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

Orthograde and retrograde axoplasmic transport have been studied in the optic nerve heads of 37 Macaca fascicularis eyes with normal or elevated intraocular pressure (IOP) produced by cannulation of the anterior chamber. Orthograde transport was labeled by 3H-amino acids injected intravitreally and incorporated into retinal ganglion cell proteins. Retrograde transport was studied in the same eyes by injecting horseradish peroxidase (HRP) into one or both optic tracts and dorsal lateral geniculate nuclei (dLGN). Both tracers accumulated in the lamina scleralis (LS) of eyes maintained at pressures of 25 to 150 mm. Hg for 12 to 28 hours (pressure in normal controls = 10 to 14 mm. Hg) but the HRP technique was markedly more sensitive. The degree of retrograde transport obstruction in the LS appeared to be directly proportional to both the height and the duration of elevated IOP. In one experiment, the blockades of orthograde and retrograde transport induced at 50 mm. Hg were demonstrated to be reversible. Serial reconstructions of radioautographs and peroxidase-reacted sections of the optic nerve heads demonstrated that the orthograde and retrograde transport obstructions were coincidental anatomically by light microscopy in the LS and occurred most prominently in the temporal quadrants of the nerve head. These transport obstructions occurred at moderate elevations of IOP (25 TO 50 mm. Hg) despite (1) elevated arterial PO2 levels during inhalation of 100 percent oxygen and (2) intact nerve head capillary circulation, as demonstrated by perfusion with nucleated avian erythrocytes.
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PMID:Orthograde and retrograde axoplasmic transport during acute ocular hypertension in the monkey. 6 96

Orthograde and retrograde axoplasmic transport were studied in optic nerve heads of seven hypotensive Macaca fascicularis eyes. Orthograde transport was studied by radioautography after intravitreal radioisotope injections. Retrograde transport was studied in the same eyes by horseradish peroxidase injection into the dorsal lateral geniculate nuclei or optic tracts. Three eyes had developed marked papilledema before injections. Orthograde axoplasmic transport was blocked in swollen axons of the optic disc anterior to Bruch membrane and in the lamina scleralis. Retrograde transport was blocked in axons within the lamina scleralis along the posterior edges of transverse scleral beams and in axons in the choroidal portion of the nerve head posterior to Bruch membrane. These results support the general concept that axoplasmic transport in the optic nerve head is sensitive to alterations in intraocular pressure, either increases or decreases. The edges of Bruch membrane and the openings in the lamina scleralis may constrict axon bundles in ocular hypotony.
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PMID:Axoplasmic transport in ocular hypotony and papilledema in the monkey. 7 Feb

Rhesus monkeys were injected intravenously with hypertonic urea (9 ml/kg body weight of 30% urea in 10% invert sugar) and the intraocular pressure was measured with an applamatic tonometer. When this pressure reached its minimum (20% of the normal value) horseradish peroxidase (molecular weight 40,000; radius of an equivalent hydrodynamic sphere about 2.5 nm; 0.5 g/kg body weight), was injected intravenously. Twenty minutes following peroxidase administration, either aqueous humor was sampled from the anterior chamber for biochemical determination of peroxidase activity, or one eyeball was enucleated and processed for light and electron microscopic localization of the enzymatic tracer. This experiment showed that: (1) therapeutic doses of hypertonic urea do not cause a breakdown of either the blood-retina or the blood-aqueous barriers; (2) as intraocular pressure decreases, peroxidase-containing blood flows back from the episcleral veins into the Schlemm canal; (3) macromolecules up to the dimensions of horseradish peroxidase leak through the intercellular clefts of the endothelium of the Schlemm canal, permeate the juxtacanalicular connective tissue and trabecular meshwork, and finally enter the anterior chamber. Thus, blood-borne substances can circumvent the blood-aqueous barrier when intraocular pressure is decreased, and administration of a hypertonic agent may represent a simple pharmacological device to cause penetration into the ocular chambers by drugs that are normally excluded from the interior of the eye.
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PMID:Blood-aqueous barrier can be circumvented by lowering intraocular pressure. 81 31

