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Study on the mechanisms of leukocyte-endothelial interactions in retinal microcirculation

视网膜微循环中白细胞与内皮相互作用的机制研究

基本信息

批准号：
10470364
负责人：
OGURA Yuichiro
金额：
$ 8.45万
依托单位：
NAGOYA CITY UNIVERSITY
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B).
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 2000
项目状态：
已结题

项目摘要

Acridine orange leukocyte fluography was applied to study leukocyte dynamics in the following experimentally induced microcirculatory disturbance of the retina : ischemia-reperfusion injury of the retina and experimental diabetes mellitus.1. Ischemia-reperfusion injury of the retinaDuring reperfusion period after transient (60 min) retinal ischemia by optic nerve ligation, the rolling of leukocytes in the retinal veins was prominent and numerous leukocytes were trapped in the retinal capillaries. The numbers of rolling leukocytes were at maximum 12 hours after reperfusion. Leukocyte entrapment was peaked at 24 hours after reperfusion. By blocking adhesion molecules on the vascular endothelium, these leukocyte-endothelial interactions were effectively inhibited. Postischemic retinal atrophy was also inhibited by blocking adhesion molecules. These results suggested that leukocytes may be major players in the pathophysiology of ischernia reperfusion injury of the retina.2 Experimental diabetes mellitusLeukocyte dynamics in the retina were studied in streptozotocin-induced disbetes and spontaneous diabetes (OLEIF rat). In the both diabetic models, leukocytc entrapment in the retinal capillaries was increased even in the early stages of diabetes. Fluorescein angiography revealed that trapped leukocyte disturbed the regional capillary blood flow in the downstream. Enhanced expression of adhesion molecules was observed in the capillary endothelium of the retina in the diabetic rats. Leukocyte entrapment in the retinal capillaries might cause microvascular occlusions and dysfunction, in tum causing diabetic retinopathy.

应用吖啶橙白细胞荧光造影术研究实验性视网膜微循环障碍：视网膜缺血再灌注损伤和实验性糖尿病的白细胞动力学。视网膜缺血再灌注损伤视神经结扎视网膜短暂缺血再灌注期(60min)，视网膜静脉内白细胞滚动明显，大量白细胞滞留在视网膜毛细血管内。再灌流后12h，滚动的白细胞数最多。再灌流后24小时，白细胞包裹率达到高峰。通过阻断血管内皮细胞上的黏附分子，这些白细胞与内皮细胞的相互作用被有效地抑制。阻断黏附分子也可抑制缺血后视网膜萎缩。这些结果提示白细胞可能是视网膜缺血再灌注损伤的主要病理生理机制。2.实验性糖尿病大鼠在链脲佐菌素诱导的糖尿病和自发性糖尿病(OLEIF)大鼠中，观察了视网膜中白细胞的动态变化。在两种糖尿病模型中，即使在糖尿病的早期，白细胞在视网膜毛细血管中的滞留也增加了。荧光素血管造影术显示被困的白细胞干扰了下游的局部毛细血管血流。糖尿病大鼠视网膜毛细血管内皮细胞黏附分子表达增强。白细胞卡在视网膜毛细血管内可能导致微血管闭塞和功能障碍，最终导致糖尿病视网膜病变。