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)

This study found that pretreatment with 4-(o-benzylphenoxy)-N- methylbuty-lamine hydrochloride (bifemelane hydrochloride, Celeport) reduced ischemia-reperfusion injury in rat eyes. Bifemelane (25 mg/kg) was injected intraperitoneally 30 minutes before an ischemic insult, then acute ischemia of the retina and optic disc was induced by increasing intraocular pressure to 110 mmHg for 45 minutes. After one week, the axonal count of the optic nerve was investigated using electron microscopy. The control group consisted of vehicle-treated eyes which received normal saline. The axon count was 93.4 +/- 7.9 for the bifemelane treated group, and 79.2 +/- 6.4 for the controls. The axon count in the treated group was significantly higher. These results suggest that bifemelane, which prevents cerebral nerve cell damage from ischemia, can reduce ischemic retinal nerve cell injury.
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PMID:Treatment with bifemelane for optic nerve damage following high intraocular pressure in rat eyes. 899 85

Brief ischemia caused by high intraocular pressure induced tolerance to subsequent ischemia-reperfusion injury in rats. Male Wistar rats were subjected to 15 minutes of ischemia. This ischemic injury did not show distinct axonal damage in the optic nerve in electron microscopy. 1, 2, 4, 7, and 14 days after the first 15 min ischemia, the rats were subjected to a second ischemia for 45 minutes (ischemic tolerance). After 1 week, the rats were perfusion fixed and the optic nerves were processed for light and electron microscopy. Samples of the axonal density in the central optic nerve 2 mm behind the lamina cribrosa were observed and counted an electron micrographs. In axonal morpometric findings, 2 days and more after brief ischemia, the damage was lessened more than after 45 minutes ischemia (control) and the difference was significant. This 'ischemic tolerance' induced by brief ischemia might be considered the same stress as brain ischemia-reperfusion injury.
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PMID:['Ischemic tolerance' in ischemia-reperfusion injury in the optic nerve in rats]. 902 3

It is known that NO is involved in the regulation of intraocular pressure (IOP) and retinal function recovery after ischemia. Thus, S-nitrosoglutathione (RVC-588) and 4-phenyl-3-furoxancarbonitrile (RVC-589) as NO donor and precursor, respectively, were studied in terms of their ability to increase b-wave recovery of electroretinogram (ERG) and ocular blood flow. It was found that RVC-588 increased b-wave amplitude markedly from 28% (control) to 67% (treated) and the blood flow significantly in the retina, choroid, and ciliary body. In the case of RVC-589, the b-wave recovery was significantly increased from 30% (control) to 51% (treated) but was less marked than that of RVC-588. The blood flow in the eye tissues was not significantly increased by RVC-588, but there was a clear tendency to enhance in the retina, choroid and iris. These results indicate that NO can be released effectively from S-nitrosothiols but less significantly from furoxans.
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PMID:Nitric oxide donors: effects of S-nitrosoglutathione and 4-phenyl-3-furoxancarbonitrile on ocular blood flow and retinal function recovery. 909 Jun 11

The efficacy of MK-801, an N-methyl-D-aspartate receptor antagonist, was evaluated in a rat model of retinal ischemia induced by elevated intraocular pressure. Intraperitoneal injection of MK-801 at 0, 1, 3 and 10 mg/kg was given immediately after reperfusion. At 7 days after reperfusion, the inner retinal thickness, as measured from histologic sections of the retinas, of the 10 mg/kg treated group showed significant beneficial effect, while the other doses had no significant effect. Retinal ganglion cell counts on flat preparations of the retinas showed a beneficial dose dependent effect of MK-801 with the lowest dose showing no effect, 3 mg/kg showing marginal effects and 10 mg/kg showing significant effects. Intravitreal infusion of MK-801 during the ischemic period suppressed ischemia/reperfusion-induced internucleosomal DNA fragmentation measured at 18 hours after the insult as well as retinal tissue responses measured at 7 days. These findings suggested that the NMDA receptors may have an important role in ischemia-reperfusion insult as well as in mediating ischemia-induced apoptosis of retinal neurons. In addition, we demonstrated that pharmacological modulation of apoptotic cell death may affect the final tissue responses in vivo.
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PMID:Ameliorative effect of MK-801 on retinal ischemia. 909 Jun 13

