Electroretinography, retinal ischaemia and carotid artery disease

Coleman, Kate; Fitzgerald, Desmond J.; Eustace, P.; Bouchier‐Hayes, David

doi:10.1016/s0950-821x(05)80809-6

Cited by 30 publications

(14 citation statements)

References 14 publications

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“…An alternative reason underlying the inability of the Rho-kinase inhibitor to improve the b-wave amplitudes might be the remodelling of the actin cytoskeleton at the synapses of the depolarizing bipolar cells in an activity dependent manner. The b-wave represents the combined response of the depolarizing bipolar, amacrine, and Müller cells, which are dependent on the hyperpolarization of the photoreceptors upon the perception of light [6,35]. In response to the light stimulus, the hyperpolarizing bipolar cells project thin extrusions called spinules into the synaptic processes of the amacrine cells, which possibly strengthens the synaptic connections.…”

Section: Discussionmentioning

confidence: 99%

“…Consistently the recovery of the b-wave depends on the severity of the experimental model and the duration of hypoxia/ischemia. The reduction in the amplitude of the b-wave is therefore regarded as a sensitive indicator of reduced oxygen delivery in humans as well as the in vivo and in vitro models [6,35,36]. In our study we evaluated the outcomes of Rho-kinase inhibition in an ex-vivo model of retinal hypoxia, using H-1152P to modulate the Rho-kinase activity.…”

Section: Introductionmentioning

confidence: 99%

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The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

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Hilgers

Tura

et al. 2013

Cell Physiol Biochem

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Aims: To investigate the outcomes of Rho-kinase inhibition in the electrophysiological ex vivo model of the isolated perfused vertebrate retina under hypoxia. Methods: Bovine retinas were perfused with an oxygen saturated nutrient solution with or without the Rho-kinase inhibitor H-1152P. The retinas were stimulated repeatedly until stable amplitudes were reached and the electroretinogram was recorded at five minute intervals. Hypoxia was induced for 15, 30, and 45 minutes, after which the oxygen saturation was restored. The extent of the cell damage and glial reactivity was determined by Ethidium homodimer-1 staining, immunohistochemistry, and Western blot. Results: Hypoxia caused a time-dependent reduction of the b-wave amplitudes, which could not be prevented by the H-1152P. Although the Rho-kinase inhibitor maintained higher b-wave amplitudes, these effects did not reach statistical significance. Hypoxia also resulted in an increase in cell damage and the activation of the glial cells in the untreated retinas whereas the administration of H-1152P significantly reduced the extent of these events. Conclusion: H-1152P exerted a neuroprotective effect against necrosis on the isolated bovine retina under hypoxia together with a reduction in glial cell reactivity. However, the inhibitor could not prevent the hypoxia induced retinal dysfunction possibly due to the interference with synaptic modulation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

Alt

Hilgers

Tura

et al. 2013

Cell Physiol Biochem

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“…80 This is reflected in a postreceptoral-mediated b-wave amplitude loss and possibly amacrine cell-mediated reduction in oscillatory potentials electrophysiologically. [80][81][82][83] Chronic (as opposed to acute) ischaemia is less likely to cause massive damage to retinal tissue and a delay in implicit times has been reported. 64,80 For example in diabetes, a chronic ischaemic disease, delayed multifocal electroretinogram (mfERG) peak implicit times but no amplitude loss are seen; these findings predict the onset of diabetic retinopathy before ophthalmoscopically visible changes in subjects with diabetes.…”

Section: Eyementioning

confidence: 99%

Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Feigl

Brown

Lovie‐Kitchin

et al. 2006

Eye

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We review proposed models and psychophysical and electrophysiological tests performed in many studies for early agerelated maculopathy (ARM). We suggest that ischaemia is the trigger for impaired retinal pigment epithelium function causing imbalance of secretion of vascular growth factors, reduced disc degradation capability and reduced metabolic activity and possible inflammatory response. This results in increased deposition of cell debris, such as drusen and thickens Bruch's membrane causing even more ischaemia of the overlying neurosensory retina. The photoreceptors are more resistant to ischaemia given their proximity to the choroid. Furthermore, being 'upstream' from the inner retinal layers, they act as an oxygen sink depriving retinal layers further from the choroid. Postreceptoral cell layers and especially parts of the inner nuclear layer that are located in the watershed zone between two sources of blood supply are preferentially vulnerable to ischaemia. Based on psychophysical and electrophysiological findings we propose that most of the function impairment in early ARM starts postreceptorally.

