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

视网膜缺血再灌注后，白细胞开始沿着静脉壁滚动。再灌注后12小时，滚动白细胞流量显著增加，达到峰值（10240个/mm）。再灌注48小时后，流量明显下降，约为最大值的1/6.再灌注96小时后可见少量滚动的白细胞。缺血再灌注损伤各时间点粘附分子的种类和密度的差异可能是其原因之一。再灌注后12小时白细胞滚动速度明显低于再灌注前和再灌注后。这种降低可能是由于粘附分子的种类和密度在每个时间点的差异，而不是血流速度的降低。血管在再灌注后即刻即出现收缩，再灌注后4 h达高峰（动脉66.8%，静脉90.1%）。 关于我们 在动脉和静脉中。动脉血管舒张在再灌注后12 ~ 24小时达高峰（1.23 ~ 1.29%），再灌注后96小时消退。静脉血管舒张在再灌注后24小时达到高峰，48小时消退。再灌注4 h后白细胞开始增多。随着时间的推移，细胞数逐渐增加，再灌注后24小时达到高峰，为931 × 187个/mm。结果表明，ICAM-1的mRNA表达在短暂脑缺血后上调，并在再灌注后12小时达到高峰。糖尿病大鼠视网膜微循环中白细胞的速度为1.38 × 0.31 mm/sec，对照组为1.27 × 0.20 mm/sec。两组间无显著性差异，未观察到阻塞或滚动的白细胞。与此相反，白细胞截留在视网膜微循环的数量显着高于糖尿病大鼠比对照组。因此，提示糖尿病大鼠的白细胞具有增加的变形性和降低的变形性。尽管白细胞性质发生了这些变化，但糖尿病大鼠视网膜微循环中白细胞的速度可能保持不变，因为白细胞可以避开受损的通路循环。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