeine-induced contracture at 22 C increased over a dose range of 5-40 mM caffeine. Procaine, which inhibits caffeine-induced calcium release at doses between 5 and 20 mM, progressively reduced contracture caused by addition of 20 mM caffeine at 22 C. Hearts perfused with calcium-free solution containing 16 mM K+ showed a reduction in caffeine-induced contracture. Extended calcium-free perfusion (20 minutes) at temperatures from 18 to 37 C resulted in a progressive reduction of caffeine-induced contracture. Each of these interventions was also found to inhibit caffeine-induced injury at 37 C. Low temperature was found to have complex effects. Hypothermia enhanced caffeine contractures but also protected hearts from cell separations and CK release. Increasing intracellular sodium was found to enhance caffeine-induced contracture at 37 C. There was a direct correlation between measured intracellular sodium levels and the magnitude and duration of caffeine-induced contracture. These results demonstrate a direct correlation between the magnitude of contracture and myocardial injury in calcium-free hearts. It is proposed that contracture is the primary mediator of sarcolemmal membrane injury in hearts with intercalated disks weakened by prior calcium-free perfusion.
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PMID:Modification of caffeine-induced injury in Ca2+-free perfused rat hearts. Relationship to the calcium paradox. 370 96

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


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