CAJ | 학술논문

目的：建立离体大鼠心肌缺血／再灌注损伤模型，观察二氮嗪（ diazoxide，D）后处理对缺血／再灌注损伤离体大鼠心功能及线粒体心磷脂的影响，并探讨ATP敏感性钾通道在二氮嗪后处理心肌保护中的作用。方法：采用Langendorff装置建立离体大鼠心肌缺血／再灌注损伤模型，将SD大鼠随机分为对照组（ control）、缺血再灌注模型组（I／R）、二氮嗪后处理组（I／R＋D）、5-羟葵酸拮抗二氮嗪后处理组（I／R＋5-HD＋D），每组8只，均先灌注平衡20 min。 Control组：灌注平衡后续灌70 min；I／R组：缺血前灌注4℃ST．Thomas停跳液，全心缺血40 min，再灌30 min；I／R＋D组：全心缺血40 min，缺血后给予含二氮嗪（50μmol／L）的K-H液灌注5 min后，再灌25 min；I／R＋5-HD＋D组：二氮嗪后处理前给予含5-羟葵酸（100μmol／L）的K-H液灌注5 min，再灌20 min。观察各组续（再）灌注末心率、冠脉流出液量、心功能、心肌酶学及心肌线粒体心磷脂的变化。结果：各组续（再）灌注末比较， I／R组较control组及I／R＋D组心率减慢、冠脉流出液量降低，心功能明显受损，心肌酶增加，心磷酯含量减少，但与I／R＋5-HD＋D无明显差异。结论：二氮嗪后处理通过增加线粒体心磷脂含量，减少心肌酶的释放，改善心脏功能，减轻心肌的再灌注损伤，产生心肌保护作用。5-羟葵酸能够完全阻断二氮嗪的心肌保护作用。
목적：건립리체대서심기결혈／재관주손상모형，관찰이담진（ diazoxide，D）후처리대결혈／재관주손상리체대서심공능급선립체심린지적영향，병탐토ATP민감성갑통도재이담진후처리심기보호중적작용。방법：채용Langendorff장치건립리체대서심기결혈／재관주손상모형，장SD대서수궤분위대조조（ control）、결혈재관주모형조（I／R）、이담진후처리조（I／R＋D）、5-간규산길항이담진후처리조（I／R＋5-HD＋D），매조8지，균선관주평형20 min。 Control조：관주평형후속관70 min；I／R조：결혈전관주4℃ST．Thomas정도액，전심결혈40 min，재관30 min；I／R＋D조：전심결혈40 min，결혈후급여함이담진（50μmol／L）적K-H액관주5 min후，재관25 min；I／R＋5-HD＋D조：이담진후처리전급여함5-간규산（100μmol／L）적K-H액관주5 min，재관20 min。관찰각조속（재）관주말심솔、관맥류출액량、심공능、심기매학급심기선립체심린지적변화。결과：각조속（재）관주말비교， I／R조교control조급I／R＋D조심솔감만、관맥류출액량강저，심공능명현수손，심기매증가，심린지함량감소，단여I／R＋5-HD＋D무명현차이。결론：이담진후처리통과증가선립체심린지함량，감소심기매적석방，개선심장공능，감경심기적재관주손상，산생심기보호작용。5-간규산능구완전조단이담진적심기보호작용。
AIM: To investigate the effect of diazoxide (D) postconditioning on Cardiac function and mito-chondrial cardiolipin in isolated rat heart and to explore the protective effect of ATP sensitive potassium channel on diazo-xide postconditioning myocardium.METHODS: The myocardial ischemia/reperfusion injury model in isolated rat hearts was established by Langendorff apparatus.The isolated rat hearts were randomized into 4 groups ( n=8): control group ( control) , myocardial ischemia/reperfusion injury group ( I/R) , diazoxide postconditioning group ( I/R+D) , 5-hydroxy decanoic acid (5-HD) plus diazoxide postconditioning group (I/R+5-HD+D).The hearts in each group were started with 20 min perfusion for equilibration.The hearts in control group perfused for 70 min;The hearts in I/R group was global ischemia for 40 min after ischemia reperfusion at 4℃ST.Thomas cardioplegia, then reperfusion for 30 min;The hearts in I/R+D group were treated with diazoxide (50μmol/L) in K-H perfusion for 5 min after global ischemia for 40 min, then reperfusion for 25 min;The hearts in I/R+5-HD+D group were treated with 5-HD (100μmol/L) in K-H perfusion for 5 min before diazoxide postconditioning, then reperfusion for 20 min.The heart rate, coronary outflow volume, heart func-tion, myocardial enzymes and myocardial mitochondrial cardiolipin at the end of perfusion in each group were determined. RESULTS:Compared with control group and I/R+D group, the heart rate, the concentration of heart phospholipid and the coronary outflow volume were reduced, the heart function was significantly impaired the contents of myocardial enzymes were increased in I/R group.However, no significant difference between I/R group and I/R+5-HD+D group was ob-served.CONCLUSION:The diazoxide postconditioning protects the myocardium by increasing mitochondrial cardiolipin content, reducing the release of myocardial enzymes, improving heart function and reducing myocardial reperfusion injury. The myocardial protective effect of diazoxide is completely blocked by 5-hydroxy decanoic acid.