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

Acute retinal ischemia was induced in adult albino rabbits by clamping the retrobulbar blood vessels or raising the intraocular pressure. As the level of ischemia was increased, the b-wave amplitude and implicit time of response increased. However, the hyperresponsivity and delay of response were inversely related to the intensity of stimulation used, although at levels of ischemia above 70% there was a significant delay of response even with high-intensity stimulation. Thus, if early signs of acute ischemia are to be successfully monitored, low intensities of stimulation must be used.
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PMID:Effects of intensity of stimulation on signs of acute ischemia in the electroretinogram. 665 75

Having examined in literature the intraocular pressure changings due to periocular encirclement, the Authors analyse a casenstry of 135 eyeballs in which a silicone band encirclement was performed. They conclude emphasizing the hypotonizing action of this technique, due to ciliary body ischemia, hypothesizing the use of this surgical technique in case of neovascular glaucoma.
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PMID:[Effect of scleral buckling on ocular tone]. 670 49

Iodoantipyrine was used to record relative blood flow in the retina, choroid, optic nerve head, lamina cribrosa, and postlaminar optic nerve of cats at different levels of intraocular pressure. The IOP could be elevated to within 25 mm Hg of mean femoral arterial pressure, with only a slight effect on blood flow in the retina, choroid, and optic nerve head. At higher IOPs, the blood flow is reduced in the retina, choroid, and optic nerve head, but, in the lamina cribrosa, the blood flow is reduced only with extreme pressure elevation and is not reduced at all in the intraorbital optic nerve. Thus, there is no demonstrated effect of IOP on blood flow preferentially in the normal optic nerve. It is concluded that there is an efficient autoregulation in the optic nerve head and lamina cribrosa so that the IOP over a wide range does not much influence blood flow under normal circumstances. These findings do not rule out a role of ischemia in the pathophysiology of glaucomatous cupping, which may be caused by faulty autoregulation.
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PMID:Effect of elevated intraocular pressure on blood flow. Occurrence in cat optic nerve head studied with iodoantipyrine I 125. 684 62

Acute ischemia was induced in 11 adult albino rabbits by clamping the retrobulbar blood vessels and in 5 others by raising the intraocular pressure. Total ischemia was achieved by raising the pressure in the hydraulic remote control system until total collapse of the retinal circulation was observed by indirect ophthalmoscopy and the response on the electroretinogram (ERG) disappeared. The level of ischemia was increased by 15% increments from 25% to 100%, and ERGs were recorded with a constant intensity of stimulation. The amplitude increased up to a peak at 55% ischemia, then decreased to extinction at 100% ischemia. The time of response increased to a maximum at 100% ischemia. The tentative conclusion is drawn that it is important to appreciate that ischemia, and not just degeneration, can cause a delay of the ERG response in humans.
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PMID:Hyper-response and delay in the electroretinogram in acute ischemia. 688 95

A 14-year-old black boy with sickle cell trait, who sustained a traumatic hyphema, developed moderately elevated intraocular pressure that failed to respond to carbonic anhydrase inhibitors and osmotic agents. On the tenth postinjury day, a sudden increased cupping of the optic disc and partial central retinal artery obstruction caused painless loss of vision. Reversal of the cupping, the retinal ischemia, and the intraocular pressure was documented following anterior chamber paracentesis, and visual acuity returned to 6/6. Pathophysiology of the posterior ischemia is discussed. This case documents the potentially debilitating course of traumatic hyphema in "benign" sickle cell trait and its avoidance with proper management. The authors endorse recent suggestions for careful observation of any sickle cell patient with traumatic hyphema, and recommend anterior chamber paracentesis, supplemental oxygen, and avoidance of osmotic agents, if secondary glaucoma develops following the initial trauma.
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PMID:Reversal of retinal and optic disc ischemia in a patient with sickle cell trait and glaucoma secondary to traumatic hyphema. 712 55

Four cases of acute angle closure glaucoma with different types of ocular vascular accidents are presented: one case of optic nerve head ischemia; two cases of central retinal vein occlusion, and one case of vitreous hemorrhage. One of the patients had vitreous hemorrhage following the lowering of intraocular pressure in acute angle closure glaucoma. The possible predisposition to ocular vascular accidents of patients with poor hematologic and cardiovascular status is discussed.
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PMID:Vascular accidents in acute angle closure glaucoma. 723 10

