{"title":"[Protective effect of dantrolene in post-ischemic reperfusion myocardial damage].","authors":"E O Balam Ortiz, K Carvajal, D Cruz","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>This study shows that the hydantoin drug, dantrolene, protects against myocardial damage induced by reperfusion. This effect was analyzed after 5 minutes of left coronary artery occlusion in Wistar rats hearts. The results made evident that dantrolene protects the myocardium against myocardial dysfunction (stunning heart) and reperfusion arrhythmias. Furthermore, it decreases the release of the enzymes creatine cinase and lactate dehydrogenase to the plasma, and protects from the structural damage of myocardium. We propose that the protective effect of the drug, might be due to its blocking effect on cardiac calcium release channel (ryanodine receptor) of the sarcoplasmic reticulum; thus, decreasing the high level of cytoplasmic calcium concentration (calcium overload), that is a characteristic of reperfusion injury.</p>","PeriodicalId":75556,"journal":{"name":"Archivos del Instituto de Cardiologia de Mexico","volume":"69 4","pages":"311-9"},"PeriodicalIF":0.0000,"publicationDate":"1999-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archivos del Instituto de Cardiologia de Mexico","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
This study shows that the hydantoin drug, dantrolene, protects against myocardial damage induced by reperfusion. This effect was analyzed after 5 minutes of left coronary artery occlusion in Wistar rats hearts. The results made evident that dantrolene protects the myocardium against myocardial dysfunction (stunning heart) and reperfusion arrhythmias. Furthermore, it decreases the release of the enzymes creatine cinase and lactate dehydrogenase to the plasma, and protects from the structural damage of myocardium. We propose that the protective effect of the drug, might be due to its blocking effect on cardiac calcium release channel (ryanodine receptor) of the sarcoplasmic reticulum; thus, decreasing the high level of cytoplasmic calcium concentration (calcium overload), that is a characteristic of reperfusion injury.