Myocardial neutrophil accumulation during reperfusion after reversible or irreversible ischemic injury.
Myocardial neutrophil accumulation during reperfusion after reversible or irreversible ischemic injury.
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DOI：
10.1152/ajpheart.1988.255.5.h1188
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发表时间：
1988-11
期刊：
影响因子：
--
通讯作者：
L. O. Go;C. Murry;VINCENT J. Richard;G. R. Weischedel;R. Jennings;K. Reimer
中科院分区：
文献类型：
--
作者：
L. O. Go;C. Murry;VINCENT J. Richard;G. R. Weischedel;R. Jennings;K. Reimer
最近的研究表明，多形核白细胞（PMNs）在缺血心肌再灌注过程中可能引起额外的心肌细胞损伤。本研究旨在探讨可逆性或不可逆性心肌缺血再灌注早期中性粒细胞是否在心肌内积聚。开胸麻醉的狗经历了回旋支冠状动脉闭塞12分钟（n = 5），40分钟（n = 8），或90分钟（n = 8），然后再灌注1小时。用111 In标记自体PMN，并重新注射以定量再流期间心肌PMN内流。同时注射125 I标记的白蛋白以校正心肌组织中与血浆蛋白相关的111 In。测定非缺血和缺血再灌注心肌内、中、外三分之一的中性粒细胞数量。在12分钟组中，40%的中性粒细胞减少存在于再灌注比非缺血对照组织。相反，在40分钟和90分钟组中，缺血-再灌注心肌中的PMN积聚是非缺血心肌的2 - 6倍，PMN流入的跨壁梯度从外层到内层增加。用放射性微球测量的侧支血流量在三组之间没有显著差异。在缺血12分钟后再灌注过程中，中性粒细胞未能聚集，这并不支持中性粒细胞导致可逆性损伤的心肌细胞缺血后功能障碍的假设。是否中性粒细胞引起的细胞死亡，在早期再灌注后较长的缺血发作仍然未知，但是，在预测的梗死区的PMN积累的速度与这种可能性是一致的。
Recent studies suggest that polymorphonuclear leukocytes (PMNs) may cause additional myocyte injury during reperfusion of ischemic myocardium. The present study was done to investigate whether PMNs accumulate in myocardium during early reperfusion after reversible or irreversible ischemic injury. Open-chest anesthetized dogs underwent circumflex coronary occlusions for 12 min (n = 5), 40 min (n = 8), or 90 min (n = 8), followed by 1 h of reperfusion. Autologous PMNs were radiolabeled with 111In and reinjected to quantitate myocardial PMN influx during reflow. 125I-labeled albumin was injected simultaneously to correct for 111In associated with plasma proteins in myocardial tissue. The number of PMNs was determined in the inner, middle, and outer one-third of nonischemic and ischemic-reperfused myocardium. In the 12-min group, 40% fewer PMNs were present in the reperfused than in the nonischemic control tissue. In contrast, in both the 40- and 90-min groups, PMN accumulation was two- to sixfold greater in the ischemic-reperfused than nonischemic myocardium, with a transmural gradient of PMN influx increasing from the outer to inner layers. Collateral blood flow, measured with radioactive microspheres, was not significantly different among the three groups. The failure of PMNs to accumulate during reperfusion after 12 min of ischemia does not support the hypothesis that PMNs contribute to postischemic dysfunction of reversibly injured myocytes. Whether PMNs caused cell death during early reperfusion after longer ischemic episodes remains unknown; however, the rapidity of PMN accumulation in the zones of predicted infarction is consistent with this possibility.