摘要
目的:评价卡维地洛防治猪急性心肌梗死(AMI)再灌注后无再流的作用.方法:将中华小型猪24只随机分成对照组、卡维地洛组1mg/(kg·d)和假手术组,每组8只.冠状动脉结扎3h,松解1h制备AMI再灌注模型.AMI前、后和再灌注后均行血流动力学测定和心肌声学造影(MCE)检查,最终行病理学分析.结果:①与AMI前相比,对照组AMI后3h主动脉收缩和舒张压(SBP和DBP)、左室收缩压(LVSP),心排量(CO)和左心室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05),肺毛细血管楔压(PCWP)和左室舒张末压(LVEDP)均显著升高(P<0.01);再灌注后1h仅LVSP显著恢复(P<0.05),±dp/dtmax继续显著下降(P<0.05);而卡维地洛组AMI后3h各项指标变化与对照组相同;但再灌注后1hLVSP,LVEDP,±dp/dtmax和CO均显著恢复(P<0.05)且比对照组更显著(P<0.05).②对照组MCE和病理染色所测的冠脉结扎区心肌范围(LA)高度一致,再灌注后无再流面积(ANR)分别为78.5%和82.3%,心肌坏死面积(NA)占LA的98.5%;而卡维地洛组%LA虽与对照组相当,但两方法所测ANR仅分别为24.9%和25.8%,NA仅为74.4%,均显著小于对照组(P<0.05).③对照组再灌注即刻和再灌注后1h冠脉血流量仅占AMI前的45.8%和50.6%(P<0.01),而卡维地洛组冠脉血流量分别提高到70.6%和74.1%,均比对照组显著增加(P<0.01).结论:卡维地洛能有效地防治AMI再灌注后无再流,改善其心功能,缩小梗死面积.
AIM： To evaluate the effects of carvedilol （beta blocker） on myocardial no-reflow in a mini-swine model of acute myocardial infarction （AMI） and reperfusion. METHODS： Twenty-four mini-swine were randomized into 3 groups： control, carvedilol-treatment [ 1 mg/（ kg · d） ] and sham-operation groups （ n = 8 ）. Animals in the former 2 groups were subjected to 3 h of coronary occlusion followed by 60 min of reperfusion. Data on hemodynamics and coronary blood flow volume （CBV） were collected and the area of no-reflow （ANR） was evaluated with both myocardial contrast echocardiography （MCE） in vivo and pathological means. Necrosis area （NA） was measured with triphenyltetrazolium chloride （TTC） staining. RESULTS： ① In control group, left ventricular systolic pressure （ LVSP ）, maximal rate of increase and decline in left ventricular pressure （± dp/dtm max） and cardiac output （ CO ） significantly declined （ P 〈 0.05 ）, while pulmonary capillary wedge pressure （PCWP） and left ventricular end-diastolic pressure （LVEDP） significantly increased at the end of 3 h of left anterior descending （LAD） occlusion （ P 〈 0.01 ）. Compared with those at the end of 3 h of occlusion, ± dp/dt further significantly declined （ P 〈 0.05 ） at 60 min of reperfusion. In carvedilol group, the changes of LVSP, ± dp/dt CO and LVEDP were the same as those in the control group after 3 h of AMI. In contrast, LVSP, ±dp/dt max CO, LVEDP and pulmonary capillary wedge （PCWP） recovered significantly at 60 min of reperfusion. ② In control group, the coronary ligation areas （LA） were similar （P〉0.05） on both MCE in vivo and pathological evaluation and ANR was also both similar as high as 78.5% and 82.3% respectively, with final NA reaching 98.5% of LA. There was no significant difference in LA by both MCE and pathological evaluation between carvedilol and control groups, though ANR by both methods was significantly decreased to 24.9% and 25.8% respectively （ both P 〈 0.01 ）, with final NA being also significantly decreased to 74.4% of LA in carvedilol group （P 〈 0.05 ）. ③ In control group, CBV was significantly declined to 45.8% and 50.6% of the baseline immediately after release of occlusion （3 h） and at 60 min of reperfusion （ both P 〈 0.01 ）. In carvedilol-treated group, CBV was also significantly declined immediately after release of occlusion （3 h ） and at 60 min of reperfusion （ both P 〈 0. 05 ） , though significantly increased to 70.6% and 74.1% of the baseline, which were both significantly higher than those in control group （ both P 〈 0.01 ）. CONCLUSION： Carvedilol is effective in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area during AMI and reperfusion in mini-swines.
出处
《第四军医大学学报》
北大核心
2006年第1期14-18,共5页
Journal of the Fourth Military Medical University
基金
国家自然科学基金(90209038)
