Influence of neutrophil depletion on myocardial function and flow after reversible ischemia.
Influence of neutrophil depletion on myocardial function and flow after reversible ischemia.
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DOI：
10.1152/ajpheart.1989.256.2.h341
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发表时间：
1989-02
期刊：
影响因子：
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通讯作者：
P. O’Neill;M. L. Charlat;L. Michael;R. Roberts;R. Bolli
中科院分区：
文献类型：
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作者：
P. O’Neill;M. L. Charlat;L. Michael;R. Roberts;R. Bolli
我们探讨了中性粒细胞(PMN)在心肌收缩功能障碍(心肌“顿抑”)和可逆性缺血后血管异常的发生中的作用。开胸犬冠状动脉结扎15min，再灌注4h，实验组(n=16)静脉注射抗犬PMN山羊抗血清，对照组(n=15)静脉注射非免疫性山羊血清。治疗组的平均血液PMN水平是生理盐水对照组的10%。在缺血期间，中性粒细胞减少的狗的侧支血流趋于增加，矛盾的收缩期室壁变薄趋于减少，但尽管如此，这些动物在REP后的室壁增厚的恢复并没有增强。同样，缺血或复跳期间的心律失常在三组之间也没有不同。REP后4小时，与非缺血心肌相比，顿抑心肌的静息阻力和最小冠脉阻力(通过腺苷注射评估)都更高；然而，这些血管紊乱在所有三组中都是相似的。因此，严重的中性粒细胞减少未能减轻机械功能障碍，减少心律失常，并防止冠状动脉闭塞15分钟后的血管异常。虽然先前的研究表明，中性粒细胞介导了长时间缺血时的细胞死亡，但目前的发现表明，PMN在短暂的、可逆的缺血相关的损害中并不起重要作用。血流减少的持续时间可能是决定PMN是否加重缺血性损伤的关键因素。
We explored the role of polymorphonuclear leukocytes (PMN) in the genesis of contractile dysfunction (myocardial "stunning") and of vascular abnormalities after reversible ischemia. Open-chest dogs underwent a 15-min coronary occlusion and 4 h of reperfusion (REP); treated animals (n = 16) received intravenous goat antiserum against canine PMN, whereas controls received nonimmune goat serum (n = 10) or saline (n = 15). In treated dogs, the average blood PMN levels were 10% of those in saline controls. During ischemia, collateral flow tended to be higher, and paradoxical systolic wall thinning tended to be less in neutropenic dogs, but despite this, recovery of wall thickening after REP was not enhanced in these animals. Similarly, arrhythmias during ischemia or REP did not differ among the three groups. Four hours after REP, both resting and minimal coronary resistance (the latter assessed by adenosine infusion) were higher in the stunned compared with the nonischemic myocardium; these vascular derangements, however, were similar in all three groups. Thus profound neutropenia failed to attenuate mechanical dysfunction, to reduce arrhythmias, and to prevent vascular abnormalities after a 15-min coronary occlusion. Although previous studies have suggested that neutrophils mediate cell death during prolonged ischemia, the present findings suggest that PMN do not contribute importantly to the damage associated with brief, reversible ischemia. The duration of flow reduction may be a critical factor determining whether PMN exacerbate ischemic injury.