del Zoppo G J, Schmid-Schönbein G W, Mori E, Copeland B R, Chang C M
Department of Molecular and Experimental Medicine, Scripps Clinic and Research Foundation, La Jolla, Calif 92037.
Stroke. 1991 Oct;22(10):1276-83. doi: 10.1161/01.str.22.10.1276.
Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear.
In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3-hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency.
Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 microns diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capaillaries in two subjects, indicating a significant reduction of perfusion from normal (2p = 0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 3.5% of postcapillary venules, and occluded 40% (four of 10) of capillaries in linear reconstruction along a 110 microns length. Circumferential contact between polymorphonuclear leukocytes and the luminal endothelial cell membranes was documented, with an intrecellular gap of, at most, 160 nm. Fibrin was found with degranulated platelets when the latter were associated with granulocytes, but not with polymorphonuclear leukocytes alone.
The finding of capillary-obstructing polymorphonuclear leukocytes in the microvascular bed following middle cerebral artery reperfusion in focal ischemia in this model satisfies an essential requirement for postulating their role in early microvascular injury and the "no-reflow" phenomenon.
微血管灌注缺陷可能伴随大脑中动脉的持续闭塞及随后的再灌注；然而，这种“无再流”缺陷的本质仍不清楚。
在未进行抗血栓预处理的情况下，我们通过两种方法记录了狒狒闭塞/再灌注模型中大脑中动脉闭塞3小时和再灌注1小时后豆纹状核微血管血流完整性，这两种方法分别用于识别1）微血管闭塞和2）微血管通畅情况。
微血管“无再流”累及豆纹状核区域的毛细血管（直径4.0 - 7.5微米的血管）。两名受试者的毛细血管再流占所有毛细血管的27% - 39%，表明灌注较正常水平显著降低（P = 0.045）。在相同的实验准备中，单个多形核白细胞在随机选择的视野中完全阻塞了4.7%的毛细血管直径的微血管，部分阻塞了3.5%的毛细血管后微静脉，并在沿110微米长度的线性重建中阻塞了40%（10个中的4个）的毛细血管。记录到多形核白细胞与管腔内内皮细胞膜之间的周向接触，细胞间隙最大为160纳米。当脱颗粒血小板与粒细胞相关时可发现纤维蛋白，但单独与多形核白细胞相关时则未发现。
在该模型中局灶性缺血大脑中动脉再灌注后微血管床中发现阻塞毛细血管的多形核白细胞，满足了假定其在早期微血管损伤和“无再流”现象中作用的一个基本要求。
