Menger M D, Rücker M, Vollmar B
Institute for Clinical & Experimental Surgery, University of Saarland, Germany.
Shock. 1997 Jul;8(1):2-7.
The major dysfunction of capillaries after prolonged periods of ischemia is the lack of re-establishment of nutritive blood flow upon onset of reperfusion, i.e., capillary no-reflow. Several mechanisms have been proposed to cause capillary no-reflow, including intravascular hemoconcentration and thrombosis, leukocyte plugging, endothelial cell swelling, vasomotor dysfunction, and interstitial edema formation. Electron microscopic studies suggest that thrombus formation and intravascular clotting are not significant mechanisms. Moreover, intravital microscopic studies have demonstrated that plugging of capillaries by leukocytes is not a primary cause for the manifestation of no-reflow in postischemic striated muscle. In contrast, both in vivo studies and histological examinations support the concept that ischemia/reperfusion induces the disruption of the endothelial integrity with loss of fluid to endothelial cells and the interstitial space. As a consequence, these pathological sequelae are associated with intravascular hemoconcentration, endothelial cell swelling and interstitial edema formation, which contribute to capillary lumenal narrowing, increase of hydraulic resistance, and, thus, impairment of perfusion. Whether the postischemic diameter response with dilation of reperfused capillaries and lumenal narrowing of no-reflow capillaries involves endothelin/nitric oxide-triggered capillary pericyte function remains to be determined.
长时间缺血后毛细血管的主要功能障碍是再灌注开始时营养性血流无法重新建立，即毛细血管无复流现象。已提出多种机制来解释毛细血管无复流现象，包括血管内血液浓缩和血栓形成、白细胞阻塞、内皮细胞肿胀、血管舒缩功能障碍以及间质水肿形成。电子显微镜研究表明血栓形成和血管内凝血并非主要机制。此外，活体显微镜研究已证明白细胞阻塞毛细血管并非缺血后横纹肌无复流表现的主要原因。相反，体内研究和组织学检查均支持这样的观点，即缺血/再灌注会导致内皮完整性破坏，液体从内皮细胞流失到间质间隙。因此，这些病理后遗症与血管内血液浓缩、内皮细胞肿胀和间质水肿形成有关，这些因素会导致毛细血管腔狭窄、水力阻力增加，进而损害灌注。缺血后再灌注毛细血管扩张和无复流毛细血管腔狭窄的直径反应是否涉及内皮素/一氧化氮触发的毛细血管周细胞功能仍有待确定。
