PROLONGED BILATERAL CAROTID-ARTERY OCCLUSION INDUCES ELECTROPHYSIOLOGICAL AND IMMUNOHISTOCHEMICAL CHANGES TO THE RAT RETINA WITHOUT CAUSING HISTOLOGICAL DAMAGE
PROLONGED BILATERAL CAROTID-ARTERY OCCLUSION INDUCES ELECTROPHYSIOLOGICAL AND IMMUNOHISTOCHEMICAL CHANGES TO THE RAT RETINA WITHOUT CAUSING HISTOLOGICAL DAMAGE
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DOI：
10.1016/s0014-4835(95)80061-1
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发表时间：
1995-07-01
影响因子：
3.4
通讯作者：
OSBORNE, NN
中科院分区：
文献类型：
--
作者：
BARNETT, NL;OSBORNE, NN
现在，通过阻断双侧颈总动脉减少视网膜血，抑制了大鼠视网膜电波的b波。短暂阻断颈总动脉45min，b波减少46%，a波幅度不受影响。血流恢复30min后，ERG活动恢复正常。长时间阻断颈动脉7d后，b波完全消失，a波幅度增加。虽然b波波幅抑制被认为是视网膜缺血的一个指标，但在光镜下观察到双血管阻塞45min或7d的大鼠视网膜没有组织学变化。此外，GABA、GABA(A)受体、Calretinin和PKC-α免疫反应未见改变。然而，颈动脉阻断确实诱导了视网膜Muller细胞中细胞骨架蛋白--胶质纤维酸性蛋白(GFAP)的表达。Muller细胞GFAP免疫反应增强与阻断颈动脉的时间长短及再灌流时间有关。长时间阻断7d后，视网膜GFAP增加了356%。这些发现表明，现在由于阻断颈总动脉而导致的视网膜血液减少会对视网膜造成代谢压力，并引发与胶质增生相关的事件，而不会导致“缺血性”的形态变化。(C)1995年学术出版社有限公司
Reduction of the retinal blood now by occlusion of both common carotid arteries suppressed the b-wave of the rat's electroretinogram. Transient occlusion of the carotids for 45 min reduced the b-wave by 46% without affecting the amplitude of the a-wave. The normal ERG activity returned 30 min after restoration of blood flow. Prolonged carotid occlusion for 7 days totally abolished the b-wave but enhanced the a-wave amplitude. Although b-wave amplitude suppression has been considered as an indicator of retinal ischaemia, no histological changes were seen in retinas of rats subjected to 45 min or 7 days of two-vessel occlusion, when observed by light microscopy. Moreover, GABA, GABA(A) receptor, calretinin and PKC-alpha immunoreactivities were unaltered. Carotid artery occlusion did, however, induce the expression of the cytoskeletal protein, glial fibrillary acidic protein (GFAP), in retinal Muller cells. The increase in the Muller cell GFAP immunoreactivity was related to how long the carotids were occluded as well as the reperfusion time. Prolonged occlusion for 7 days resulted in a 356% increase in retinal GFAP. These findings show that a reduction of retinal blood now by occlusion of the carotids causes a metabolic stress to the retina and elicits events associated with gliosis without resulting in 'ischaemic-like' morphological changes. (C) 1995 Academic Press Limited