15 research outputs found
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Short-Term Effect of Intraocular Pressure Elevation on the Human Electroretinogram
In six human volunteers, serial electroretinograms (ERGs) were performed over five minutes at intraocular pressure artificially elevated with a suction cup. Compared to the base line ERG, there was no decrease in b-wave amplitude unless intraocular pressures approached or exceeded diastolic ophthalmic artery pressure, as determined by suction cup ophthalmodynamometry. Although reduced severely, the b-wave was not completely obliterated within five minutes, even at intraocular pressures above the mean ophthalmic artery pressure and in some cases above systolic artery pressure
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Low-frequency damped electroretinographic wavelets in young asymptomatic patients with dominant retinitis pigmentosa: A new electroretinographic finding
To describe a previously unreported electroretinographic (ERG) pattern in early retinitis pigmentosa (RP).
Two case reports.
Two unrelated young asymptomatic patients with autosomal-dominant retinitis pigmentosa were studied.
Clinical findings and ERG responses were assessed.
No ERG responses were detected scotopically with low-luminance stimuli. With increasingly brighter stimuli, a series of three to five low-frequency damped wavelets developed under both scotopic and photopic conditions. The period of the wavelets was 25 to 37 msec.
Low-frequency damped ERG wavelets occur in some young asymptomatic patients with autosomal-dominant RP. The ERG pattern suggests that these wavelets are predominantly cone-generated
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Pressure Effect on ERG and Optic Nerve Conduction of Visual Impulse: Short-Term Effects in Owl Monkeys
The effects of increased intraocular pressure on optic tract responses and the electroretinogram (ERG) b-wave were studied in owl monkeys. Both responses showed a decrease in amplitude only if the intraocular pressures exceeded a certain critical level, which was about 30 mm Hg below mean femoral blood pressure. Above this intraocular pressure, the magnitude of the depressed ERG and optic tract responses were linearly related to the perfusion pressure. The maximum effect occurred within five minutes, and after the intraocular pressure was restored to normal, the optic tract response and ERG returned to normal in four to five minutes. It is not clear whether the phenomena studied here have any relationship to the optic nerve damage seen in chronic open-angle glaucoma, where the perfusion pressure is usually greater than 30 mm Hg
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Complex neurodegeneration in retina following moderate ischemia induced by bilateral common carotid artery occlusion in Wistar rats
Bilateral common carotid artery occlusion (BCCAO) produces moderate levels of ischemia in the retina of rats, which may simulate the inflow disturbances in severe carotid artery disease. ERG changes following acute BCCAO have been well described, but the effects of chronic BCCAO on the histopathology of the retina remain to be characterized in a reproducible model. Chronic BCCAO was induced in halothane-anaesthetized male Wistar rats and the retina fixed after 3, 6, or 24
hr, 1 week, and 2, 4, or 6 months. Cell counts and measurements of retinal layers were performed in H&E stained paraffin sections. Immunohistochemistry with a panel of fourteen antibodies served to examine the survival of different retinal cell class, astrocytic reactions and the expression of acute stress response proteins. A lectin method was used to label activated microglial cells. Microglial activation, heme oxygenase-1 upregulation and caspase-3 cleavage occurred during the first 24
hr in the absence of overt cell death of retinal ganglion cells (RGC). Three waves of neurodegeneration followed. RGCs were affected after 1 week, followed by neurons in the inner nuclear layer at 2 months, and finally photoreceptors at 4 months. Immunomarkers indicated acute damage to horizontal cells and prolonged survival of amacrine cells. In conclusion, chronic BCCAO produced delayed neuronal death in the retina of adult male Wistar rats. The window of moderate changes of at least 1 day may facilitate molecular studies on retinal ganglion cell loss
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Intravitreal acetylsalicylic acid in silicone oil: pharmacokinetics and evaluation of its safety by ERG and histology
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Photoreceptor synapses degenerate early in experimental choroidal neovascularization
