Johnston W H, Latta H
Am J Pathol. 1977 Oct;89(1):153-66.
The purpose of these experiments was to define changes in glomeruli of rats kidneys which could account for a marked reduction of blood flow immediately following temporary ischemia. After the renal artery had been clamped for 60 minutes, mesangial and endothelial cellular swelling was sufficiently severe to compress and trap intracapillary erythrocytes, obstruct capillary lumens, and prevent reflow of an isotonic carbon suspension. Perfusion of saline solution before the renal arteries were clamped washed blood from the kidney, and the resulting cellular swelling alone was not sufficient to block capillary lumens. Erythrocyte trapping did not occur after 15 minutes of ischemia. Swelling of glomerular and tubular epithelial cells produced some extrinsic capillary compression that could contribute to erythrocyte trapping, but this appeared to be of minor importance in producing the no-reflow phenomenon.
这些实验的目的是确定大鼠肾脏肾小球的变化,这些变化可以解释短暂缺血后血流量的显著减少。肾动脉夹闭60分钟后,系膜和内皮细胞肿胀严重到足以挤压并困住毛细血管内的红细胞,阻塞毛细血管腔,并阻止等渗碳悬浮液的回流。在肾动脉夹闭前灌注盐溶液可将肾脏中的血液冲洗掉,仅由此产生的细胞肿胀不足以阻塞毛细血管腔。缺血15分钟后未发生红细胞被困现象。肾小球和肾小管上皮细胞的肿胀产生了一些外部毛细血管压迫,这可能有助于红细胞被困,但这在产生无复流现象中似乎不太重要。