There are many unanswered questions about chronic glaucoma which cannot be investigated in the available animal models. The present experiments were designed to develop a rabbit model of chronic intraocular hypertension with characteristics similar to human chronic glaucoma by ligating vortex veins or by making single or multiple intraocular injections of 0.5% or 1% alpha-chymotrypsin, 20% chondroitin sulphate, 2% hydroxypropyl methylcellulose, 2% sodium carboxymethylcellulose or 1% or 2% methylcellulose. Evaluation was based on the clinical findings, intraocular pressure and the retrograde axoplasmic transport function of the optic nerve using a horseradish peroxidase histochemical technique. Most methods either failed to produce moderate chronic intraocular hypertension or were associated with other complications. However, a reliable and relatively long period (eight weeks) of intraocular hypertension was developed by a series of four intra-anterior chamber injections of 1% or 2% methylcellulose. This model has been proved suitable for the study of structural and functional damage to the retina and optic nerve caused by chronic glaucoma.
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PMID:Development of experimental chronic intraocular hypertension in the rabbit. 144 75

In order to determine thresholds for irreversible cellular injury in the rat retina, timed acute no-flow ischemic episodes of 30-180 min duration were produced by elevation of intraocular pressure (IOP) above systolic pressure. Quantitation of irreversible degeneration and cell loss following a 2-week post-ischemic interval was performed by computer-assisted measurements from histologic sections. Alterations of thickness of retinal layers and linear cell density were determined for ischemia of selected durations (30, 60, 80, 90, 120 and 180 min). Different thresholds were evident for inner and outer retinal damage. Neurons of the inner nuclear layers showed extensive loss with episodes at 60 min. Decrease in the thickness of the inner plexiform layer provided the best index of this inner nuclear damage. The outer retina was more resistant, with photoreceptors showing extensive damage only after 90 min in conjunction with pigment epithelial metaplasia and degeneration. Two-hour episodes produced full-thickness degeneration with loss of pigment epithelium and sparing of the peripheral retina. Greater sensitivity of the inner retina suggested problems with restoration of the retinal circulation. Horseradish peroxidase infusions did reveal central microcirculatory defects in retinal wholemounts of some specimens with episodes longer than 60 min. Refinements of the methods resulted in outcomes sufficiently reproducible for quantitative assessment of acute ischemic injury. The rat retina provides an economical basic tissue model of acute ischemic injury affecting neurons, glia, and microvasculature. Quantitation of this injury promises great utility in testing agents with potentially protective effects on acute ischemic injury.
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PMID:Quantitation of ischemic damage in the rat retina. 174 56

Horseradish peroxidase (HRP) injected into one lateral geniculate nucleus of male inbred PVG/Mol hooded rats is taken up by terminals of the optic nerve and transported retrogradely towards the opposite retina. Four hours after injection when a small portion of HRP had reached the retina, the eye and optic nerve were excised and incubated in vitro at 38 degrees C for another 3.5 hr during which the intraocular pressure (IOP) was set at 30 or 0 mmHg. During the in vitro period additional HRP entered the retina by axonal transport if the incubation medium contained enough Ca2+. Transport occurred at 0.45-1.1 mM Ca2+, but not at 0.30mM Ca2+. When transport occurred, no significant difference in degree of transport was found between the two pressures. The amount of HRP transported at 30 and 0 mmHg was very similar to that at 20 mmHg but significantly higher than that at 50 mmHg, (values at 20 and 50 mmHg from an earlier study). Thus, fast retrograde HRP transport was equally efficient at or near a physiological IOP as at zero pressure. Also, the degree of transport inhibition was not proportional to the height of the IOP, but started to increase above 30 mmHg. This is probably due to the presence of supporting tissue in the optic nerve head and inherent strength of the nerve fibers themselves. The lamina cribrosa in the rat eye is poorly developed and a shearing force on the nerve fibers due to laminar hole misalignment can largely be excluded. Effects on blood circulation are also excluded by the in vitro situation.
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PMID:Influence of low IOP and low calcium on retrograde axoplasmic transport in rat optic nerve in vitro. 242 Jun 29

