Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22-year-old man with Eales' disease with secondary rhegmatogenous retinal detachment with a break five disc diameters from the disc underwent radial scleral buckling using a silicone sponge episcleral explant with local cryopexy. Five hours after surgery the patient had no light perception. There was no intraoperative or postoperative rise of intraocular pressure or central retinal artery ischemia. Immediate removal of the explant brought a return of light perception and postoperative visual acuity improvement. The episcleral explant may have caused the direct optic nerve trauma that resulted in loss of vision.
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PMID:Sudden vision loss following retinal detachment surgery. 157 71

Intracellular calcium overload has been implicated to be a major factor in triggering cell death after ischemic neuronal injury. We investigated the effects of flunarizine hydrochloride, a calcium-overload blocker, on pressure-induced retinal ischemia in a rat model. Retinal ischemia was induced in intraocular pressure to 110 mm Hg for 45 minutes. Two regimens of treatment with flunarizine were examined: (1) prophylactic treatment, in which flunarizine was administered before ischemia and in the early phase of reperfusion; and (2) postischemic treatment, in which flunarizine was administered only in the early phase of reperfusion. Injury was evaluated morphologically and morphometrically by measuring the thickness of the inner retinal layers on plastic-embedded retinal sections and by counting the retinal ganglion cells on retinal flat preparations. By morphologic and morphometric criteria, a significant but partial protection of the inner retinal layers was noted in the groups given either regimen. This protective effect of flunarizine suggests that elevated intracellular calcium concentration may play an important role in ischemic retinal injury.
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PMID:Protective effects of flunarizine on ischemic injury in the rat retina. 159 36

In order to determine thresholds for irreversible cellular injury in the rat retina, timed acute no-flow ischemic episodes of 30-180 min duration were produced by elevation of intraocular pressure (IOP) above systolic pressure. Quantitation of irreversible degeneration and cell loss following a 2-week post-ischemic interval was performed by computer-assisted measurements from histologic sections. Alterations of thickness of retinal layers and linear cell density were determined for ischemia of selected durations (30, 60, 80, 90, 120 and 180 min). Different thresholds were evident for inner and outer retinal damage. Neurons of the inner nuclear layers showed extensive loss with episodes at 60 min. Decrease in the thickness of the inner plexiform layer provided the best index of this inner nuclear damage. The outer retina was more resistant, with photoreceptors showing extensive damage only after 90 min in conjunction with pigment epithelial metaplasia and degeneration. Two-hour episodes produced full-thickness degeneration with loss of pigment epithelium and sparing of the peripheral retina. Greater sensitivity of the inner retina suggested problems with restoration of the retinal circulation. Horseradish peroxidase infusions did reveal central microcirculatory defects in retinal wholemounts of some specimens with episodes longer than 60 min. Refinements of the methods resulted in outcomes sufficiently reproducible for quantitative assessment of acute ischemic injury. The rat retina provides an economical basic tissue model of acute ischemic injury affecting neurons, glia, and microvasculature. Quantitation of this injury promises great utility in testing agents with potentially protective effects on acute ischemic injury.
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PMID:Quantitation of ischemic damage in the rat retina. 174 56

The advent of treatment modalities with the potential to ameliorate retinal ischemic injury calls for methods allowing their quantitative assessment. We thus established a model of pressure-induced retinal ischemia/reperfusion injury in rats. The intraocular pressure (IOP) was raised to 110 mm Hg by cannulation of the anterior chamber for a duration of 0, 90 or 120 min. The eyes were reperfused for 3 or 7 days. Morphologically, retinal injury occurred in a pattern consistent with retinal and choroidal vascular occlusion. Damage increased in severity with prolonged durations of ischemia. Morphometric determination of the mean thickness of inner retinal layers (MTIRL) revealed significant differences between controls and the 90- or 120-min ischemia groups (p less than 0.05 and p less than 0.01, respectively). The difference in MTIRL between 3 and 7 days of reperfusion was not significant. Replacement of normal saline by a solution of 5% dextrose in the hydrostatic device used to increase the IOP led to a decrease in retinal injury after 120 min of ischemia (p less than 0.01). This model combines a relatively simple methodology, cost-effective execution and a fast, semicomputerized method of quantitation. Depletion of carbohydrates during ischemia may contribute to retinal injury in this model.
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PMID:Pressure-induced retinal ischemia in rats: an experimental model for quantitative study. 177 2

Survival of the rabbit retinal pigment epithelium (RPE) after ischemia was studied. The ischemia was induced by elevating intraocular pressure; retinal and RPE function were monitored by electrophysiologic recordings. The b-wave recovered to control amplitude in 1-4 hr after 30-60 min of ischemia, but it never recovered more than about 50% amplitude after 90 min of ischemia. The c-wave recovered after 30 min of ischemia but was replaced by a negative response after 60-90 min of ischemia. The RPE hyperosmolarity response was normal after 60 min of ischemia, but it was severely depressed after 90 min of ischemia. The RPE response to acetazolamide (cornea positive in the rabbit) was lost after both 60 and 90 min of ischemia. These results suggest that different components of RPE function have different tolerances to ischemia and is consistent with evidence that the RPE electrophysiologic responses differ in mechanism and response to disease.
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PMID:Recovery of retinal pigment epithelial function after ischemia in the rabbit. 198 7

