Schmid-Schönbein G W
Fed Proc. 1987 May 15;46(7):2397-401.
Granulocytes are large, stiff viscoelastic cells that adhere naturally to the vascular endothelium. On their passage through the capillary network they have to be deformed, and recent evidence indicates that they may impose a significant hemodynamic resistance. The entry time of granulocytes into capillaries is about three orders of magnitude longer than that for red cells. Inside the capillary the granulocytes move with a lower velocity than red cells. Under conditions when the capillary perfusion pressure is reduced and/or elevated levels of inflammatory products are present that increase the adhesion stress to the endothelium, granulocytes may become stuck in the capillary. In such a situation, the granulocytes form a large contact area with the capillary endothelium, they obstruct the lumen, and they may initiate tissue injury. After the restoration of the perfusion pressure the granulocytes may not be removed from the capillary owing to the adhesion to the endothelium. Capillary plugging by granulocytes appears to be the mechanism responsible for the no-reflow phenomenon, and together with oxygen free radical formation and lysosomal enzyme activity may constitute the origin for ischemic injury as well as other microvascular occlusive diseases.
粒细胞是大的、具有刚性粘弹性的细胞，它们自然地粘附于血管内皮。在通过毛细血管网络时，它们必须发生变形，最近的证据表明它们可能会产生显著的血流动力学阻力。粒细胞进入毛细血管的时间比红细胞长约三个数量级。在毛细血管内，粒细胞的移动速度比红细胞慢。当毛细血管灌注压力降低和/或存在炎症产物水平升高导致对内皮的粘附应力增加时，粒细胞可能会卡在毛细血管中。在这种情况下，粒细胞与毛细血管内皮形成大的接触面积，阻塞管腔，并可能引发组织损伤。灌注压力恢复后，由于与内皮的粘附，粒细胞可能无法从毛细血管中清除。粒细胞造成的毛细血管堵塞似乎是无复流现象的原因，并且与氧自由基形成和溶酶体酶活性一起可能构成缺血性损伤以及其他微血管闭塞性疾病的起源。
