Influence of collateral flow on the ischemic tolerance of the heart following acute and subacute coronary occlusion.
Influence of collateral flow on the ischemic tolerance of the heart following acute and subacute coronary occlusion.
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作者：
W. Schaper;S. Pasyk
急性闭塞的回旋支分支的左冠状动脉中产生的慢性仪器清醒的狗。示踪剂微球被用来测量在一个既定的时间段内，梗塞心肌内的侧支血流的分布。冠状动脉闭塞后2小时，侧支血流的数量和分布保持不变。冠状动脉闭塞后2 ~ 4小时，心内膜下血流几乎为零，心外膜下血流上升。6 ~ 48小时，心外膜下和总侧支血流明显升高。无复流现象是导致内动脉下侧支血流减少的原因。通过在闭塞后1、2、4和6小时释放动脉，为该假设提供了证据。不能再灌注的内膜下动脉的量在闭塞1小时后较小，在闭塞6小时后较大。当总侧支血流非常低时，心外膜下不能再灌注，发生透壁性心肌梗死。我们的结论是缺血发作和无复流现象的出现之间的时间延迟取决于侧支血流的量。心内膜下无复流现象的发生增加了流向心外膜下的流量，这增加了其存活的机会。闭塞后超过6小时，侧支血流总量增加，这被解释为侧支血管被动口径变化导致侧支阻力降低。通过细胞增殖发出活性管径变化信号的DNA合成总是在冠状动脉完全闭塞后24小时检测到，而不管狭窄发作至完全闭塞之间的时间是否在36小时至5天之间变化。当完全闭塞时间为4天时，由于预先存在的侧支血管的生长转化，心肌梗死得以预防。观察到急性冠状动脉闭塞时的四个阶段的侧支反应：有利于心外膜下的有效侧支血流再分布（闭塞后t = 1至4小时），2）由于侧支血管的被动“拉伸”，总侧支血流增加（闭塞后t = 4至24小时），3）由于活跃的细胞增殖，侧支血管放射状生长，（t = 24小时至5天）4）细胞增殖以确保生长转化的侧支中的正常壁厚度（冠状动脉闭塞后t = 5天至20天）。当然，在亚急性冠状动脉闭塞中，第一阶段不适用。
Acute occlusion of the circumflex branch of the left coronary artery was produced in chronically instrumented conscious dogs. Tracer microspheres were used to measure during an established time period, the distribution of collateral flow within the infarcting myocardium. For up to 2 hours after coronary occlusion the amount and distribution of the collateral flow remained unchanged. Two to 4 hours after coronary occlusion the subendocardial flow fell to almost zero and the subepicardial flow rose. Between 6 and 48 hours subepicardial and total collateral flow rose markedly. A no-reflow phenomenon is responsible for the decline of collateral flow in the subendocardium. Evidence for this hypothesis was provided by releasing the artery 1,2, 4 and 6 hours after occlusion. The amount of subendocardium that could not be reperfused was small after 1 hour and large after 6 hours of occlusion. When the total collateral flow was very low, the subepicardium was not able to be reperfused and a transmural myocardial infarction developed. We conclude that the time delay between onset of ischemia and the appearance of a no-reflow phenomenon depends upon the amount of collateral flow. The occurrence of a no-reflow phenomenon in the subendocardium increases the amount of flow to the subepicardium which increases its chances of survival. Beyond the sixth hour after occlusion the total amount of collateral flow increases which is interpreted as a reduction of collateral resistance by passive caliber changes of the collateral vessels. DNA-synthesis that signal active caliber changes through cellular proliferation were always detected 24 hours after complete occlusion of a coronary artery regardless whether the time between onset of stenosis until complete occlusion was varied between 36 hours and 5 days. When the time to complete occlusion was 4 days, myocardial infarction was prevented due to growth-transformation of pre-existing collaterals. Four phases of collateral reactions in acute coronary occlusion were observed: redistribution of available collateral flow in favor of the subepicardium (t = 1 to 4 hours after occlusion), 2) increase of total collateral flow due to passive "stretch" of collateral vessels (t = 4 to 24 hours after occlusion), 3) radial growth of collateral vessels due to active cellular proliferation, (t = 24 hours to 5 days) 4) cellular proliferation to ensure a normal wall thickness in growth'transformed collaterals (t = 5 days to 20 days after coronary occlusion). In subacute coronary occlusion the first phase does, of course, not apply.