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

It has been suggested that glaucomatous field loss may progress on the basis of ischemia of the optic nerve head alone after the intraocular pressure has been controlled. Bishydroxycoumarin (Dicumarol) has been reported to be of benefit in such situations. A review of 551 consecutive glaucoma records did not support this theory. Apparent progression of field loss at intraocular pressures of 20 mm Hg or less was either due to artifacts in field testing or to a pressure that was still too high. A pilot study suggested that bishydroxycoumarin was of no benefit in these situations.
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PMID:An evaluation of anticoagulation in glaucoma therapy. 7 Oct 7

Anterior segment ischemia changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. They were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma and frank necrosis. The variables which lead to this reaction is described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle surgeries, are discussed.
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PMID:Production of anterior segment ischemia. 10 21

Anterior segment ischemic changes can occur without detachment of any muscles. The most common cause of such ischemic changes of the anterior segment is the removal of too many rectus muscles in one operation. Twenty dog eyes and eight monkey eyes were subjected to the disinsertion and detachment of various combinations of extraocular muscles. The dogs were sacrificed at intervals from 30 to 90 days. During the observation period, they were observed for gross and slit-lamp changes. The enucleated eyes were studied microscopically for signs of ischemic and necrotic changes. Two patients who were studied, observed, and treated for anterior segment ischemia following muscle surgery are described. The changes which occur after extraocular muscle surgery are extensive and include corneal edema, cataract, chemosis, corneal changes, decreases in intraocular pressure, decreases in outflow or glaucoma, and frank necrosis. The variables which lead to this reaction are described in detail. Also, some unanswered queries, such as the duration of the reaction and the time interval of the reaction after multiple muscle operations are discussed.
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PMID:Production of anterior segment ischemia. 41 49

In a study of 130 cases of unilateral retinal vein occlusion uncomplicated by rubeosis, we found that more than 80% of the patients had a lower intraocular pressure (IOP) in the eye with the occlusion than in the fellow normal eye. The reduction of IOP was greater with central than with branch vein occlusion, greater with hemorrhagic than with venous stasis retinopathy, and greater in patients who had high pressures in their fellow eyes. The pressure reductions persisted during follow-up periods of up to two years. How retinal vein occlusion lowers IOP is obscure and may involve more than one mechanism. Outflow facility was increased (compared to the fellow eye) in hemorrhagic retinopathy and in branch vein occlusion, both of which are association with retinal ischemia, but not in venous stasis retinopathy. Calculated rates of aqueous formation were low in central vein occlusion but not in branch vein occlusion.
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PMID:Ocular hypotony following retinal vein occlusion. 65 20

Stereophotographs of the optic disc were reviewed in 78 patients with ischemic optic neuropathy (ION). Only 10% (6) of 61 nonarteritic (idiopathic) ION eyes developed optic disc cupping similar to that seen in glaucomatous eyes. Five of ten eyes with ION due to giant cell arteritis had cupping simulating glaucoma; however, two had elevated intraocular pressure, and the other three had large physiologic cups in the opposite eye. Optic disc pallor was proportionately more severe in ION eyes than in glaucomatous eyes of similar cup size. While there are similarities in the type of visual field loss in ION and glaucoma, the two disorders differ in the usual appearance of the disc after field loss has occurred and in the portion of the field most frequently affected. These observations suggest that if both disorders have an ischemic mechanism, there is a difference in the nature or distribution of the ischemia. There should be little difficulty under most circumstances in making the clinical differentiation between a disc that has suffered ION and a disc that has suffered pressure-induced damage, although occasional instances of ION may be classified as low-tension glaucoma on the basis of field loss and cupping without elevated intraocular pressure.
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PMID:Cupping of the optic disc in ischemic optic neuropathy. 92 94

Susceptibility to pressure amaurosis was measured in young research subjects before and during blood pressure elevation induced by intravenous infusions of phenylephrine. Intraocular pressure elevations were produced by paralimbal suction; we measured the highest level to which intraocular pressure could be raised without obliterating perception of a slowly flickering stimulus in the nasal field of vision. Elevation of systemic blood pressure was accompanied in all subjects by a corresponding increase in the highest "safe" level of intraocular pressure. This observation confirms the commonly held hypothesis that pressure amaurosis is the result of pressure-induced neuroretinal ischemia.
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PMID:Blood pressure and pressure amaurosis. 111 22