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“…Studies of dark adaptation and electroretinographic oscillatory potentials show that subclinical abnormalities in patients with carotid artery stenosis precede the OIS. 4,5 OIS in humans is unique in that no experimental paradigm can reproduce the protracted onset and long duration of retinal hypoperfusion of this condition. Transient ocular ischemia of a duration of ϳ5 minutes leads to immediate conditioning of the retina and improved ischemia tolerance, but little is known about long-term conditioning in chronic ischemia where electroretinography has shown reduced amplitude of a-waves, b-waves, 2,6 -8 and oscillatory potentials.…”

mentioning

confidence: 99%

Prolonged Multifocal Electroretinographic Implicit Times in the Ocular Ischemic Syndrome

Kofoed

Munch

Sander

et al. 2010

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.To examine retinal function in chronic ocular ischemia using multifocal electroretinography (mfERG). METHODS. Thirteen patients with unilateral ocular ischemic syndrome (OIS) underwent assessment of ophthalmic systolic blood pressure by ocular pneumoplethysmography, carotid artery patency by ultrasonography, intraocular pressure (IOP) by applanation tonometry, retinal perfusion by fluorescein angiography, and retinal function by mfERG. RESULTS. Ophthalmic systolic blood pressure was 67.0 Ϯ 11.6 mm Hg in eyes with OIS and 106.1 Ϯ 18.0 mm Hg in fellow eyes, whereas IOP was 13.8 Ϯ 3.2 and 14.4 Ϯ 1.7 mm Hg, respectively. Summed mfERG implicit times (N1, P1, N2) were prolonged in eyes with OIS, by 7.6%, 6.2%, and 7.5%, respectively, compared with fellow eyes (P Յ 0.0048). The retardation of retinal function was significant outside the macula, whereas the assessment of responses from the central retina was limited by high variance. Second-order kernel (first slice) summed implicit times (N1, P1, N2) were also prolonged in OIS, by 6.6%, 7.3%, and 6.8%, respectively (P Յ 0.0058). Of the amplitudes, only the second-order N2 amplitude was significantly abnormal, being reduced by 23.2% in OIS (P ϭ 0.011). CONCLUSIONS. The function of the outer and middle layers of the retina was found to be suppressed in chronic ocular hypoperfusion. The moderate delay in retinal function does not appear to explain the prominent photopic symptom of diffuse glare in bright light, and the delay could be evidence of a functional adaptation that serves to maintain and optimize signaling under conditions of compromised perfusion. (ClinicalTrials.gov number, NCT00403195.) (Invest Ophthalmol Vis Sci.O cular ischemic syndrome (OIS) was first recognized as a result of severe carotid artery obstruction in 1963. 1 Definite diagnostic criteria have not been established. The principal symptoms are mild to severe visual loss, ocular pain that can be relieved by lying down, and diffuse glare in bright light. Findings include aqueous flare, iris rubeosis, cataract, narrow retinal arteries, dilated nontortuous retinal veins, retinal hemorrhages, microaneurysms, cotton-wool spots, and preretinal neovascularization. Fluorescein angiography reveals delayed and patchy choroidal filling and diffuse leakage from the retinal vessels and the optic nerve head. 2 OIS is relatively rare. The largest study so far included 52 eyes with OIS in 43 patients collected retrospectively from a background of 1.5 million outpatient visits. 3 Patients found to have OIS are often referred with a diagnosis of diabetic retinopathy, central retinal vein occlusion, or neovascular glaucoma, showing that OIS is underdiagnosed in general clinical practice.There is no strict correlation between the degree of carotid artery stenosis and the presence or severity of ipsilateral OIS, probably because there is considerable variation in the capacity of collateral and retrograde filling of the ophthalmic artery from the external carotid artery and the contralateral internal carotid arter...

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Electroretinography, retinal ischaemia and carotid artery disease

Cited by 30 publications

References 14 publications

The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

The Neuroprotective Potential of Rho-Kinase Inhibition in Promoting Cell Survival and Reducing Reactive Gliosis in Response to Hypoxia in Isolated Bovine Retina

Functional loss in early age-related maculopathy: the ischaemia postreceptoral hypothesis

Prolonged Multifocal Electroretinographic Implicit Times in the Ocular Ischemic Syndrome

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