The effects of acute intraocular pressure (IOP) on the reduction/oxidation ratio of cytochrome a, a3 were measured from intact cat optic nerve by microfiber reflection spectrophotometry. This enabled the real-time analysis of optic nerve-head oxidative metabolism following IOP or mean arterial pressure (MAP) changes. Findings included: (1) cytochrome a, a3 became more reduced and relative blood volume decreased at lower perfusion pressures, even at IOP of less than 20 mm Hg; (2) metabolic inhibition began at variable perfusion pressures but invariably progressed as perfusion pressure declined; and (3) increased IOP or decreased MAP caused metabolic inhibition. These findings demonstrate that: (1) optic nerve metabolic dysfunction is possible at low IOPs; (2) lowering IOP can reverse metabolic dysfunction; (3) the metabolic response is dependent on IOP and/or MAP changes; and (4) the metabolic inhibition is related to optic nerve ischemia.
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PMID:Intraocular pressure effects on optic nerve-head oxidative metabolism measured in vivo. 215 40

Studies on retinal oxygen and glucose consumption in cats and pigs are reviewed and recent experiments with the deoxyglucose method in monkeys are described. In all three species, the retina is supplied with nutrients by both the retinal and the choroidal blood vessels. Studies on regional blood flow and differences in arteriovenous concentration in cats have indicated that under conditions of general anesthesia and exposure to laboratory light, the oxygen supply from the choroid is about 5.6 microliters/min and that from the retinal vessels, 1.3 microliters/min. In pigs the corresponding figures were about 4 and 2.9 microliters/min, respectively. Moderate reductions in perfusion pressure caused by increments in intraocular pressure or reductions in arterial blood pressure resulted in little change in oxygen tension in the inner retina, due to efficient autoregulation of retinal blood flow. Reduced choroidal blood flow was to a large extent compensated by increased differences in arteriovenous concentration. Studies using the deoxyglucose method in monkeys indicated that pentobarbital anesthesia and constant illumination tend to reduce the metabolism of the retina. In darkness, glucose consumption in the photoreceptors was higher than that recorded under conditions of constant illumination with white light. Flickering light at 4 Hz enhanced glucose consumption in the inner retina. At very high intraocular pressures glucose consumption in the retina was enhanced, probably as a result of partial ischemia, with a shift to more anaerobic glucose metabolism.
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PMID:Aspects of oxygen and glucose consumption in the retina: effects of high intraocular pressure and light. 233 49

Carotid artery obstructive disease, although infrequently diagnosed as a primary or contributing cause of neovascular glaucoma, can produce distinctive characteristics. Decreased perfusion of the ciliary body may decrease aqueous humor production. As a result, such eyes with neovascular glaucoma may occasionally be normotensive or even hypotensive. Fluorescein angiography may show an increased arm-to-retina time and leakage from the major retinal arterioles. Panretinal photocoagulation may not eliminate the anterior segment neovascularization because of anterior segment ischemia. Endarterectomy can significantly increase intraocular pressure as perfusion to the ciliary body returns to normal. These characteristics were found in two patients, a 67-year-old woman and a 49-year-old man, with diabetes and hypertension. In both cases cyclocryotherapy significantly reduced the intraocular pressure and the rubeosis iridis regressed.
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PMID:Neovascular glaucoma and carotid artery obstructive disease. 240 76

Two patients are presented with neovascularization of the iris due to ischemia secondary to decreased blood flow through the carotid arteries. Panretinal photocoagulation was followed by regression of the new iris blood vessels to a greater extent in one patient than in the other. Following carotid endarterectomy, intraocular pressure increased, and, in one case, filtering surgery was required. Possible mechanisms for the rise in intraocular pressure following carotid endarterectomy are discussed.
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PMID:Increased intraocular pressure following endarterectomy. 244 46

The responses of X and Y type retinal ganglion cells were extracellularly recorded from the cat optic chiasm or tract before and during brief intraocular pressure (IOP) elevation. The responses of both X and Y cells to stimulus flashes decreased monotonically with increase of IOP. Y cells had significantly higher tolerance to IOP than did X cells. This systematic difference was independent of the cell's retinal position. The findings support the conclusion that during brief IOP elevation pressure-induced ischemia is the main factor causing a decrease in ganglion cell responsiveness. Our findings also suggest a means of selectively eliminating the contribution of X cells to visual function. At moderate levels of IOP elevation X cells, but not Y cells, virtually cease to function.
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PMID:Y cells in the cat retina are more tolerant than X cells to brief elevation of IOP. 279 52


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