Six patients experienced ischemic oculopathy, a condition in which there is ischemia in both the anterior and posterior segments of the eye caused by occlusive carotid artery disease. The abnormalities in the anterior segment include episcleral vascular congestion, anterior chamber flare and cells, a mid-dilated, sluggish, or unreactive pupil, rubeosis iridis, and abnormal intraocular pressure. The posterior segment abnormalities include ischemic insults to the retina or optic nerve, venous-stasis retinopathy, and low ophthalmodynamometry values. Ophthalmodynamometry is particularly helpful in recognizing the pathogenesis of this disorder. Superficial temporal artery-middle cerebral artery anastomosis surgery may have particular merit for patients with ischemic oculopathy.
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PMID:Ischemic oculopathy. A manifestation of carotid artery disease. 723 64

Three patients developed apparent choroidal ischemia after phacoemulsification. The outer half of the posterior retina appeared white after operation, with confluent lesions in the posterior pole and splotchy white areas in the midperiphery. The separate lesions appeared similar in pattern to the lobular division of the choriocapillaris, and the retinal vessels were not involved. The white lesions resolved in two to three weeks, leaving alterations in the pigment epithelium. Vision was transiently reduced in each eye but returned to a nearly normal level in two of three affected eyes, although paracentral scotomas persisted. In each case of phacoemulsification, the posterior lens capsule was either damaged or was removed. In all three cases, an investigational type of irrigating solution (BSS Plus) containing balanced salt, glutathione, and other constituents was used. Controlled ocular compression was performed before operation using a pneumatic device in two cases. However, the cause of retinal and choroidal damage now described was probably excessively elevated intraocular pressure during the operation.
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PMID:Choroidal ischemia after extracapsular cataract extraction by phacoemulsification. 734 48

We evaluated quantitatively the protective effect of local fundus hypothermia under pressure-induced ischemia using morphometric analysis. Retinochoroidal ischemia was produced in albino rabbit eyes by increasing the intraocular pressure for 60 minutes. During the ischemic procedure, a copper plate was inserted behind the eyeball. The retinal temperature in the posterior pole was thus reduced to 29 degrees C by placing solid carbon dioxide, and to 32 degrees C by placing an ice cube at the anterior end of the plate. Histopathological changes in the group with ischemia alone were obvious in visual cells and retinal pigment epithelial cells (RPE), but the retina treated with additional hypothermia was well preserved. In the retina with hypothermia at 29 degrees C, there was no significant difference from the controls in the mean thickness of the photoreceptor layer (PRL) and the RPE, and the average count of nuclei in the outer nuclear layer (ONL). In the retina with hypothermia at 32 degrees C, there was also no significant difference from the controls in the thickness of the PRL and the RPE. Otherwise, the count of nuclei in the ONL decreased significantly when compared to that of controls (p < 0.001). These findings indicate that even mild hypothermia at 29 degrees C preserves the outer retina from ischemic damage and that the protective effect of hypothermia at 32 degrees C is insufficient.
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PMID:[Fundus hypothermia at 29 degrees C prevents ischemic injury of the outer retina]. 748 99

Significant hyperemia results after 1 h of retinal ischemia in cats. Adenosine receptor blockade significantly attenuates the increase in retinal blood flow that occurs in response to systemic hypoxia. Synthesizing these findings, I hypothesized that adenosine receptor antagonism would attenuate the increase in blood flow that follows retinal ischemia. In these experiments, blood flows were measured with radioactively labeled microspheres in the retina and choroid of adult cats anesthetized with chloralose and acepromazine. Ischemia was induced for 1 h in both eyes by elevation of intraocular pressure above systolic arterial pressure. Blood flows were measured before ischemia and 5 min after the return of normal intraocular pressure. In each animal, after baseline blood flows were determined and approximately 10-15 min before ischemia was induced, one eye received 0.1 ml of intravitreal 0.01M 8-sulfophenyltheophylline, a polar adenosine receptor antagonist, while the opposite eye, the control, received an equal volume of intravitreal saline. Arterial blood gas tensions, systemic arterial pressure, hematocrit, and anesthetic level were kept constant during the experimental protocol. Compared with control eyes, hyperemia was significantly attenuated in the retinal circulation after ischemia in eyes injected with 8-sulfophenyltheophylline. Increase in post-ischemic choroidal blood flow was not affected. Although adenosine is involved in the vasodilatation that occurs when blood flow is restored after retinal ischemia, adenosine receptor blockade did not completely abolish hyperemia, implying that blockade was incomplete or other vasoactive substances also affect post ischemic hyperemia in the retina.
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PMID:Post-ischemic hyperemia in the cat retina: the effects of adenosine receptor blockade. 760 19


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