Prolonged bilateral carotid artery occlusion induces electrophysiological and immunohistochemical changes to the rat retina without causing histological damage.

Reduction of the retinal blood flow 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, GABAA 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 Müller cells. The increase in the Müller 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 flow 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.