Yamamoto K, Wilson D R, Baumal R
Am J Pathol. 1984 Aug;116(2):253-61.
Changes in medullary circulation may contribute significantly to the pathogenesis of ischemic acute renal failure. The microcirculation of the outer medulla of the rat kidney was studied by morphometry, carbon injection, and scanning electron microscopy of vascular casts after temporary renal ischemia. Morphometry showed a markedly reduced vascular area and an increased tubular epithelial cell area in the outer stripe of the medulla 2 hours after blood reflow. Maximum diminution in vascular area occurred 24-48 hours after reflow, with swollen and later necrotic tubular epithelium compressing the surrounding vascular compartment. Outflow blockade of venous vasa recta in the outer stripe caused congestion of the inner stripe. Carbon injection and scanning electron microscopy of vascular casts confirmed the perfusion defects of the outer stripe. These results suggest that decreased blood reflow to the outer stripe of the medulla secondary to tubular epithelial cell swelling and necrosis plays a significant role in the pathogenesis of ischemic acute renal failure in the rat.
髓质循环的改变可能在缺血性急性肾衰竭的发病机制中起重要作用。通过形态计量学、碳灌注以及对大鼠肾脏短暂缺血后血管铸型进行扫描电子显微镜检查,对大鼠肾外髓质的微循环进行了研究。形态计量学显示,再灌注2小时后,髓质外带的血管面积显著减少,肾小管上皮细胞面积增加。血管面积在再灌注后24 - 48小时减少到最大程度,此时肿胀并随后坏死的肾小管上皮细胞压迫周围的血管腔。髓质外带直小静脉的流出道阻塞导致内带充血。碳灌注和血管铸型的扫描电子显微镜检查证实了外带的灌注缺陷。这些结果表明,继发于肾小管上皮细胞肿胀和坏死的髓质外带血流减少在大鼠缺血性急性肾衰竭的发病机制中起重要作用。