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Query: UMLS:C0595921 (intraocular pressure)
11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The interaction of retinal dopamine depletion and partial ischemia on the a- and b-wave amplitudes and implicit times of the electroretinogram was examined in adult pigmented rabbits. Seven days after 6-hydroxydopamine treatment, which resulted in a depletion of the amine, partial retinal ischemia was induced by raising the intraocular pressure. As expected, moderate elevation of intraocular pressure produced increases in both a- and b-wave amplitudes. Amplitude hyperresponses were significantly reduced in dopamine-depleted retinas. These reductions were more prominent with relatively lower intensities. However, response delays were not shortened but lengthened by 6-hydroxydopamine pretreatment. Together, these results point to a selective role of dopamine in partial retinal ischemia induced by moderate elevation of intraocular pressure in rabbits.
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PMID:Selective effects of retinal dopamine depletion on partial ischemia-induced electroretinographic hyperresponses in rabbits. 774 16

In experimental work on retinal ischemia and its medical management, we have been disturbed by the large variations in the electroetinogram (ERG) recovery of rabbit eyes subjected to similar degrees of ischemia. We investigated whether body temperature might be one of the critical factors. We studied pigmented Dutch rabbits that had been subjected to 60 min of ocular ischemia followed by 4 h of reperfusion at different body temperatures. Ischemia was produced by cannulating the anterior chamber and raising the intraocular pressure. Scotopic ERGs and rectal temperatures were recorded at regular intervals. Rabbits with a subnormal mean temperature of 35.5-37.7 degrees C throughout the experiment showed mean a- and b-wave recoveries of 131.52% and 107.68% of preischemic values after 4 h reperfusion. At temperatures between 37.8-38.9 degrees C, the a- and b-waves only recovered to 88.43% and 32.0% respectively. Even small degrees of cooling greatly enhanced post-ischemic ERG recovery. This may explain some of the variations in ERG recovery that have been reported in the literature. We suggest that body temperature should be tightly controlled between 37.8 and 38.9 degrees C during ischemia experiments to stabilize results and minimize errors in judging therapeutic effects. Retinal cooling may be a means to protect the retina against ischemic damage in clinical situations.
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PMID:Post-ischemia ERG recovery is influenced by temperature. 776 10

The effects of antioxidant drugs on retinal ischemia-reperfusion damage were studied by electroretinograms (ERGs) from reperfused Dutch rabbit eyes. After inducing retinal ischemia by increasing the intraocular pressure (IOP) up to 140 mmHg for 60 minutes, the reperfusion was started by lowering the IOP to the normal level. Mannitol, polyethylene glycol superoxide dismutase (PEG-SOD), or ascorbic acid was administered by drip-infusion to the rabbits immediately after (early group) or 1 hr after (delayed group) the start of reperfusion. Saline, as a control, was administered by the same method as the early group. The a- and b-waves were recorded before the ischemia and during the reperfusion. In the early group treated by each drug, the recovery rates of the b-wave amplitudes at 4 hrs after the start of reperfusion were significantly greater than those in the controls. In the delayed group, the ERG recovery rate in rabbits treated with PEG-SOD was significantly better than in the controls. These results indicated that all these drugs were effective in protecting from the retina from the ischemia-reperfusion damage, and that some antioxidant drugs might be effective even when they were administered after the start of reperfusion.
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PMID:[An electrophysiological study on the effect of antioxidant drugs against retinal ischemia-reperfusion damage]. 778 13

Optic neuropathy occurred in two patients suffering from Graves' disease with marked limitation of eye movement. Optic nerve changes were moderate. They consisted of parapapillary flame-shaped hemorrhages, swelling of the disc, and bundle defects in the visual field on the involved side. This clinical pattern suggested that the optic neuropathy was anterior and ischemic in nature. In one patient, symptoms of optic neuropathy were noted 3 days after starting stretching exercises with the ocular muscles, performed following a friend's advice in an attempt to prevent increase in restrictive myopathy. In patients with Graves' disease, it is conceivable that mild optic neuropathy occasionally occurs as a result of elevation in intraocular pressure, and stretching exercises of the ocular muscles might consequently favor such ischemic events. In the mechanisms of optic nerve involvement associated with Graves' disease, the role of ischemia should be considered in addition to the widely accepted role of optic nerve compression by enlarged extraocular muscles, at the level of the orbital apex.
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PMID:Anterior ischemic optic neuropathy in Graves' disease. 780 22