Horseradish peroxidase (HRP) injected into one lateral geniculate nucleus of male inbred PVG/Mol hooded rats is taken up by terminals of the optic nerve and transported retrogradely towards the opposite retina. One hr after injection, the eyes were cannulated and set at an intraocular pressure (IOP) of either 35 mmHg or 15 mmHg. The IOP were set for 4 hr at which time the trial was terminated and retinal HRP content measured. It was found that in eyes set at 35 mmHg (18 eyes) the axoplasmic transport was partially blocked compared with that in eyes set at 15 mmHg (10 eyes), absorbances were 0.034 +/- 0.003 (S.E.) and 0.044 +/- 0.003 (S.E.), respectively, P less than 0.05. In a third group of eyes (nine eyes) set at 50 mmHg for 2 hr (beginning 1 hr after the intrageniculate injection), succeeded by another 2 hr of 15 mmHg IOP, there was no statistically significant difference in retinal HRP content compared to that in eyes set at 15 mmHg throughout, absorbances were 0.040 +/- 0.006 and 0.044 +/- 0.003, respectively. Two hr of 50 mmHg IOP blocks the axonal transport in the rat optic nerve (Johansson, 1986a). The result shows that also moderately increased IOP blocks axonal transport in the rat optic nerve. It also shows the presence of a rapid recovery when the pressure is normalized. A direct mechanical factor underlying axonal transport blockage is proposed.
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PMID:Inhibition and recovery of retrograde axoplasmic transport in rat optic nerve during and after elevated IOP in vivo. 245 Jul 68

The presence and distribution of laminin, heparan sulfate proteoglycan and collagen types I, III and IV were immunohistologically determined in cynomolgus monkey optic nerve heads using the avidin-biotin-peroxidase complex technique. Collagen types I and III were detected within the collagenous plates of the scleral lamina cribrosa, in the septa and pia mater of the postlaminar optic nerve and in blood vessel walls in all regions of the optic nerve head. Collagen type IV, laminin and heparan sulfate proteoglycans were all localized to the margins of the collagenous laminar plates of the scleral lamina cribrosa and along the margins of the optic nerve septa and the pia mater. All three components also appeared beneath the blood vessel endothelium throughout the optic nerve head. Within the lamina cribrosa, collagen types I and III occupy the core of the scleral laminar plates and may provide structural support for optic nerve bundles exiting the eye. The distribution of collagen type IV, laminin and heparan sulfate proteoglycan corresponds to basement membranes from two sources: vascular endothelial cells and glial cells lining the axonal bundles. Abnormalities of these substances may influence optic nerve function and susceptibility to elevated intraocular pressure by altering their mechanical support functions within the nerve head, by interfering with axonal nutrition, or both.
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PMID:The extracellular matrix composition of the monkey optic nerve head. 304 74

Horseradish peroxidase (HRP) injected into one lateral geniculate nucleus of hooded rats, is taken up by terminals of the optic nerve and transported retrogradely towards the opposite retina. Four hours after injection, a small portion of HRP has reached the retina. After excision of the bulb and optic nerve and another 4 hours of in vitro transport during which different levels of intraocular pressure (IOP) were set, more HRP accumulated in the retina. The amounts entering in vitro at IOPs of 35 and 50 mmHg were 29% and 76% less, respectively, than at 20 mmHg. The lamina cribrosa of the rat strain used was studied by scanning electron microscopy. It consisted of only one complete laminar sheet, a fact that minimizes optic nerve fiber strangulation by laminar shearing in raised IOP. Thus, moderately increased IOP can inhibit fast retrograde transport of HRP in the optic nerve of the rat by direct mechanical pressure, and does not involve either the blood circulation or a multilayered structure of the lamina cribrosa.
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PMID:Inhibition of retrograde axoplasmic transport in rat optic nerve by increased IOP in vitro. 619 89

Morphological changes in the ciliary epithelium and blood-aqueous barriers were observed with a tracer, horseradish peroxidase, after 10 microliters of 10(-5) M endothelin-1 was injected intravitreally. A decrease of intraocular pressure and an increase of anterior chamber flare were found, and the structure of the ciliary epithelium changed drastically 6-7 hr after the injection. Swelling of mitochondria appeared in both non-pigmented and pigmented epithelial cells of the ciliary body. Intercellular spaces and ciliary channels were markedly dilated in the iridial processes. Some non-pigmented epithelial cells in both iridial and ciliary processes appeared to be degenerated and necrotic. Horseradish peroxidase leaked into the posterior chamber via extremely dilated ciliary channels and necrotic cells. The dose of 10(-5) M endothelin-1 seems to be so large that a toxic action occurred. The mechanism of the effect of endothelin on intraocular pressure was also discussed.
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PMID:Morphological changes in rabbit ciliary epithelium and blood-aqueous barriers after intravitreal 10(-5) M endothelin-1. 898 42


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