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

Bilateral blindness resulting from optic atrophy is an unusual complication following shock and cardio-respiratory arrest. This report describes a patient with acute respiratory failure due to pneumococcal pneumonia being treated with very high levels of positive end expiratory pressure who developed bilateral blindness following cardiac arrest. This unfortunate complication most likely resulted from increased intraocular pressure and low systemic perfusion pressure synergistically causing ischemia of the optic nerves.
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PMID:Bilateral optic atrophy after cardiac arrest in a patient with acute respiratory failure on positive pressure ventilation. 283 2

No satisfactory treatment is available to supply the metabolic needs of the retina in vascular occlusion. Consequently, necrosis occurs. We devised vitreoperfusion, a technique of perfusing the vitreous cavity after vitrectomy-lensectomy with selected fluids containing glucose and oxygen. We tested whether vitreoperfusion could protect the retina from severe combined retinal and choroidal ischemia. An intraocular pressure of 170 mm Hg was induced in each eye of nine cats for up to four hours, and simultaneously one eye of each cat underwent vitreoperfusion. After one week, histopathologic examination revealed retinal atrophy and dissolution in untreated eyes but not in eyes treated with vitreoperfusion. To our knowledge, such severe ischemia has never been treated successfully before. Vitreoperfusion is a potential treatment modality in various forms of ocular ischemia. Additional studies are warranted to refine the technique and determine any clinical applicability.
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PMID:Vitreoperfusion. A new approach to ocular ischemia. 255 70

Severe occlusive disease of the carotid artery may produce a rare syndrome of chronic ocular ischemia. Prolonged retinal hypoxia is associated with characteristic funduscopic changes and neovascularization of the iris, with subsequent obstruction of aqueous humor resorption. A case of neovascular glaucoma as a result of severe bilateral carotid occlusive disease and the pathophysiology involved are discussed. Definitive treatment consisted of carotid endarterectomy and aggressive control of intraocular pressure, including operative placement of a drainage implant in the anterior chamber of the eye. Seizure activity and an exacerbation of glaucoma developed after successful revascularization, exemplifying the derangements in cerebral and ocular function that may result from chronic hypoperfusion.
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PMID:Chronic ocular ischemia and neovascular glaucoma: a result of extracranial carotid artery disease. 318 12

The authors report on the behavior of the intraocular pressure of 20 patients who had sustained severe head injury. The 8 patients who retained normal intraocular pressure all survived. The 12 patients who developed intraocular hypotony all suffered brain death. Although optic disc edema was not noted in any brain-dead patients, we did find signs of fundus ischemia in most.
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PMID:Brain death and intraocular pressure. 321 15

After retinal detachment operations 1-5% of the patients develop glaucoma. If this occurs directly after the operation it is the result of mechanical narrowing of the chamber angle. This can be the result of indentation due to an exoplant or encircling band causing forward displacement of the lens/iris diaphragm. Other causes are torsion of the ciliary body or a ciliary block due to serous detachment of the choroid caused by venous compression or diathermy. Ischaemia of the anterior segment sometimes leads to glaucoma in the long run; this is then the result of rubeosis iridis. Conducive factors are detachment of the recti muscles, arterial and venous compression by the exoplant or encircling band and the use of diathermy. When performing such operations it is advisable to take these risks into account and to keep a check on the intraocular pressure after the operation. A patient is described who, as the result of ischaemia, eventually developed ribeosis iridis with neovascular glaucoma, leading to loss of the eye.
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PMID:Glaucoma following retinal detachment operations. 342 98

Glucose consumption and regional blood flow were determined using the [14C]-2-deoxyglucose (2-DG) method and microspheres in the optic nerve, the retina and different parts of the brain in monkeys. The relationship between the 2-DG accumulation and blood flow in the optic nerve head region was similar to that in grey matter of the brain under pentobarbital anaesthesia as well as under urethan anaesthesia. Pentobarbital anaesthesia resulted in lower values for blood flow and glucose metabolism in most regions. In the optic nerve the highest values were observed in the distal part; there was a fall in blood flow and metabolism along the nerve. There was a corresponding increase in myelin content. Artificial increments in intraocular pressure resulting in a perfusion pressure (mean arterial pressure minus intraocular pressure) of 40 cm H2O had no appreciable effect on the 2-DG accumulation. At a perfusion pressure of 20 cm H2O 2-DG accumulation in the retina and prelaminar part of the optic nerve was markedly increased indicating partial ischemia resulting in anaerobic glycolysis. At intraocular pressures higher than the systolic arterial blood pressure there was still some accumulation of 2-DG in the intraocular tissues, but no blood flow, which indicates that glucose could diffuse into the eye through the sclera. Behind the lamina cribrosa there was no indication of a reduction in blood flow or a metabolic disturbance. The results indicate that the blood flow and metabolism of the retina and prelaminar part of the optic nerve is disturbed only at very high intraocular pressures, and that even at extreme pressures there is no disturbance behind the lamina cribrosa in acute experiments. The 2-DG method will be useful in further studies on the nutritional status of the optic nerve head since it can detect abnormal glycolysis even in very discrete regions due to its high spatial resolution.
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PMID:Blood flow and glucose consumption in the optic nerve, retina and brain: effects of high intraocular pressure. 409 55

