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

通过白细胞运动学分析研究视网膜循环障碍的发病机制。

基本信息

批准号：
09671792
负责人：
KIRYU Junichi
金额：
$ 1.73万
依托单位：
KYOTO UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09671792/
关键词：
lenkocytes retina endothelium adhesion molecules 網膜循環障害非侵襲的評価

项目摘要

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

视网膜缺血再灌流后4h，白细胞开始沿静脉壁滚动。再灌流后12小时，滚转的白细胞流量显著增加，达到峰值(10240个/mm)。再灌流后48小时，血流量明显下降至最大值的六分之一左右。再灌流96h后可见少量滚动的白细胞。各时间点在缺血再灌注损伤过程中参与的黏附分子种类和密度的差异可能解释了这一发现。再灌注12h后，白细胞滚动速度明显低于再灌注前和再灌注后。这种减少可能是由于各时间点黏附分子的种类和密度的不同，而不是由于血流速度的降低。血管收缩在再灌注后即刻出现，再灌注后4h达高峰(动脉66.8%，静脉90.1%)，…出现明显的血管扩张更多的动脉和静脉。动脉血管扩张在再灌注后1、2~2 4h达高峰(1 2 3~1 2 9%)，再灌注96h后血管扩张减弱。静脉血管扩张在再灌流后24小时达高峰，48小时后消退。再灌流4h后，聚集的白细胞数开始增加。细胞数随时间延长而增加，再灌流后24小时达高峰，达931×187个/mm。结果表明，短暂性脑缺血后细胞间黏附分子-L基因表达上调，再灌注12h达高峰。糖尿病大鼠视网膜微循环中白细胞的运动速度为1.38×0.31 mm/s，对照组为1.27×0.20 mm/s。两组间差异无统计学意义，未见白细胞堵塞或卷曲。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。因此，糖尿病大鼠的白细胞具有更高的粘附性和更低的变形性。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的白细胞速度仍有可能保持不变，这是因为白细胞可能绕过了损伤途径而循环。较少