PROGRESSIVE IMPAIRMENT OF REGIONAL MYOCARDIAL PERFUSION AFTER INITIAL RESTORATION OF POSTISCHEMIC BLOOD-FLOW
PROGRESSIVE IMPAIRMENT OF REGIONAL MYOCARDIAL PERFUSION AFTER INITIAL RESTORATION OF POSTISCHEMIC BLOOD-FLOW
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DOI：
10.1161/01.cir.80.6.1846
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发表时间：
1989-12-01
期刊：
影响因子：
37.8
通讯作者：
BECKER, LC
中科院分区：
文献类型：
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作者：
AMBROSIO, G;WEISMAN, HF;BECKER, LC
“无复流”现象是指在缺血后再灌流的心脏中出现非常低血流的区域，被认为主要是由于缺血引起的微血管损伤而在再灌流时建立的。在目前的研究中，我们试图确定在再灌流过程中是否也可能发生额外的组织灌注量损害。开胸犬冠状动脉左回旋支结扎90min，再灌流2min(n=7)或3.5h(n=8)。在活体注射荧光染料硫代黄素-S后，在处死前的左心室切片上显示心肌灌注。血流灌注受损的面积(缺乏硫代黄素)平均为9.5±-。3.0%的狗的危险区域再灌流2分钟，而在再灌流3.5小时的狗(25.9±-)小时，其危险区几乎是狗的三倍。风险区域的8.2%，p<；0.05)。再灌流期间微球连续测量血流显示缺血后心肌内的区域在再灌流2分钟后充血，30分钟时仍有充足的血流，但随后灌注量显著下降。3.5小时后，这些区域的血流可忽略不计(0.13±-)。0.03ml/min/g)，不摄取硫代黄素。显示缺血后灌注受损的组织样本在缺血期间几乎没有侧支血流(<；0.01ml/min/g)，而相邻硫代黄素阳性区的侧支血流显著增加(0.04±-)。心内膜标本0.01ml/min/g，0.07±-。0.02ml/分钟/g来自中段心肌的样本，p<；0.001对硫代黄素阴性区域)。表现为晚期血流障碍的区域总是表现为收缩带坏死，这与“真实”(即立即)无再流区所观察到的凝固性坏死的模式形成对比。毛细血管内红细胞停滞和明显的血管内中性粒细胞聚集(在再灌流2分钟后达到20倍)在迟发性血流障碍区域典型地被观察到。在死后心脏注射硅橡胶以描绘微血管充盈模式的另一只狗中，证实了毛细血管水平的血流阻塞。再灌流3.5h后，毛细血管充盈缺失区域较再灌流2min时更为广泛。因此，这项研究表明，缺血后心肌出现明显的灌注区仅在一定程度上与不能在回流时再灌流某些区域有关。一个更重要的因素是流向最初接受充分再灌注的区域的血流延迟、渐进性下降。这种现象发生在缺血期间没有侧支循环的区域，并与再灌流过程中中性粒细胞聚集和晚期毛细血管堵塞有关。
The "no-reflow" phenomenon, the occurrence of areas with very low flow in hearts reperfused after ischemia, is thought to be largely established at the time of reperfusion as a result of microvascular damage induced by ischemia. In the present study we sought to determine whether additional impairment of tissue perfusion might also occur during the course of reperfusion. Open-chest dogs were subjected to 90 minutes of left circumflex coronary artery occlusion and reperfused for 2 minutes (n = 7) or 3.5 hours (n = 8). Myocardial perfusion was visualized in left ventricular slices following in vivo injection of the fluorescent dye thioflavin-S just before killing. The area of impaired perfusion (absent thioflavin) averaged 9.5 .+-. 3.0% of the risk region in dogs reperfused for 2 minutes, whereas it was nearly three times as large in dogs reperfused for 3.5 hours (25.9 .+-. 8.2% of the risk region, p < 0.05). Serial measurements of flow by microsphereas during reperfusion demonstrated zones within the postischemic myocardium that were hyperemic 2 minutes after reperfusion, with adequate flow still present at 30 minutes, but with a subsequent marked fall in perfusion. After 3.5 hour these areas showed negligible flow (0.13 .+-. 0.03 ml/min/g) and no thioflavin uptake. Tissue samples showing postischemic impairment in perfusion had received virtually no collateral flow during ischemia (< 0.01 ml/min/g), whereas collateral flow was significantly higher in adjacent thioflavin-positive zones (0.04 .+-. 0.01 ml/min/g in endocardial samples and 0.07 .+-. 0.02 ml/min/g in samples from the midmyocardium, p < 0.001 vs. thioflavin-negative areas). Areas that showed late impairment of flow invariably demonstrated contraction band necrosis, which contrasted with the pattern of coagulation necrosis observed in areas of "true" (i.e., immediate) non-reflow. Intracapillary erythrocyte stasis and marked intravascular neutrophil accumulation (to levels > 20-fold that found after 2 minutes reperfusion) were typically observed in areas of delayed impairment to flow. Obstruction to flow at the capillary level was confirmed in additional dogs in which the heart was injected postmortem with silicone rubber to delineate the microvascular filling pattern. Areas of absent capillary filling were much more extensive after 3.5 hours than after 2 minutes reperfusion. Thus, this study shows that the occurrence of areas of markedly impaired perfusion in postischemic myocardium is related only in part to inability to reperfuse certain areas on reflow. A more important factor is represented by a delayed, progressive fall in flow to areas that initially received adequate reperfusion. This phenomenon develops in regions receiving no collateral flow during ischemia and is associated with neutrophil accumulation and capillary plugging late during the course of reperfusion.