The aim of the study was to determine whether betaxolol is a neuroprotective agent and can therefore slow down the changes seen in the retina following ischaemia/reperfusion. Ischaemia was induced in one rat eye by raising the intraocular pressure for 45 min. Three days later electroretinograms were recorded from both eyes and the retinas were examined immunohistochemically for the localisation of calretinin and choline acetyltransferase (ChAT) immunoreactivities. The effect of glutamate agonists, hypoxia or experimental ischaemia was examined on the GABA immunoreactivity, lactate dehydrogenase (LDH) and internal calcium levels ([Ca2+]i) of the isolated rabbit retina, rat cortical cultures and chick retinal cell cultures respectively. Betaxolol was tested to see whether it can attenuate the influence of the glutamate agonists, hypoxia or experimental ischaemia. Ischaemia for 45 min causes a change in the nature of the normal calretinin immunoreactivity, an obliteration of the ChAT immunoreactivity and a drastic reduction in the b-wave of the electroretinogram after 3 days of reperfusion. When betaxolol was injected i.p. into the rats before ischaemia and on the days of reperfusion the changes to the calretinin and ChAT immunoreactivities were reduced and the reduction of the b-wave was prevented. Rabbit retinas incubated in vitro in physiological solution lacking oxygen/glucose or containing the glutamate agonists kainate or NMDA caused a change in the nature of the GABA immunoreactivity. Inclusion of betaxolol partially prevented the changes caused by NMDA and lack of oxygen/glucose. Rat cortical cultures exposed to glutamate or hypoxia/reoxygenation resulted in a release of LDH. The release of the enzyme was almost completely attenuated when betaxolol was included in the culture medium. Kainate increased the [Ca2+]i in chick retinal cultures, as measured with Indo-1. In a medium with sodium, this kainate-induced elevation of [Ca2+]i was significantly reduced by betaxolol. The combined data show that betaxolol is a neuroprotective agent and attenuates the effects on the retina induced by raising the intraocular pressure to simulate an ischaemic insult as may occur in glaucoma.
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PMID:In vivo and in vitro experiments show that betaxolol is a retinal neuroprotective agent. 909 74

Excitotoxic amino acids, such as glutamate, may play an important role in retinal ischemia/reperfusion damage. In central neurons, excitotoxicity may be mediated by nitric oxide synthase (NOS) causing DNA damage via nitric oxide (NO). The nicked DNA activates poly-adenosine diphosphate (ADP)-ribose polymerase (PARP) and may deplete intracellular ATP resulting in cell death. PARP may also be involved in apoptosis. We used 3-aminobenzamide (3-ABA), a PARP inhibitor, to examine the possible involvement of PARP in a rat model of retinal ischemia. Retinal ischemia was induced by elevating the intraocular pressure (IOP) through the insertion of a needle into the anterior chamber of a rat eye. IOP was raised to 110 mm Hg for 60 minutes. Animals were given intracameral infusion of 0, 1, 3, 10, 30, 100 mM 3-ABA in 0.1 M PBS, pH 7.4 during ischemia. Morphologic and morphometric evaluation at 7 days after reperfusion showed that 3-ABA at 3 mM and above significantly ameliorated the ischemic/reperfusion damage to the retina. In addition, at 10 mM 3-ABA inhibited the characteristic ladder pattern in DNA gel analysis seen in apoptosis of retinal neurons after ischemia/reperfusion. Hence, PARP may be involved in retinal cell loss after ischemia/reperfusion insult probably through the apoptotic pathway.
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PMID:The effect of 3-aminobenzamide, an inhibitor of poly-ADP-ribose polymerase, on ischemia/reperfusion damage in rat retina. 914 32

Although the effects of physical exertion on intraocular pressure and systemic blood pressure are well established, the retinal response to such physiologic stress has not been examined. We studied the effect of short-term intense exercise on the principal waves in the scotopic and photopic flash electroretinograms, as well as the lower-amplitude oscillatory potentials. Sixteen healthy volunteers between 20 and 30 years of age participated in this experiment. The electroretinograms and oscillatory potentials were recorded with a Nicolet CA-1000 clinical averager, using DTL-type fiber electrodes. All retinal potentials were taken immediately before and after a minimum 20-min period of stationary bicycling that increased the heart rate to about 140 beats per minute. The electroretinograms were recorded from eyes with dilated pupils, 10 min after white-light adaptation of the right eye, and 30 min after dark adaptation of the left eye. Red flashes and dim white flashes were used to elicit photopic and scotopic electroretinograms, respectively. While no changes were recorded for any of the electroretinogram components recorded under photopic conditions, the amplitude of OP5 was decreased and the implicit time of OP4 was delayed after exercise for scotopic conditions. We concluded that exercise caused component-specific changes in the scotopic oscillatory potentials. Since it is well known that oscillatory potentials are vulnerable to ischemia, scotopic oscillatory potentials may be used as simple noninvasive indices of the reactivity of the retinal vascular autoregulatory system during exercise.
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PMID:Correlation of an exercise-induced increase in systemic circulation with neural retinal function in humans. 918 42