Ocular blood flow in the retina, choroid and optic nerve head should be measured in addition to the intraocular pressure (IOP) in order to better diagnose glaucoma disease and to better evaluate the efficacy of antiglaucoma drugs. It was found that beta-adrenergic blockers, the most widely used antiglaucoma drugs, reduced ocular blood flow in animals and worsened glaucoma disease in some patients, even though the IOP was reduced to the normal range. Therefore, their use for glaucoma treatment requires careful re-evaluation. On the other hand, most dopamine antagonists were found to reduce the IOP and increase the blood flow to the retina, choroid, iris and ciliary muscle. Therefore, these agents could be used for glaucoma treatment. Further, dopamine antagonists were found to improve retinal function after ischemia and, thus, also could be used for the treatment of ischemic retinopathy.
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PMID:Treatment of open angle glaucoma and ischemic retinopathy with dopamine antagonists. 791 5

Increased intraocular pressure and vascular ligation models are often used in studies of global ocular ischemia. The purpose of this study is to perform a paired comparison of retinal recovery in these paradigms. Our data indicate that ERG b-wave recovery profiles, following identical periods of ischemia, differ significantly between models. We propose that increased intraocular pressure models induce greater retinal injury than vascular ligation models. We suggest that pressure or another aspect of the increased intraocular pressure model induces injury beyond that caused by ischemia alone and caution against direct comparison of results obtained using these two models.
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PMID:A paired comparison of two models of experimental retinal ischemia. 795 12

Dextromethorphan has been shown to protect against ischemic tissue damage. We investigated the effects of dextromethorphan on electroretinographic oscillatory potentials in retinal ischemia. Retinal ischemia was induced in rabbits by increasing intraocular pressure to 120 mm Hg for 30, 60 or 90 minutes. Dextromethorphan was intravenously administered before ischemia and maintained throughout the whole period of experiments. Oscillatory potentials were recorded before and during ischemia as well as 4 hours of recirculation after ischemia. As expected, all oscillatory potentials were decreased after 60 and 90 minutes of ischemia. However, after 30 minutes of ischemia followed by 4 hours of recirculation, amplitudes of P2 were elevated whereas those of P3 and P4 were decreased with normal P1 amplitudes. Dextromethorphan administration diminished the effects of 30 minutes of ischemia on oscillatory potentials and partially attenuated the effects of 60 minutes of ischemia, whereas the effects of 90 minutes of ischemia could not be reversed by dextromethorphan treatment. These results indicate that electroretinographic oscillatory potentials could be useful indicators to evaluate retinal function in the ischemic condition and that dextromethorphan can attenuate the effects of relatively short periods of ischemia on rabbit electroretinographic oscillatory potentials.
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PMID:Dextromethorphan attenuates the effects of ischemia on rabbit electroretinographic oscillatory potentials. 811 4

The aim of investigations was to evaluate the changes in the eyeball, after extraocular rectus muscles myotomy. In 16 rabbits two muscles and in 17 four muscles were cut in one eye; the opposite eye was control. In early postoperative period intraocular pressure was statistically significantly lower, as compared with the control eyes and it depended on the number of cut muscles. In histopathological examination, the most constant changes were dilatation of conjunctival vessels and pigment migration in the anterior uvea. Decreased intraocular pressure and pigment migration in iris and ciliary body were considered to be the symptoms of anterior segment ischemia.
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PMID:[Consequences of extraocular rectus muscle myotomy in rabbits--in vivo and pathomorphologic studies]. 812 Nov 41

A bleb infection and subsequent endophthalmitis developed in the left eye of a 68-year-old man who had had a trabeculectomy. Vitreous injections of vancomycin and gentamicin were given, and vitreous cultures grew alpha-Streptococcus. Postoperatively, as the intraocular inflammation resolved, intraocular pressure (IOP) markedly decreased secondary, in our judgment, to ciliary body ischemia. A pars plana vitrectomy relieved the tractional bands and restored the IOP.
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PMID:Restoration of intraocular pressure after streptococcus endophthalmitis with vitrectomy. 818 7

The present study was undertaken to determine whether dextromethorphan (DM), a potent N-methyl-D-aspartate antagonist, could attenuate the effects of ischemia on rabbit ERG. Retinal ischemia was induced by increasing intraocular pressure to 120 mm Hg for 30, 60, or 90 min. DM was intravenously administered before ischemia and maintained throughout the entire experimental period. ERGs were recorded prior to, during, and after ischemia. The results indicate that the b-wave hyperresponses and the delays in implicit times induced by 30 min. ischemia were suppressed by the administration of DM. Similar findings were obtained when ischemia lasted for 60 min, except that DM did not improve delayed implicit times, suggesting that cellular injury is still present. ERG changes resulting from 90 min ischemia were not reversed by DM treatment. Effects of DM treatment on a-wave were less prominent. Together, our results further support that DM can to some extent alleviate ischemic injury in the rabbit retina.
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PMID:Effects of dextromethorphan on ischemia induced electroretinogram changes in rabbit. 819 64


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