NEUTROPHILS PLUG CAPILLARIES IN ACUTE EXPERIMENTAL RETINAL ISCHEMIA
NEUTROPHILS PLUG CAPILLARIES IN ACUTE EXPERIMENTAL RETINAL ISCHEMIA
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DOI：
10.1006/mvre.1994.1027
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发表时间：
1994-05-01
影响因子：
3.1
通讯作者：
SALOUPIS, P
中科院分区：
文献类型：
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作者：
HATCHELL, DL;WILSON, CA;SALOUPIS, P
嗜中性粒细胞阻塞毛细血管似乎是许多组织实验性缺血后无复流现象的机制。本研究的目的是确定是否中性粒细胞堵塞毛细血管在实验性视网膜缺血。通过将三个相邻的视网膜小动脉局部暴露于100 mW的氩蓝绿激光，在白化病大鼠中产生单侧视网膜缺血。每只眼睛至少有两条血管完全闭塞。在激光处理后3、6、8或24小时对动物实施安乐死。17只动物的非激光眼作为对照。福尔马林固定后，制备视网膜血管的胰蛋白酶消化物。使用光学显微镜计数每个视网膜的毛细血管中存在的嗜中性粒细胞的总数，并表示为每个视网膜的细胞数。其他眼睛固定在戊二醛：多聚甲醛和视网膜组织制备的光学和电子显微镜。视网膜毛细血管中的中性粒细胞进行激光治疗的平均数是显着高于未处理的对照视网膜在所有的时间段研究，并随时间增加，从3至6小时。完整的，以及脱颗粒的中性粒细胞存在于毛细血管。大量的中性粒细胞堵塞毛细血管，其数量随着缺血时间的增加而增加，这支持了急性视网膜缺血后毛细血管无灌注的假设。(C)1994年出版社出版。
Capillary plugging by neutrophils appears to be the mechanism responsible for the no reflow phenomenon following experimental ischemia in many tissues. The purpose of this study was to determine if neutrophils plug capillaries in experimental retinal ischemia. Unilateral retinal ischemia was produced in albino rats by focally exposing three adjacent retinal arterioles to argon blue-green laser light at 100 mW. Total occlusion was achieved in at least two vessels in each eye. The animals were euthanized at 3, 6, 8, or 24 hr following laser treatment. Nonlasered eyes of 17 animals served as controls. Trypsin digests were prepared of the retinal vasculature following formalin fixation. The total number of neutrophils present in the capillaries of each retina was counted using a light microscope and expressed as the number of cells per retina. Other eyes were fixed in glutaraldehyde:paraformaldehyde and the retinal tissue prepared for light and electron microscopy. The mean number of neutrophils in capillaries of retinas subjected to laser treatment was significantly higher than that in untreated control retinas at all time periods studied and increased with time from 3 to 6 hr. Intact as well as degranulated PMNs were present in the capillaries. The presence of large numbers of neutrophils plugging capillaries and their increased number with duration of ischemia supports the hypothesis that they contribute to capillary nonperfusion following acute retinal ischemia. (C) 1994 Academic Press, Inc.