We studied cellular aspects of amyloid angiopathy of the iris upon decompensation of ocular pressure and the role of microcirculatory pathology in pathogenesis of the open angle glaucoma. A total of 115 iris biopsies were studied, which were taken during antiglaucoma operations and stained by Congo rot and thioflavine for amyloid and Toluidine blue for glycosaminoglycans. The biopsies from nine patients were studied at the ultrastructural level. Intravasal increase of the concentration of preamyloid proteins during spasms of the arterioles and capillaries should be considered as a provoking moment of the iris amyloidogenesis. Blockade of reticular structures of the microcirculatory basal membranes by preamyloid serum proteins, which provides for shedding of amyloid fibrils, dystrophic changes and detachment of the endothelial cells from the basal membrane, obliteration of lumens of the capillaries and arterioles, disturbed integrity of the microvascular barrier and accumulation of preamyloid and amyloid proteins in the extracellular matrix, ischemia and focal microinfarctions of the iris, and dystrophia of the melanocytes, are subsequent key factors. Amyloid angiopathy of the iris is a cause of ischemia of the anterior eye part, thus creating conditions for increased intraocular pressure and glaucoma.
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PMID:[The cellular aspects of amyloid angiopathies of the iris in open-angle glaucoma]. 919 Feb 23

Pharmacological experiments have suggested that ocular ischemia, induced by high intraocular pressure in the rabbit, provokes an oxidative stress responsible for functional alteration of the retina. However, the nature of the oxidant chemical species and their mode of generation were not elucidated. The aim of the present studies was to characterize the oxygen-derived free radicals produced during and/or after the hyperpressure period. The technique used was based on electron spin resonance spin trapping analysis of the signals obtained in microdialysates of the retina perfused with the nitrone 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide (DEPMPO). The oxidative stress was also evaluated under ischemia and reperfusion periods by measuring the level of ascorbate in the retina via electron spin resonance detection of the ascorbyl free radical-dimethyl sulfoxide (AFR-DMSO) complex. Electroretinograms were recorded to determine the functional consequences of high intraocular pressure and free radical generation. Our results show that superoxide dismutase-inhibitable DEPMPO/hydroxyl radical adducts were generated during the high intraocular pressure period and that the oxidative stress was not increased at reperfusion as assessed by spin trapping and AFR-DMSO measurements. Functional protection provided by free radical scavengers (superoxide dismutase+catalase, TEMPO nitroxide+catalase and dimethylthiourea) against high intraocular pressure-induced electroretinogram alteration confirmed these observations. In conclusion, these experiments demonstrate for the first time by direct measurement that oxygen-derived free radicals are produced by the retina during acute ischemia. This generation could be the explanation for electroretinogram alteration.
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PMID:Free radicals in rabbit retina under ocular hyperpressure and functional consequences. 922 82

Nitric oxide (NO) is a free radical and was regarded as noxious to life. But recent studies show that NO is an important substance for transcellular signal transduction. It also seems to act as a neurotransmitter in the nervous system. In ischemic nerve tissue a release of glutamate is one of the critical factors that increase neuronal death, and some experiments suggest that NO may be involved in this process. Here we provide evidence that NO provides neuroprotection in ischemic retinas in vivo. Albino rabbits' eyes were subjected to 60 minutes of ischemia by raising intraocular pressure. Before ischemia the eyes were treated intravitreously with the NO-precursor L-arginine, the NO synthase-inhibitor nitro-L-arginine methyl ester hydrochloride (L-NAME), the NO-donor sodium nitroprusside (SNP), or solvent only. The amplitude of the b-wave was measured and the recovery ratio of the b-wave was analyzed hourly after reperfusion. The recovery ratio of b-wave in the eyes with L-arginine and with SNP increased more rapidly than in the controls, while the recovery ratio in the eyes with L-NAME increased in a way similar to that of the controls. These results suggest that NO plays a neuroprotective role in ischemic retina. It may be involved with S-nitrosylation of some proteins, including one of the glutamate receptors, the N-methyl-D-aspertate (NMDA) receptor.
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PMID:[Protective effect of nitric oxide on ischemic retina]. 928 18


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