CAJ | 학술논문

目的：观察远端缺血预处理( RIPC)对严重失血性休克大鼠在体心脏功能的保护作用及其机制。方法32只雄性SD大鼠,体重300~350 g,随机分成4组：对照组( C组)、失血性休克组( S 组)、RIPC组( R组)、RIPC +线粒体KATP通道阻滞剂组( B组),每组8只。采用经大鼠颈动脉60 min内放血占总血容量50%,观察30 min后经颈静脉30 min回输释放的血液建立严重失血性休克和复苏模型。在放血前双侧后肢以止血带捆绑阻断血流5 min,再灌注5 min,反复4个循环形成RIPC。 B组在RIPC前15 min经颈静脉注入线粒体KATP通道阻滞剂(5-羟基葵酸盐)10 mg/kg。 C组所有手术操作同S组,但不放血。持续监测心电图、平均动脉压( MAP)到血液回输后2 h,在放血前、放血后、输血前、输血后即刻、输血后1、2 h用彩色超声仪测量心输出量( CO)、左室射血分数(LVEF)、左室短轴缩短率(LVFS)、心肌做功指数(MPI)、左室后壁厚度(LVPWD)。结果在失血和休克阶段,与 C 组比较, S 组、B 组和 R 组 MAP、CO、LVEF、LVFS均降低(P<0．01),MPI、 LVPWD升高(P<0．01)；血液回输后,与 C 组比较, R 组 MAP、CO、LVEF、LVFS、MPI、LVPWD差异无统计学意义；与R组比较,S组和B组MAP、CO、LVEF、LVFS明显降低( P<0．01), MPI、LVPWD明显升高(P<0.01)；S组和B组各心脏功能指标差异无统计学意义。结论 RIPC明显保护严重失血性休克大鼠在体心脏功能,其保护作用可能与线粒体KATP通道激活有关。
목적：관찰원단결혈예처리( RIPC)대엄중실혈성휴극대서재체심장공능적보호작용급기궤제。방법32지웅성SD대서,체중300~350 g,수궤분성4조：대조조( C조)、실혈성휴극조( S 조)、RIPC조( R조)、RIPC +선립체KATP통도조체제조( B조),매조8지。채용경대서경동맥60 min내방혈점총혈용량50%,관찰30 min후경경정맥30 min회수석방적혈액건립엄중실혈성휴극화복소모형。재방혈전쌍측후지이지혈대곤방조단혈류5 min,재관주5 min,반복4개순배형성RIPC。 B조재RIPC전15 min경경정맥주입선립체KATP통도조체제(5-간기규산염)10 mg/kg。 C조소유수술조작동S조,단불방혈。지속감측심전도、평균동맥압( MAP)도혈액회수후2 h,재방혈전、방혈후、수혈전、수혈후즉각、수혈후1、2 h용채색초성의측량심수출량( CO)、좌실사혈분수(LVEF)、좌실단축축단솔(LVFS)、심기주공지수(MPI)、좌실후벽후도(LVPWD)。결과재실혈화휴극계단,여 C 조비교, S 조、B 조화 R 조 MAP、CO、LVEF、LVFS균강저(P<0．01),MPI、 LVPWD승고(P<0．01)；혈액회수후,여 C 조비교, R 조 MAP、CO、LVEF、LVFS、MPI、LVPWD차이무통계학의의；여R조비교,S조화B조MAP、CO、LVEF、LVFS명현강저( P<0．01), MPI、LVPWD명현승고(P<0.01)；S조화B조각심장공능지표차이무통계학의의。결론 RIPC명현보호엄중실혈성휴극대서재체심장공능,기보호작용가능여선립체KATP통도격활유관。
Objective To investigate the effects of remote ischemic preconditioning on cardiac dysfunction in vivo rat model of severe hemorrhagic shock and its potential mechanism. Methods Thirty-two male Sprague-Dawley rats, weighting 300~350 g, were randomized into four groups: control( C) group; shock ( S) group; Remote is-chemic preconditioning ( R) group;Remote ischemic preconditioning with mitochondrial KATP channel blocker ( B) group. Hemorrhagic shock and resuscitation were induced by reduction of 50% of total blood volume over an inter-val of 1 hour, 30 mins after bleeding, reinfusion was initiated with the shed blood over the ensuing 30 mins. RIPC was performed by four cycles of 5 mins of limbs ischemia followed by reperfusion for 5 mins. The mitochondrial KATP channel blocker (5-hydroxydeconate) was injected into the right atrium fifteen minutes before the initiation of RIPC. The procedure in control group was the same as shock group but not bleeding. Electrocardiogram and mean artery pressure ( MAP) were continuously measured to 2 h after reinfusion. Cardiac function was measured by echo-cardiography at baseline, after bleeding, before reinfusion, after reinfusion and at hourly intervals after reinfusion. Results Compared with C group, MAP, CO, LVEF,LVFS were significantly decreased and MPI, LVPWD were significantly increased in R,S and B groups (P<0. 01) during hemorrhagic and shock phase. After reinfusion, MAP,CO,LVEF,LVFS,MPI, LVPWD were not different between R group and C group. Compared with R group, MAP, CO, LVEF, LVFS were significantly decreased and MPI, LVPWD were significantly increased in S group than B group (P<0. 01). There were no differences of cardiac function indexes between S group than B group. Conclusion RIPC obviously improves cardiac dysfuntion in vivo rat following severe hemorrhagic shock and resus-citation, the result is associated with the activation of mitochondrial KATP channel.