Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The usefulness of ulinastatin for protection of reperfusion injury after myocardial ischemia was evaluated in 25 patients undergone open heart surgery (18 cases with coronary artery bypass grafting and 7 with valve replacements). Twenty five patients were divided into two groups; U (+)-group consisted of 12 patients with ulinastatin (10,000 IU/kg) injected via the aortic root just before aortic declamping, and U (-)-group of 13 patients without ulinastatin. There were no significant differences between the two groups in age, body weight, total cardiopulmonary bypass (CPB) time, and aortic cross clamp time. Blood samples were obtained from coronary sinus before the start of CPB, just before the aortic cross clamp and immediately after reperfusion, and 1 and 3 hours later. Levels of thiobarbituric acid (TBA), alpha-tocopherol (alpha TOC), polymorphonuclear elastase (PMNE), creatine phosphokinase (CK) and creatine phosphokinase isoenzyme (CK-WB) release were measured, and myocardial aerobic metabolism was also evaluated. At each time point after reperfusion, TBA levels in U (+)-group were significantly less (p less than 0.05), and alpha TOC levels were significantly higher (p less than 0.05) than those in U (-)-group. PMNE increased progressively during CPB and showed a peak at 3 hours after reperfusion. And both groups showed increased lactate production and anaerobic metabolism immediately after reperfusion and 1 hour later, as evidenced by changes in excess lactate and redox potential of lactate and pyruvate. There was, however, no significant difference between the two groups with CK-MB as well as CK release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Usefulness of ulinastatin as a radical scavenger for protection of reperfusion injury after myocardial ischemia in open heart surgery]. 177 2

The effect of oleanolic acid (OA) pretreatment on myocardial ischemia-reperfusion (I-R) injury was investigated using an ex vivo rat heart model. Pretreatment with OA at daily doses (0.6 and 1.2 mmol/kg) for 3 days significantly protected against I-R injury in isolated rat hearts, as evidenced by the decrease in the extent of lactate dehydrogenase (LDH) leakage and improvement in contractile force recovery. The cardioprotection was associated with a slight increase in mitochondrial reduced glutathione (GSH) level and a significant increase in mitochondrial alpha-tocopherol (alpha-TOC) level, when compared with the unpretreated I-R group. To further investigate the mechanism of myocardial protection, pretreatment with a single dose of OA (1.2 mmol/kg) produced a time-dependent protection against myocardial I-R injury as assessed by LDH leakage, with the maximum extent of protection occurring at 48 hour post-dosing. The maximum cardioprotection was associated with parallel increases in mitochondrial GSH and alpha-TOC levels in ischemic-reperfused hearts, with the stimulation of the alpha-TOC level being optimal. Furthermore, buthionine sulfoximine/phorone (BSO/PHO) treatment, while abolishing the enhancing effect of OA on mitochondrial GSH, did not completely abrogate the cardioprotection against I-R injury. The remnant cardioprotection was associated with an increase in mitochondrial alpha-TOC level, when compared with the unpretreated I-R group with BSO/PHO. The results suggest that the cardioprotection afforded by OA pretreatment against I-R injury may at least in part be attributed to the enhancement of mitochondrial antioxidant mechanism mediated by GSH and alpha-TOC, particularly under I-R conditions. Abbreviations. BSO:buthionine sulfoximine GSH:reduced glutathione I-R:ischemia-reperfusion alpha-LA:alpha-lipoic acid LDH:lactate dehydrogenase OA:oleanolic acid PHO:phorone alpha-TOC:alpha-tocopherol.
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PMID:Oleanolic acid protects against myocardial ischemia-reperfusion injury by enhancing mitochondrial antioxidant mechanism mediated by glutathione and alpha-tocopherol in rats. 1653 26