Zhao Jing-lin, Yang Yue-jin, Jing Zhi-cheng, Wu Yong-jian, You Shi-jie, Yang Wei-xian, Meng Liang, Tian Yi, Chen Ji-lin, Gao Run-lin, Chen Zai-jia
Department of Coronary Heart Disease, Cardiovascular Institute and Fu Wai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100037, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2005 May;33(5):453-8.
To evaluate the beneficial effects of adenosine on myocardial no-reflow in a mini-swine model of acute myocardial infarction (AMI) and reperfusion.
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.
(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.
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.
评估腺苷对小型猪急性心肌梗死(AMI)及再灌注模型中心肌无复流的有益作用。
将24只动物随机分为3组:对照组8只、腺苷治疗组8只、假手术组8只。除假手术组外,其余组均进行3小时冠状动脉闭塞,随后再灌注60分钟。收集血流动力学和冠状动脉血流量(CBV)数据。通过体内心肌对比超声心动图(MCE)和组织病理学方法评估无复流面积,并用氯化三苯基四氮唑染色测量坏死面积。
(1)对照组在左前降支闭塞3小时末,收缩压和舒张压(SBP和DBP)、左心室收缩压、左心室压力最大上升和下降速率(±dp/dtmax)及心输出量显著下降(P<0.05 - 0.01),而左心室舒张末期压力(LVEDP)和肺毛细血管楔压(PCWP)显著升高(均P<0.01),在再灌注60分钟时±dp/dtmax进一步显著下降(均P<0.05)。腺苷治疗组在AMI和再灌注后SBP、DBP、左心室收缩压、±dp/dtmax、心输出量、LVEDP和PCWP的变化与对照组相同,但与AMI 6小时时相比,再灌注60分钟时左心室收缩压、±dp/dtmax、心输出量、LVEDP和PCWP显著恢复。(2)对照组通过体内MCE和组织病理学评估检测到的冠状动脉结扎区(LA)相似(P>0.05),无复流面积分别高达67.5%和69.3%。最终坏死面积达到LA的99%。与对照组相比,腺苷治疗组在MCE和组织病理学评估中LA无显著差异,尽管两种方法的无复流面积均显著降至21%和22%(均P<0.01),最终坏死面积也显著降至LA的75%(P<0.05)。(3)对照组在闭塞3小时解除后即刻和再灌注60分钟时,CBV分别显著降至基线的45.8%和50.6%(均P<0.01)。腺苷治疗组在闭塞3小时解除后即刻和再灌注60分钟时CBV也显著下降(均P<0.05),尽管显著升至基线的79.5%和79.9%,均显著高于对照组。
腺苷在小型猪AMI及再灌注期间对预防心肌无复流、改善左心室功能和减少梗死面积具有有效作用。