To investigate the effect of dextromethorphan (DEX), N-methyl-D-aspartate (NMDA) receptor antagonist, on the retinal ischemia, 0.4%DEX hydrobromide was intravenously given to rabbits before, during and after retinal ischemia. Retinal function was monitored by electroretinogram (ERG). Retinal ischemia was induced by increasing intraocular pressure to 130 mmHg for 90 or 120 min. Amplitudes of ERG.b-waves recorded after the 90 min ischemia recovered to 72.5 +/- 9.0% in the DEX group and 38.5 +/- 8.5% in the control group which was given normal saline. The maximal recovery rates of b-wave amplitudes after the 120 min ischemia were 44.0 +/- 7.9% in the DEX group and 21.0 +/- 1.3% in the control group. The recovery rates of the b-wave amplitudes in DEX group were significantly higher than in the control group (p less than 0.01). It was found that the effective dose of DEX was 0.1-0.4%.
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PMID:[Protective effect of dextromethorphan on the ischemic retinal damage in rabbit]. 131 99

Previous studies have suggested that prophylactic treatment by dextromethorphan (DEX), N-methyl-D-aspartate (NMDA) receptor antagonist can protect the retina against ischemia. To investigate the effect of DEX on the proceeding ischemic retina, 0.1% DEX hydrobromide was intravenously administered in rabbits immediately (group A), 1 hour (group B) or 2 hours (group C) after the release from ischemia induced by increasing intraocular pressure to 130 mmHg for 90 min. Normal saline was infused immediately after the release from ischemia as control rabbits. Retinal function was monitored by recording electroretinogram (ERG). Twenty four hours after the release of ischemia, the recovery rates of ERG.b-wave amplitudes in groups A, B and C were 61.3 +/- 3.3, 52.2 +/- 9.0 and 43.6 +/- 8.4% of the preischemic amplitude, respectively. The recovery rate of the group A was higher than that of the control (41.9 +/- 10.6%), while no significant differences were seen between groups B or C and the control. The results suggest that DEX can protect the retina if it is administered immediately after the release of ischemia.
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PMID:[Delayed treatment with dextromethorphan can reduce ischemic retinal damage in rabbit]. 138 63

A 74-year-old man with the isolated complaint of uniocular transient visual loss after exposure to bright light was found to have severe ipsilateral, atherosclerotic carotid occlusive disease. Signs of ocular ischemia that were present included slightly reduced visual acuity, mild afferent pupillary defect, lowered intraocular pressure, increased photostress recovery time, and reduced opthalmodynamometry values on the affected side. After a subclavian to internal carotid artery bypass procedure, the patient's symptoms resolved completely and his ocular signs returned to normal. This patient's initial symptom, referred to as light-induced amaurosis (LIA), is an unfamiliar manifestation of the ocular ischemic syndrome. We discuss the condition and summarize the literature.
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PMID:Light-induced amaurosis associated with carotid occlusive disease. 145 7

Overstimulation of the N-methyl D-aspartate (NMDA) receptor has been implicated as a factor in the pathogenesis of ischemic injury in the central nervous system. The present study was undertaken to determine whether ketamine hydrochloride, a potent NMDA antagonist, could attenuate ischemic injury in the rabbit retina. Retinal ischemia was induced for 60 min in one eye of 18 albino rabbits by raising intraocular pressure above the systolic blood pressure. Three concentrations of ketamine, 0.5, 1.5, 5.0 mumol were dissolved in 20 microliters of saline solution and injected in the midvitreous in each eye of 14 rabbits 1 hr prior to ischemia. Four rabbits received saline solution as controls. The scotopic electroretinogram was monitored in each eye to assess the postischemic recovery of retinal function. A statistically significant reduction in the b-wave was detected in the eyes treated with saline (P less than 0.05), whereas the postischemic recovery of b-wave amplitude was enhanced by pretreatment with lower doses of ketamine. The highest dose depressed b-wave amplitude regardless of ischemia. Six rabbits underwent unilateral ocular ischemia under general anesthesia with ketamine. A small ameliorative effect was seen (P = 0.029). These results suggest that ketamine may alleviate ischemic injury in the rabbit retina, presumably by antagonizing the NMDA receptor-mediated toxicity. Thus, ketamine may have potential in the treatment of retinal vascular occlusive diseases. Moreover, a modified ischemic state may exist in experiments on ischemia conducted under general anesthesia with ketamine hydrochloride.
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PMID:Ketamine suppresses ischemic injury in the rabbit retina. 153 93


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