CAJ | 학술논문

目的评价含左西孟旦的STH-2心脏停搏液对大鼠离体心脏缺血再灌注损伤的影响.方法雄性Wistar大鼠32只,制备离体Langendorff灌注模型,随机分为4组(n=8),采用K-H液平衡灌注30 min时,C组采用STH-2心脏停搏液进行灌注,L1组、L2组和L2+G分别用含0.03μmol/L左西孟旦、0.3 μmol/L左西孟旦和0.3 μmol/L左西孟旦+10μmol/L格列苯脲(ATP敏感性钾通道阻断剂)的STH-2心脏停搏液进行灌注,灌注2 h时采用K-H液再灌注30 min.分别于灌注心脏停搏液前即刻(基础状态)、再灌注10 min、20 min、30 min时收集冠脉流出液,测定乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性.再灌注30 min时,取心肌组织,测定ATP、MDA、SOD水平及含水量.结果与C组比较,L1组CK、LDH的活性和MDA含量降低,SOD活性升高,L2组CK、LDH的活性和MDA含量降低,ATP含量和SOD活性升高(P＜0.05或0.01);与L1组比较,L2组CK和IDH的活性和MDA含量降低,SOD活性升高(P＜0.05或0.01);与L2组比较,L2+G组MDA含量、CK和LDH的活性升高,ATP含量和SOD活性降低(P＜0.05或0.01).结论含左西孟旦的STH-2心脏停搏液可减轻大鼠心肌缺血再灌注损伤,且与浓度有关,其机制与开放ATP敏感性K+通道有关.
목적 평개함좌서맹단적STH-2심장정박액대대서리체심장결혈재관주손상적영향.방법 웅성Wistar대서32지,제비리체Langendorff관주모형,수궤분위4조(n=8),채용K-H액평형관주30 min시,C조채용STH-2심장정박액진행관주,L1조、L2조화L2+G분별용함0.03μmol/L좌서맹단、0.3 μmol/L좌서맹단화0.3 μmol/L좌서맹단+10μmol/L격렬분뇨(ATP민감성갑통도조단제)적STH-2심장정박액진행관주,관주2 h시채용K-H액재관주30 min.분별우관주심장정박액전즉각(기출상태)、재관주10 min、20 min、30 min시수집관맥류출액,측정유산탈경매(LDH)화기산격매(CK)적활성.재관주30 min시,취심기조직,측정ATP、MDA、SOD수평급함수량.결과 여C조비교,L1조CK、LDH적활성화MDA함량강저,SOD활성승고,L2조CK、LDH적활성화MDA함량강저,ATP함량화SOD활성승고(P＜0.05혹0.01);여L1조비교,L2조CK화IDH적활성화MDA함량강저,SOD활성승고(P＜0.05혹0.01);여L2조비교,L2+G조MDA함량、CK화LDH적활성승고,ATP함량화SOD활성강저(P＜0.05혹0.01).결론 함좌서맹단적STH-2심장정박액가감경대서심기결혈재관주손상,차여농도유관,기궤제여개방ATP민감성K+통도유관.
Objective To investigate the effect of STH-2 cardioplegic solution containing levosimendan on ischemia-reperfusion (I/R) injury in isolated rat hearts. Methods Thirty-two male Wistar rats weighing 250-300 gwere anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg. The hearts were rapidly excised and perfused with oxygenated (95% O2-5% CO2) K-H solution for 30 min in a Langendorff apparatus and then divided into 4groups (n = 8 each) according to the composition of cardioplegic solution: group Ⅰ control (group C) was perfused with STH-2 cardioplegic solution; group Ⅱ , Ⅲ and Ⅳ were peffused with STH-2 cardioplegic solution containing levosimendan 0.03 μmol/L (L1), 0.3 μmol/L (L2) and levosimendan 0.3 μmol/L + glibenclamide 10 μmol/L (L2+ G) respectively. The isolated hearts were first perfused with different cardioplegic solutions for 2 h and then with K-H solution for 30 min. The coronary effluent was collected before ischemia (baseline) and at 10, 20 and 30 min of reperfusion for measurement of creatine kinase (CK) and lactate dehydrogenase (LDH)activities. Myocardial specimens were obtained from apex at 30 min of reperfusion for determination of myocardial ATP and MDA contents and SOD activity. Results Perfusion with STH-2 cardioplegic solution significantly increased CK and LDH activities and MDA content, and significantly decreased SOD activity. Levosinendan 0.03or 0.3 μmol/L significantly attenuated the cardioplegia-induced increase in LDH,CK and SOD activities and MDA content. The protective effects of levosimendan on myocardium against I/R injury were reversed by glibenclamide to some extent. Conclusion Levosimendan can protect myocardium from I/R injury in a dose-dependent manner by opening KATP channel.