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)

Creatine kinase BB isoenzyme (CK-BB) was detected intraoperatively in 22 of 25 patients undergoing aortocoronary bypass surgery, both in the coronary sinus and in the mixed venous blood. In a group of 10 patients in whom selective intracavitary profound hypothermic arrest was used, CK-BB values were lower than in another group of 10 patients, in whom controlled ventricular fibrillation with moderate total body hypothermia was instituted. This latter group also had higher levels of CK-MB. Patients who developed acute myocardial infarction immediately prior to or during the surgical intervention had the highest CK-BB values. This enzyme appeared as early as 15 minutes after the institution of cardiopulmonary bypass and disappeared within 6 hours. It is considered that part of the BB isoenzyme in serum of patients undergoing heart surgery is of myocardial origin.
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PMID:Detection of creatine kinase BB isoenzyme in sera of patients undergoing aortocoronary bypass surgery. 30 Jun 59

The concentration of calcium (1.2 mmol/L) in clinical St. Thomas' Hospital cardioplegic solution was chosen several years ago after dose-response studies in the normothermic isolated heart. However, recent studies with creatine phosphate in St. Thomas' Hospital solution demonstrated that additional myocardial protection during hypothermia resulted principally from its calcium-lowering effect in the solution. The isolated working rat heart model was therefore used to establish the optimal calcium concentration in St. Thomas' Hospital solution during lengthy hypothermic ischemia (20 degrees C, 300 minutes). The calcium content of standard St. Thomas' Hospital solution was varied from 0.0 to 1.5 mmol/L in eight treatment groups (n = 6 for each group). During ischemia, hearts were exposed to multidose cardioplegia (3 minutes every 30 minutes). Postischemic recovery of function was expressed as a percentage of preischemic control values. Release of creatine kinase and the time to return of sinus rhythm during the reperfusion period were also measured. These dose-response studies during hypothermic ischemia revealed a broad range of acceptable calcium concentrations (0.3 to 0.9 mmol/L), which appear optimal in St. Thomas' Hospital solution at 0.6 mmol/L. This concentration improved the postischemic recovery of aortic flow from 22.0% +/- 5.9% with control St. Thomas' Hospital solution (calcium concentration 1.2 mmol/L) to 86.0% +/- 4.0% (p less than 0.001). Other indices of functional recovery showed similar dramatic results. Creatine kinase release was reduced 84% (p less than 0.01) in the optimal calcium group. Postischemic reperfusion arrhythmias were diminished with the loser calcium concentration, with a significant decrease in the time between initial reperfusion until the return of sinus rhythm. In contrast, acalcemic St. Thomas' Hospital solution precipitated the calcium paradox with massive enzyme release and no functional recovery. Unlike prior published calcium dose-response studies at normothermia, these results demonstrate that the optimal calcium concentration during clinically relevant hypothermic ischemia is considerably lower than that of normal serum ionized calcium (1.2 mmol/L) and appears ideal at 0.6 mmol/L to realize even greater cardioprotective and antiarrhythmic effects with St. Thomas' Hospital solution.
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PMID:Lowering the calcium concentration in St. Thomas' Hospital cardioplegic solution improves protection during hypothermic ischemia. 199 42

Twenty-seven children with complex congenital heart malformations necessitating early repair were studied before and after deep hypothermic procedures. The children were allocated into two groups. One group underwent total circulatory arrest (40 +/- 6 minutes). In the other group perfusion was maintained during deep hypothermia but reduced a 25% of normal at normothermia. The temperature was reduced to 15 degrees C (nasopharynx) in both groups with a combination of topical and core cooling. To study cerebral injury, were made serial measurements of creatine kinase isoenzyme BB from arterial samples before and for 8 hours after the deep hypothermic procedure. Creatine kinase isoenzyme BB increased after both procedures from 4.3 +/- 0.9 ng/ml to 10.4 +/- 1.8 ng/ml in the circulatory arrest group and from 2.8 +/- 0.7 ng/ml to 9.9 +/- 1.9 ng/ml in the low-flow group (no significant difference). The results were analyzed in relation to age, size, study group, hemoglobin, blood glucose, and blood gases. The creatine kinase BB levels were positively related to preoperative hemoglobin and blood glucose values before the hypothermic procedures.
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PMID:No flow or low flow? A study of the ischemic marker creatine kinase BB after deep hypothermic procedures. 250 90

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

Reperfusion of an isolated heart with a calcium-containing solution after a short calcium-free perfusion may result in irreversible cell damage: the calcium paradox. In this investigation the effect of hypothermia during reperfusion with calcium-containing solution on the calcium paradox damage in the isolated rat heart was studied. In addition, the effect of pre-cooling the heart during the calcium-free period was investigated. Creatine kinase release was used to define cell damage. Normothermic (37 degrees C) calcium-free perfusion followed by normothermic reperfusion with calcium-containing solution resulted in a massive release of CK. When the normothermic calcium-free perfusion was followed by hypothermic (10 degrees C) calcium-containing reperfusion, CK release was reduced by 20% (P less than 0.005). This CK release during reperfusion was further reduced by 55% and 80% when the normothermic calcium-free perfusion was followed by 5 or 10 min respectively of hypothermic calcium-free perfusion prior to the hypothermic calcium-containing reperfusion. The results show that hypothermia during the period of calcium repletion retards the sequence of events which ultimately results in release of large amounts of intracellular components.
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PMID:The effect of hypothermia during the period of calcium repletion on the calcium paradox. 377 21

