腺苷对猪急性心肌梗死再灌注后无再流的影响

目的评价腺苷防治猪急性心肌梗死(AMI)再灌注后无再流的作用。方法中华小型猪24只随机分成对照组、腺苷组(100μg·kg-1·min-1持续静点)和假手术组,每组8只。前2组行冠状动脉结扎3h,松解1h建立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、左室收缩压、心排量和左室内压最大收缩和舒张变化速率(±dp/dtmax)均显著下降(P<0.05～0.01),肺毛细血管楔压和左室舒张末压均显著升高(P<0.01);再灌注后1h仅左室舒张末压显著恢复(P<0.05)然而±dp/dtmax继续显著下降(P<0.05);而腺苷组AMI后3h各项指标变化与对照组相同;但再灌注后1h左室收缩压、左室舒张末压、±dp/dtmax和心排量均显著恢复(P均<0.05),且比对照组更显著(P均<0.05)。(2)对照组心肌声学造影和病理染色所测的冠状动脉结扎区心肌范围高度一致,再灌注后无再流面积分别为67.5%和69.3%,心肌坏死面积(NA)占结扎区心肌面积(LA)的98.5%;而腺苷组LA均与对照组相当,但两方法所测无再流面积仅分别为21.5%和20.8%,NA仅为75.2%,均显著小于对照组(P<0.05～0.01)。(3)对照组再灌注即刻和再灌注后1h冠状动脉血流量仅占AMI前的45.8%和50.6%(P均<0.01),而腺苷组冠

Beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction and reperfusion

OBJECTIVE: To evaluate the beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction (AMI) and reperfusion. METHODS: Twenty-four animals were randomly assigned to 3 groups: 8 in controls, 8 in adenosine-treated and 8 in sham-operated. The groups were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion except the sham-operated group. Data on hemodynamics and coronary blood flow volume (CBV) were collected. The area of no-reflow was evaluated by both myocardial contrast echocardiography (MCE) in vivo and histopathological means and necrosis area was measured with triphenyltetrazolium chloride staining. RESULTS: (1) In control group, systolic and diastolic blood pressure (SBP and DBP), left ventricular systolic pressure, maximal rate of increase and decline in left ventricular pressure (+/- dp/dtmax) and cardiac output significantly declined (P < 0.05-0.01), while left ventricular end-diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP) significantly increased at the end of 3 hours of LAD occlusion (both P < 0.01), with +/- dp/dtmax further significantly declined (both P < 0.05) at 60 minutes of reperfusion. In adenosine treated group, the changes of SBP and DBP, left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP were the same as those in the control group after AMI and reperfusion, while left ventricular systolic pressure, +/- dp/dtmax, cardiac output, LVEDP and PCWP recovered significantly at 60 minutes of reperfusion compared with those at 6 hours AMI. (2) In control group, the coronary ligation areas (LA) were similar (P > 0.05) detected by MCE in vivo and histopathological evaluation, and the areas of no-reflow were both as high as 67.5% and 69.3%, respectively. The final necrosis area reached 99% of LA. Compared with those in the control group, there was no significant difference in LA on both MCE and histopathological evaluation in the adenosine-treated group, though the areas of no-reflow on both methods were significantly decreased to 21% and 22% (both P < 0.01) and final necrosis area was also significantly decreased to 75% of LA (P < 0.05). (3) In the control group, CBV were significantly declined to 45.8% and 50.6% of the baseline at immediately after release of 3 hours occlusion and at 60 minutes of reperfusion, respectively (both P < 0.01). In the adenosine-treated group, CBV were also significantly declined at immediately after release of 3 hours occlusion, and at 60 minutes of reperfusion (both P < 0.05), though significantly increased to 79.5% and 79.9% of the baseline which were both significantly higher than those in the control group. CONCLUSION: Adenosine has an effective role in preventing myocardial no-reflow, improving left ventricular function and reducing infarct area during AMI and reperfusion in mini-swine.