内皮素A受体拮抗剂BQ610对猫急性心肌缺血保护作用的超微结构观察  

Protective effect of endothelin receptor subtype Aantagonist BQ610 on the ultrastructure of acuteischemic myocardium in cats

作　　者：林丽[1] 袁文俊[1] 

机构地区：[1]第二军医大学生理学教研室,上海200433

出　　处：《中华病理学杂志》1999年第4期281-284,共4页Chinese Journal of Pathology

基　　金：国家自然科学基金;"九五"全军医学科研基金

摘　　要：目的　观察内皮素Ａ受体拮抗剂ＢＱ６１０ 对急性缺血心肌超微结构的影响，以探讨内源性内皮素是否参与急性心肌缺血的病理过程。方法　结扎１２ 只猫左冠状动脉前降支（ＬＡＤ） 造成急性心肌缺血，立即向已结扎的ＬＡＤ 内直接注射ＢＱ６１０ 或注射生理盐水作对照，观察ＬＡＤ 结扎后３０ 分钟缺血区及非缺血区心肌超微结构。结果　急性缺血区心肌出现肌细胞肿胀、肌原纤维排列紊乱及灶性溶解、线粒体肿胀及内皮细胞肿胀等超微结构损伤，ＢＱ６１０ 可减轻缺血心肌超微结构损伤，与生理盐水对照组差异明显。非缺血区心肌超微结构基本正常。Objective To observethe effectsofendothelinreceptorsubtype Aantagonist BQ610 on acute ischemic myocardialinjury by electronic microscopy to study whether endogenous endothelin is involved in the pathogenesisofacute myocardialischemia. Methods Acute myocardialischemia wasinduced byligation ofthe leftanterior descending coronary artery (LAD)in 12 cats,and BQ610 wasimmediatelyinjectedintotheoccluded LAD.Controlsreceivednormalsaline (NS)injection.Theultrastructure ofischemic myocardium and non ischemic myocardium were observed 30 min after LAD ligation. Results As compared wtih NS controls, BQ610 significantly protected the acute ischemic myocardium from ultrastructuralinjury,including cardiac muscle fiber swelling,myofibrildisorganizationand breakdown ,mitochondrialswelling and endothelialswelling.In general,the non ischemic myocardialultrastructure wasnormal.Conclusions Theresultsindicatethatendogenousendothelin, through endothelin receptor subtype A, plays an important role in ultrastructure injury of acute ischemic myocardium in cats.

关 键 词：心肌缺血 内皮素A受体 拮抗剂 猫 超微结构 

分 类 号：R542.2[医药卫生—心血管疾病]