Severe visual loss in patients with age-related macular degeneration is associated with the development of choroidal neovascularization (CNV). The pathogenic mechanisms for CNV formation have been extensively investigated, but remarkably little research has addressed the mechanisms for dysfunction of the retina in CNV. Using laser-induced CNV in mice, we evaluated the mechanisms of retinal dysfunction. At 3 days, 1 week, 2 weeks, and 4 weeks after laser application, retinas under experimental CNV were characterized physiologically (ERG recordings, synaptic uptake of the exocytotic marker FM1-43, and light-induced translocation of transducin), histologically, and immunohistochemically. ERG amplitudes were reduced by 20% at 1 week after CNV. Depolarization-induced FM1-43 uptake in photoreceptor synapses was selectively reduced by 45% at 1 week after CNV. Although photoreceptor outer segments were shortened by 36%, light adaptation as measured by transducin translocation was mostly preserved. Early in CNV (3 days to 1 week), Muller cells demonstrated induction of c-fos and pERK expression. Also, the density of macrophage-like, F4/80 immunoreactive cells increased approximately 3-fold. Minimal photoreceptor death occurred during the first week, and was variable thereafter. At later times in CNV formation (> or =2 weeks), expression of photoreceptor synaptic markers was reduced in the outer plexiform layer, indicating loss of photoreceptor synaptic terminals. ERG amplitudes, synaptic uptake of FM1-43, and the induction of c-fos and pERK in Muller cells were altered within 1 week of experimental CNV, suggesting that during CNV formation, deficits in retinal function, in particular photoreceptor synaptic function, precede degeneration of photoreceptor terminals and photoreceptor cell death
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Ocular delivery of acetylsalicylic acid by repetitive coulomb-controlled iontophoresis
To investigate the potential of transscleral coulomb-controlled iontophoresis (CCI) for repetitive delivery of acetylsalicylic acid (ASA) into the eye, a total of 50 rabbits was included in this study. Fourteen animals received serial CCI treatment. Fourteen animals underwent CCI with either ASA or balanced salt solution (BSS) for at least 6 days at 24- and 48-hour intervals. Eighteen animals received a single CCI application, while 18 animals were injected with 15 mg ASA/kg body weight intravenously. HPLC analysis was performed to determine the levels of salicylic acid (SA) in ocular tissues. Apart from clinical follow-up, 2 rabbits in the ASA and BSS groups were examined by electroretinography, and 2 animals were examined histologically. Though high concentrations of SA were measured, no alterations were observed clinically, histologically and electrophysiologically. Repetitive CCI demonstrated its potential as a topical drug delivery system for ASA into the eye. This transscleral delivery of ASA resulted in significant and sustained intraocular concentrations of SA without side effects. Iontophoresis may be advantageous in clinical administration maintaining therapeutic levels of ASA while avoiding adverse effects associated with the systemic administration of nonsteroidal anti-inflammatory drugs
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Astrocytes react to oligemia in the forebrain induced by chronic bilateral common carotid artery occlusion in rats
The effects of oligemia (moderate ischemia) on the brain need to be explored because of the potential role of subtle microvascular changes in vascular cognitive impairment and dementia. Chronic bilateral common carotid artery occlusion (BCCAO) in adult rats has been used to study effects of oligemia (hypoperfusion) using neuropathological and neurochemical analysis as well as behavioral tests. In this study, BCCAO was induced for 1 week, or 2, 4, and 6 months. Sensitive immunohistochemistry with marker proteins was used to study reactions of astrocytes (GFAP, nestin), and lectin binding to study microglial cells during BCCAO. Overt neuronal loss was visualized with NeuN antibodies. Astrocytes reacted to changes in the optic tract at all time points, and strong glial reactions also occurred in the target areas of retinal fibers, indicating damage to the retina and optic nerve. Astrocytes indicated a change in the corpus callosum from early to late time points. Diffuse increases in GFAP labeling occurred in parts of the neocortex after 1 week of BCCAO, in the absence of focal changes of neuronal marker proteins. No significant differences emerged in the cortex at longer time points. Nestin labeling was elevated in the optic tract. Reactions of microglia cells were seen in the cortex after 1 week. Measurements of the basilar artery indicated a considerable hypertrophy, indicative of macrovascular compensation in the chronic occlusion model. These results indicate that chronic BCCAO and, by inference, oligemia have a transient effect on the neocortex and a long-lasting effect on white matter structures