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

Reperfusion of an isolated heart with calcium-containing solution after a short period of calcium-free perfusion may result in irreversible cell damage (calcium paradox). Experiments were undertaken to determine whether rat hearts could be predisposed to the calcium paradox by perfusion with Bretschneider's calcium-free histidine-buffered cardioplegic solution. Creatine kinase (CK) release during the reperfusion phase was used to quantitate cell damage. Perfusion with cardioplegic solution was performed at 37 degrees and 20 degrees C. Reperfusion after 10 minutes of perfusion with this solution at 37 degrees C resulted in a full calcium paradox. After 120 minutes of perfusion with cardioplegic solution at 20 degrees C, CK release during reperfusion amounted to 30% of the release during a full calcium paradox. This CK release could be further reduced by lowering the coronary flow rate or by adding 50 mumol X L-1 CaCl2 to the cardioplegic solution. It is concluded that a combination of hypothermia, a low coronary flow rate, and a limited duration of exposure to Bretschneider's histidine-buffered cardioplegic solution will minimize the risk of evoking the calcium paradox.
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PMID:Bretschneider's histidine-buffered cardioplegic solution and the calcium paradox. 688 57

Creatine kinase (CK) isoenzymes were determined on 15 patients undergoing open heart surgery with bypass. The study was performed to examine the relationship between the hypothermia under which the surgery is conducted and the appearance of CK isoenzymes in the serum both during and after surgery. All patients showed dramatic rises in total CK activity commencing during surgery. Myocardial CK (CK-MB or CK-2) was seen in fourteen patients and brain CK (CK-BB or CK-1) was seen in ten patients. Peak activities of CK-BB did not coincide with peak activities of CK-MB. The serum elevations of CK-BB in these patients appear to arise from a mechanism different from that responsible for the elevations of CK-MB, and it is assumed that the former is due to intermittent disruptions in the perfusion and/or oxygenation of tissues rich in CK-BB. CK-MB elevations appear to be due directly to the surgical intervention. Hypothermia alone does not in itself appear to be solely responsible for elevations of CK-BB although it can not be completely excluded from playing some role in its production.
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PMID:Creatine kinase (CK) isoenzyme activities in cardiac surgery. 716 90

The benefit of cardioplegic cardiac arrest for the protection of immature myocardium is controversial. We therefore investigated the efficacy of (1) topical hypothermia alone, (2) slow cooling by coronary perfusion hypothermia, and (3) cardioplegic cardiac arrest for the protection of isolated immature rats hearts (28 days) during 8 hours of global ischemia at 10 degrees C. The study was conducted in hearts from rats that were kept hypoxemic by lifelong exposure to simulated high altitude. Left ventricular function, endothelial function, the metabolic status, and the extent of myocardial injury were all assessed. Topical hypothermia provided superior protection in hypoxic hearts, with recovery of the maximum developed left ventricular pressure by 70.6% +/- 18.0% (mean +/- standard deviation) of its preischemic value (p < 0.01 versus slow cooling and versus cardioplegic protection). The same pattern of recovery was observed among control hearts. The degree of recovery of endothelial function after sole topical hypothermia measured 54% +/- 36% in hypoxic hearts and 62% +/- 37% in control hearts, but was not recordable in any of the other groups. Creatine kinase leakage and the myocardial high-energy content did not differ significantly among any of the groups. Rapid cooling by topical hypothermia alone provides superior protection in chronic hypoxic, immature rat hearts versus the protection conferred by slow cooling. St. Thomas' Hospital cardioplegic solution II does not afford additional protection. Endothelial injury caused by cold asanguineous perfusates, including cardioplegia, interferes with the recovery of vascular function, which, in turn, may limit mechanical function.
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PMID:Protection of the chronic hypoxic immature rat heart during global ischemia. 788 15

The effects of diltiazem, a sarcolemmal Ca2+ channel blocker, and ryanodine, an inhibitor of sarcoplasmic reticulum function, were investigated in isolated newborn rabbit hearts (2 to 5 days old) subjected to ischemia and reperfusion. After cardioplegic arrest with St. Thomas' Hospital solution, global ischemia was induced at 37 degrees C (normothermia) for 45 minutes or at 20 degrees C (hypothermia) for 180 minutes. The hearts were then reperfused at 37 degrees C for 30 minutes. Diltiazem or ryanodine, at concentrations that have minimal to moderately negative inotropic effects under nonischemic conditions, was added to the cardioplegic solution. After normothermic ischemia, reperfusion of untreated hearts resulted in recovery of left ventricular developed pressure to 52.9% +/- 2.5% of the preischemic level. In hearts treated with diltiazem, recovery of left ventricular developed pressure was significantly improved (84.2% +/- 2.9% at 3 x 10(-8) mol/L; p < 0.01). Comparable improvement was achieved with ryanodine (90.5% +/- 4.1% at 10(-9) mol/L; p < 0.01). Creatine kinase leakage and structural derangement of mitochondria were also reduced by both agents. With hypothermic ischemia, left ventricular developed pressure recovered in untreated hearts to 72.7% +/- 3.3% of preischemic values. Treatment with diltiazem improved the recovery of left ventricular developed pressure to 96.9% +/- 3.5% at 3 x 10(-8) mol/L and reduced creatine kinase leakage and mitochondrial damage. Ryanodine also improved the recovery of left ventricular developed pressure and attenuated ultrastructural damage. These findings suggest that Ca2+ handling by the sarcoplasmic reticulum, like transsarcolemmal Ca2+ influx, plays an important role in the pathogenesis of myocardial ischemia-reperfusion injury in the neonatal heart despite the morphologic and functional immaturity of the sarcoplasmic reticulum in the neonate.
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PMID:Protective effects of diltiazem and ryanodine against ischemia-reperfusion injury in neonatal rabbit hearts. 832 Oct 5


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