Investigation of pathogenesis in retinal circulatory disturbances with the analysis of lenkocyte clynamics.

视网膜缺血再灌注后，白细胞在再灌注后4小时开始沿静脉壁滚动。滚动白细胞通量显著增加，在再灌注12小时后达到峰值（10240个细胞/mm）。再灌注48小时后，血流通量显著下降至最高水平的六分之一左右。再灌注96 h后，可观察到少量滚动白细胞。各时间点缺血再灌注损伤过程中粘附分子种类和密度的差异可能解释了这一发现。再灌注12 h后滚动白细胞的速度明显低于再灌注前后。这种减少可能是由于每个时间点粘附分子种类和密度的不同，而不是血流速度的减少。血管收缩在再灌注后立即发生，在再灌注后4小时达到峰值（动脉收缩66.8%，静脉收缩90.1%）。动脉血管舒张在再灌注后12 ~ 24小时达到峰值（1 23-1 29%），在再灌注后96小时消退。静脉血管舒张在再灌注后24小时达到峰值，48小时消退。再灌注后4小时，白细胞数量开始增加。细胞数随时间增加而增加，再灌注后24 h达到931*187个/mm。结果表明，短暂性脑缺血后icam - 1 mRNA表达上调，再灌注后12小时达到峰值。我们在视网膜上的结果与这一观察结果一致。糖尿病大鼠视网膜微循环白细胞速度为1.38*0.31 mm/秒，对照组为1.27*0.20 mm/秒。两组间无显著性差异，未见白细胞堵塞或滚动。相比之下，糖尿病大鼠视网膜微循环中的白细胞数量明显高于对照组大鼠。由此可见，糖尿病大鼠白细胞黏附性增强，变形性降低。在糖尿病大鼠视网膜微循环中，尽管白细胞的特性发生了这些变化，但白细胞的速度可能是保持不变的，因为白细胞可能会避免损伤通路而循环。少

After retinal ischemia reperfusion, leukocytes began to roll along the venous walls 4 hours after reperfusion. The flux of rolling leukocytes substantially increased and reached a peak (10240 cells/mm) 12 hours after reperfusion. The flux decreased notably to approximately one six the maximum level 48 hours after reperfusion. Few rolling leukocytes could be observed 96 hours after reperfusion. The difference in kind and density of adhesion molecules involved during ischemia reperfusion injury at each time point may account for this finding. The velocity of rolling leukocytes 12 hours after reperfusion was significantly lower than that recorded before or after then. The reduction could be due to the difference in kind and density of adhesion molecules at each time point, not to reduction of velocity of blood flow. Vasoconstriction occurred immediately after reperfusion and peaked 4 hours after reperfusion (66.8% in arteries, 90.1% in veins) Afterward, significant vasodilation occurred i … More n arteries and veins. In arteries, vasodilation peaked 1 2 to 24 hours after reperfusion (1 23-1 29%) and subsided 96 hours after reperfusion. Venous vasodilation peaked 24 hours after reperfusion and subsided 48 hours. The number of accumulated leukocytes began to increase 4 hours after reperfusion. The number increased with time and peaked at 931*187 cells/mm 24 hours after reperfusion. It is shown that mRNA expression of ICAM-l is upregulated after transient cerebral ischemia and peaks 12 hours after reperfusion. Our results in the retina are consistent with this observation.In diabetic rats, the velocity of leukocytes in the retinal microcirculation was 1.38*0.31 mm/sec, and 1.27*0.20 mm/se in control rats. There was no significant difference between these two groups and no plugging or rolling leukocytes were observed. In contrast, the number of leukocytes entrapped in the retinal microcirculation was significantly higher in diabetic rats than in control rats. Thus, leukocytes of the diabetic rats were suggested to have increased adhesiveness and reduced deformability. It is possible that the velocity of leukocytes in retinal microcirculation is preserved in diabetic rats in spite of these changes of leukocyte properties, because leukocytes may circulate avoiding the injured pathway. Less