Hale Sharon L, Mehra Ankur, Leeka Justin, Kloner Robert A
Heart Institute, Good Samaritan Hospital, 1225 Wilshire Boulevard, Los Angeles, CA 90017, USA.
Am J Physiol Heart Circ Physiol. 2008 Jan;294(1):H421-5. doi: 10.1152/ajpheart.00962.2007. Epub 2007 Nov 9.
Postconditioning (PoC) with brief intermittent ischemia after myocardial reperfusion has been shown to lessen some elements of postischemic injury including arrhythmias and, in some studies, the size of myocardial infarction. We hypothesized that PoC could improve reflow to the risk zone after reperfusion. Anesthetized, open-chest rabbits were subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion. In protocol 1, rabbits were randomly assigned to the control group (n = 10, no further intervention after reperfusion) or to the PoC group, which consisted of four cycles of 30-s reocclusions with 30 s of reperfusion in between starting at 30 s after the initial reperfusion (4 x 30/30, n = 10). In protocol 2, rabbits were assigned to the control group (n = 7) or the PoC group, which received PoC consisting of four cycles of 60-s intervals of ischemia and reperfusion starting at 30 s after the initial reperfusion (4 x 60/60, n = 7). No reflow was determined by injecting thioflavine S (a fluorescent marker of capillary perfusion), risk zone by blue dye, and infarct size by triphenyltetrazolium chloride. In protocol 1, there were no statistical differences in hemodynamics, ischemic risk zone, or infarct size (35 +/- 6% of the risk zone in the PoC group vs. 29 +/- 4% in the control group, P = 0.38) between the groups. Similarly, in protocol 2, PoC failed to reduce infarct size compared with the control group (45 +/- 4% of the risk zone in the PoC group vs. 42 +/- 6% in the control group, P = 0.75). There was a strong correlation in both protocols between the size of the necrotic zone and the portion of the necrotic zone that contained an area of no reflow. However, PoC did not affect this relationship. PoC did not reduce infarct size in this model, nor did it reduce the extent of the anatomic zone of no reflow, suggesting that this intervention may not impact postreperfusion microvascular damage due to ischemia.
心肌再灌注后进行短暂间歇性缺血的后适应（PoC）已被证明可减轻缺血后损伤的某些因素，包括心律失常，并且在一些研究中还可减小心肌梗死面积。我们推测PoC可改善再灌注后危险区域的再灌注情况。对开胸麻醉的兔子进行30分钟冠状动脉闭塞，随后进行3小时再灌注。在方案1中，兔子被随机分为对照组（n = 10，再灌注后无进一步干预）或PoC组，PoC组在初始再灌注后30秒开始，进行四个周期的30秒再闭塞，中间间隔30秒再灌注（4×30/30，n = 10）。在方案2中，兔子被分为对照组（n = 7）或PoC组，PoC组在初始再灌注后30秒开始，接受由四个周期的60秒缺血和再灌注间隔组成的PoC（4×60/60，n = 7）。通过注射硫黄素S（毛细血管灌注的荧光标记物）测定无复流情况，用蓝色染料测定危险区域，用氯化三苯基四氮唑测定梗死面积。在方案1中，两组之间在血流动力学、缺血危险区域或梗死面积方面无统计学差异（PoC组梗死面积占危险区域的35±6%，对照组为29±4%，P = 0.38）。同样地，在方案2中，与对照组相比，PoC未能减小梗死面积（PoC组梗死面积占危险区域的45±4%，对照组为42±6%，P = 0.75）。在两个方案中，坏死区域大小与包含无复流区域的坏死区域部分之间均存在强相关性。然而，PoC并未影响这种关系。在该模型中，PoC既未减小梗死面积，也未降低无复流解剖区域的范围，这表明该干预措施可能不会影响缺血所致的再灌注后微血管损伤。
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