PROLONGED IMPAIRMENT OF CORONARY VASODILATION AFTER REVERSIBLE ISCHEMIA - EVIDENCE FOR MICROVASCULAR STUNNING
PROLONGED IMPAIRMENT OF CORONARY VASODILATION AFTER REVERSIBLE ISCHEMIA - EVIDENCE FOR MICROVASCULAR STUNNING
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DOI：
10.1161/01.res.67.2.332
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发表时间：
1990-08-01
影响因子：
20.1
通讯作者：
JEROUDI, MO
中科院分区：
文献类型：
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作者：
BOLLI, R;TRIANA, JF;JEROUDI, MO
短暂的可逆性心肌缺血后的再灌注与收缩功能的长期抑制（心肌“震颤”）有关；然而，对冠状血管功能的影响尚未确定。因此，开胸狗 (n = 14) 接受了 15 分钟的左冠状动脉前降支 (LAD) 闭塞，然后进行回流。再灌注后四小时，与非缺血心内膜相比，缺血后区域心肌血流量（微球）显着降低（p < 0.01），冠状血管阻力显着升高（p < 0.01）。此外，在静脉注射腺苷引起最大血管舒张期间（n = 6），与非缺血心肌相比，缺血后心肌血流量较低（p < 0.05），冠状血管阻力较高（p < 0.05），无论是心内膜层还是心外膜层。同样，在静脉注射罂粟碱引起的最大扩张期间（n = 8），与非缺血心内膜相比，缺血后心肌血流量较低（p < 0.05），血管阻力较高（p < 0.05）。在心外膜中观察到方向相似的趋势。再灌注后 4 小时，LAD 冠状动脉闭塞 40 秒后反应性充血的所有指标均显着低于对照回旋支冠状动脉 (n = 8)。顿挫心肌的收缩期壁增厚与 1) 静息心肌灌注，2) 腺苷或罂粟碱期间达到的充血，以及 3) 对 40 秒冠状动脉闭塞的充血反应之间没有明显的相关性。在未接受 15 分钟 LAD 闭塞的对照狗 (n = 15) 中，在使用腺苷 (n = 7) 或罂粟碱 (n = 8) 之前或期间，LAD 依赖床和回旋依赖床之间的心肌血流量或血管阻力没有差异。此外，40 秒闭塞后，LAD 和回旋动脉之间的反应性充血没有差异 (n = 8)。总之，短暂（15 分钟）的可逆性缺血性损伤会导致静息血管阻力长期增加和血管舒张反应性长期受损，两者均持续至少 4 小时。这些血管紊乱的严重程度与收缩抑制的严重程度无关，表明它们可能代表一种相对独立的现象。有人提出，除了心肌“震颤”之外，可逆性缺血也会引起微血管“震颤”。
Reperfusion after brief, reversible myocardial ischemia is associated with prolonged depression of contractile function (myocardial "stunning"); however, the effect on coronary vascular function has not been defined. Thus, open-chest dogs (n = 14) underwent a 15-minute left anterior descending coronary artery (LAD) occlusion followed by reflow. Four hours after reperfusion, regional myocardial blood flow (microspheres) was significantly (p < 0.01) lower and coronary vascular resistance significantly (p < 0.01) higher in the postischemic as compared with the nonischemic endocardium. Furthermore, during maximal vasodilation elicited by intravenous adenosine (n = 6), myocardial blood flow was lower (p < 0.05) and coronary vascular resitance higher (p < 0.05) in the postischemic as compared with the nonischemic myocardium, both in the endocardial and in the epiocardial layers. Similarly, during maximal dilation elicited by intravenous papaverine (n = 8), myocardial blood flow was lower (p < 0.05) and vascular resistance higher (p < 0.05) in the postischemic as compared with the nonischemic endocardium; a directionally similar trend was observed in the epicardium. Four hours after reperfusion, all indexes of reactive hyperemia after a 40-second coronary occlusion were significantly lower in the LAD than in the control circumflex coronary artery (n = 8). There was no appreciable correlation between systolic wall thickening in the stunned myocardium and 1) the resting myocardial perfusion, 2) the hyperemia attained during adenosine or papaverine, and 3) the hyperemic response to a 40-second coronary occlusion. In control dogs that did not undergo a 15-minute LAD occlusion (n = 15), there were no differences in myocardial blood flow or vascular resistance between the LAD-dependent and the circumflex-dependent bed, either before or during adenosine (n = 7) or papaverine (n = 8). Furthermore, reactive hyperemia after a 40-second occlusion did not differ between the LAD and the circumflex artery (n = 8). In conclusion, a brief (15 minute), reversible ischemic insult causes a prolonged increase in resting vascular resistance and a prolonged impairment in vasodilator responsiveness, both of which persist for at least 4 hours. The severity of these vascular derangements is not related to the severity of contractile depression, suggesting that they may represent a relatively independent phenomenon. It is proposed that, in addition to myocardial "stunning", reversible ischemia also causes a microvascular "stunning.".