Yin M, Kurvers H A, Tangelder G J, Booster M H, Buurman W A, Kootstra G
Department of Surgery, University Hospital Maastricht, The Netherlands.
Ren Fail. 1996 Mar;18(2):211-23. doi: 10.3109/08860229609052791.
Several pathophysiological mechanisms have been purported to be involved in the development of acute ischemic renal failure, such as impairment of tubular function and/or of the renal microcirculation. However, it has not been elucidated as yet which of these mechanisms relates to the extent of kidney damage. Besides, little is known about the time course relationship between tubular and microcirculatory disturbances during the development of ischemia-reperfusion injury. We therefore performed intravital videomicroscopy of the proximal tubules as well as the peritubular microcirculation of the rat renal cortex during the first 24 hr of reperfusion after varying lengths of warm ischemia (30 min, 30 WI group; 60 min, 60 WI group; 90 min, 90 WI group). In a separate group of animals subjected to the same protocol, the survival rate (SR) was determined. The SR in these groups were 100%, 20% and 0%, respectively. Initially, the tubular and microcirculatory changes (i.e., increased tubular diameter and reduced capillary blood flow) relate well to the length of warm ischemia as well as the SR. At a later stage of reperfusion, however, we observed that peritubular capillary blood flow and tubular diameter recovered more quickly in the 90 WI group than in the 30 WI and 60 WI groups. As a result, these parameters as obtained at 24 hr of reperfusion did not relate anymore to the survival rate. Besides, at this stage a severe loss of integrity of the tubular wall was noted in the 60 WI and 90 WI groups. These findings suggest that kidney viability is not determined by the extent of recovery of microcirculatory blood flow and/or tubular diameter during early reperfusion, but by the integrity of the tubular wall.
据推测，几种病理生理机制与急性缺血性肾衰竭的发生有关，如肾小管功能和/或肾微循环受损。然而，目前尚未阐明这些机制中哪一种与肾损伤程度相关。此外，对于缺血再灌注损伤发展过程中肾小管和微循环紊乱之间的时间进程关系知之甚少。因此，我们在不同时长的热缺血（30分钟，30WI组；60分钟，60WI组；90分钟，90WI组）后再灌注的最初24小时内，对大鼠肾皮质近端肾小管以及肾小管周围微循环进行了活体视频显微镜检查。在另一组接受相同实验方案的动物中，测定了存活率（SR）。这些组的存活率分别为100%、20%和0%。最初，肾小管和微循环变化（即肾小管直径增加和毛细血管血流量减少）与热缺血时长以及存活率密切相关。然而，在再灌注后期，我们观察到90WI组肾小管周围毛细血管血流量和肾小管直径的恢复比30WI组和60WI组更快。因此，再灌注24小时时获得的这些参数与存活率不再相关。此外，在这个阶段，60WI组和90WI组出现了肾小管壁完整性的严重丧失。这些发现表明，肾脏的存活能力不是由早期再灌注期间微循环血流量和/或肾小管直径的恢复程度决定的，而是由肾小管壁的完整性决定的。