By means of microelectrode recordings receptive field properties and flicker responses of cat retinal ganglion cells were studied during elevated intraocular pressure (IOP). At moderate IOP elevation (perfusion pressure, PP, approx. 50 mm Hg), a slight increase in the maintained activity and the neuronal activation obtained from the receptive field (RF)-center or RF-periphery occurred in some of the neurons. At critical perfusion pressure (PP 30-10 mm Hg), the RF-periphery mechanisms were less sensitive to ischemia than the RF-center mechanisms. The spontaneous activity was completely suppressed at an average PP of 36.6 +/- 9.0 mm Hg, the flicker-evoked responses at 17.7 +/- 9.6 mm Hg. At critical perfusion pressures, the stimulus-response latency increased by 20 ms at stimulation frequencies of 10-20 Hz. The critical flicker frequency was already slightly reduced at a PP of 50 mm Hg and decreased further with a further decrease in PP. The threshold values of the intensity function shifted to higher luminance levels when PP was reduced to less than 40 mm Hg, but the slope remained constant. A close interneuronal correlation was found in simultaneous recordings of pairs of ganglion cells during different levels of increased IOP. This finding indicates that the interneuronal response variability to IOP increase appearing in successively recorded neurons was predominantly caused by experimental factors. The main impairment in retinal neuronal function during increased IOP seems to occur proximal to the receptors but distal to the retinal ganglion cell somata.
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PMID:Effect of short-term intraocular pressure increase on cat retinal ganglion cell activity. 609 84

Previous experiments showed that optic nerve axonal transport can be blocked at the level of the lamina cribrosa by elevated intraocular pressure. In an effort to discover if this blockage might be secondary to pressure-induced ischemia, we studied the effect of unilateral common carotid artery ligation upont the pressure-induced interruption of axonal transport. In 13 owl monkeys (Aotus trivirgatus), the right common carotid artery was ligated within the anterior cervical triangle. Three days later, ophtalmodynomometry was performed on all experimental eyes. In nine of the 13 animals, this estimate of ophthalmic artery pressure was 10 to 20 mm Hg less in the right compared to the left eye. Optic nerve axonal transport was studied in right and left eyes during 5 hours of increased intraocular pressure (ocular pressure 35 mm Hg less than mean femoral artery blood pressure). No significant difference in the extent to which the transport mechanisms were interrupted could be demonstrated when comparing right and left eyes of the experimental animals. These observations fail to support a vascular mechanism for this pressure-induced interruption of axonal transport.
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PMID:Failure of unilateral carotid artery ligation to affect pressure-induced interruption of rapid axonal transport in primate optic nerves. 615 74

Five hours of elevated intraocular pressure produced evidence of an altered blood-brain barrier at the optic nerve head in 27 of 29 monkey eyes. The change in vascular permeability was documented by fluorescein angiography (18 of 21 eyes), by Evans blue fluorescence microscopy (21 of 23 eyes), or by both methods. Leakage occurred from major blood vessels as well as from microvasculature of the nerve head. In 22 eyes, rapid axonal transport was studied after intravitreal injection of tritiated leucine. In 18 of these 22 eyes, autoradiography demonstrated a local interruption of axonal transport. In 15 eyes examined by all three methods, leakage from microvasculature (as opposed to leakage from the major vessels) was loosely associated with severe and widespread blockade of axonal transport at the lamina cribrosa. Although cause-and-effect relationships are not proved, ischemia may be responsible both for the focal endothelial damage with breakdown of the normal blood-brain barrier and for the local abnormalities of axonal transport.
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PMID:Breakdown of the normal optic nerve head blood-brain barrier following acute elevation of intraocular pressure in experimental animals. 615 39

Previous studies have shown that elevation of intraocular pressure blocks rapid axonal transport at the lamina cribrosa of the optic nerve. In this study, IOP-induced blockage of axonal transport was greater in cats with elevation of BP induced by angiotensin I than in control animals with normal BP. The fact that cardiovascular factors influenced IOP-induced blockage of axonal transport suggests that it is due to ischemia; if the blockage were a direct mechanical effect of the IOP on the axons, it should be unaffected by BP. The data also suggest that the vasoconstrictive properties of angiotensin I reduced the ability of the vasculature of the optic nerve head to autoregulate when challenged by elevation of IOP.
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PMID:Blockage of axonal transport in optic nerve induced by elevation of intraocular pressure. Effect of arterial hypertension induced by angiotensin I. 618 8


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