Experimental carotid occlusion: funduscopic and fluorescein angiographic findings.

Abstract

SUMMARY A characteristic fundus picture was consistently produced following acute bilateral common carotid artery ligation in mature rats, reminiscent of human carotid occlusive disease. Two days after ligation it consisted of dilatation and tortuosity of retinal veins, blurring and swelling of the optic disc, retinal whitening primarily along the venous distribution, and straightening of retinal arteries. Fluorescein angiography showed hyperfluorescence of the disc, delay in the rate of retinal arterial and venous filling, venous dilatation, disc oedema, disruption of the retinal capillary bed pattern, and late peripapillary staining/leakage. This pattern was not seen in rats which underwent acute unilateral ligation, although some mild changes were seen on fluorescein angiography. The vascular alterations seemed to regress spontaneously within one week. A peripapillary 'halo' and a granular-appearing nerve fibre layer developed later, exclusively in bilaterally ligated animals.Neurologists and ophthalmologists have extensively reported the signs and symptoms of carotid artery disease in humans. 11 The term 'venous-stasis retinopathy' was used by Kearns and HollenhorstI to characterise the appearance of the retinal venous circulation in carotid occlusive disease. It consisted of dilatation and tortuosity of the major retinal veins, microaneurysms, and small punctate haemorrhages. These findings were observed in approximately 5% of their patients with unilateral internal carotid artery occlusion or stenosis. They also reported sludging of blood within retinal veins in several of their patients with both carotid artery occlusion and an elevated sedimentation rate. Cotton-wool spots,23 retinal oedema,34 pale optic discs with blurred margins,4 and retinal neovascularisation4 have also been reported in patients with carotid occlusion. David etal.7 reported a delay between the retinal arterial and venous phases of fluorescein angiography during digital carotid compression in human subjects. They found that slow venous filling, in the absence of venous obstruction, was most closely correlated with insufficiency of the retinal circulation. In another fluorescein angiographic study4 one patient with bilateral common Correspondence to Paul Henkind, MD,

Evidence for an enduring ischaemic penumbra following central retinal artery occlusion, with implications for fibrinolytic therapy

“…The full fundus picture of "partial" CRAO has never been reproduced experimentally albeit some of the essential components can be replicated in certain rodent species undergoing bilateral carotid arterial occlusion (Spertus et al, 1984;Osborne et al, 2004). In non-human primates, however, a single young healthy rhesus macaque (out of 63 animals undergoing temporary CRA clamping) exhibited a "Christmas tree pattern of normal-looking retina around the arterioles" on a background of diffuse opacification (Hayreh and Weingeist, 1980a).…”

Why cotton wool spots should not be regarded as retinal nerve fibre layer infarcts

“…6 7 50-54 Interestingly, ligation of both carotid arteries in rat strains with limited collateral flow through the circle of Willis produced an equivalent fundus picture 2 days post-occlusion associated with a marked retardation in dye transit on FFA. 55 In most animals, retinal ''whitening'' (here presumed to be accumulated axoplasm) developed in a wide zone around the optic discs bilaterally but, redolent of the pattern of clinical presentation, the axoplasmic debris was restricted to the immediate peripapillary retina if the ischaemia was particularly severe.…”

Protection Against Chronic Hypoperfusion-Induced Retinal Neurodegeneration by PARP Inhibition via Activation of PI-3-kinase Akt Pathway and Suppression of JNK and p38 MAP Kinases

“…It leads to a moderate reduction of blood flow, causing subtle morphological, biochemical, and behavioral changes (Osborne et al 2004;Farkas et al 2007;Kalesnykas et al 2008). Among the numerous models of retinal ischemia, BCCAO induces functional and morphological damage in the rat retina such as electrophysiological alterations, loss of the pupillary reflex, detectable neurodegenerative changes both retinal or visual system level, as well as fundoscopic and fluorescein angiographic findings paralleling the retinopathy of carotid artery occlusive disease in humans (Spertus et al 1984;Vidal-Sanz et al 2000;Lavinsky et al 2006). We have shown earlier that local treatment with pituitary adenylate cyclase-activating polypeptide or diazoxide counteracted mitochondrial dysfunction, and resulted in amelioration of BCCAO-induced retina degeneration in rats (Atlasz et al 2007a, b).…”