Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0595921 (intraocular pressure)
 11,750 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In owl monkeys, elevation of intracranial pressure to 500 mm. saline for 4 to 7 hours failed to cause an accumulation at the optic nerve head of protein carried by rapid axonal transport. This suggests that the block of rapid transport observed by others during papilledema may be the result of axon swelling, not its cause. Alternatively, more than 8 hours may be required for intracranial pressure to show an effect, only the slow transport may be affected initially, or other factors than simple hydrostatic pressure may be operative in papilledema. In addition, the elevated intracranial pressure did not prevent the block of axonal transport at the lamina cribrosa produced by elevated intraocular pressure, even though the elevated intracranial pressure reduced the pressure gradient to which the axon is subjected as it crosses the lamina cribrosa. Perhaps the block produced by intraocular pressure is not due to a simple mechanical or hydrostatic mechanism.
 ...
PMID:Failure of increased intracranial pressure to affect rapid axonal transport at the optic nerve head. 6 95

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.
 ...
PMID:Orthograde and retrograde axoplasmic transport during acute ocular hypertension in the monkey. 6 96

Sixteen patients with primary open-angle gaucoma (POAG) were matched as to age, sex, and race with an equal number of patients with secondary glaucoma. Although initial intraocular pressures were comparable, treatment with topical epinephrine hydrochloride, decreased intraocular pressure more than 5 mm Hg in 14 (88%) of the 16 patients with POAG but in only five (31%) of the 16 patients with secondary glaucoma (p less than .005). Eleven (69%) of the 16 patients with POAG demonstrated premature ventricular contractions during tonography as opposed to three (19%) of the 16 patients with secondary glaucoma (p less than .025). These findings suggested greater ocular as well as cardiac responsiveness to epinephrine in patients with POAG.
 ...
PMID:Increased ocular and systemic responsiveness to epinephrine in primary open-angle glaucoma. 6 37

We studied the degree of axonal transport blockade in various areas of the optic nerve head with acute intraocular pressure (IOP) elevation in 19 squirrel monkey eyes. When IOP was raised to 20 to 50 mm. Hg for 7 hr., mild axonal transport blockade occurred in each area of the disk, most prominently in nerve fiber bundles of the superior pole. With 7 hr. IOP elevations between 50 and 90 mm. Hg, a somewhat greater degree of transport blockade occurred throughout the nerve head, although again the superior and inferior poles were somewhat more affected. The distribution of short-term transport blockade over the entire nerve head corresponds to the diffuse damage of acute glaucoma, but the pattern hints at the preference for damage near the poles of the disk seen in chronic glaucoma. However, before these results can be fully evaluated, further information is needed on axonal pathways through the optic nerve head and on the relationship between transport obstruction and ganglion cell death.
 ...
PMID:Distribution of axonal transport blockade by acute intraocular pressure elevation in the primate optic nerve head. 6 42

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.
 ...
PMID:Axoplasmic transport in ocular hypotony and papilledema in the monkey. 7 Feb

Tritiated leucine was injected intravitreously into the eyes of rhesus monkeys that had developed papilledema secondary to implantation of intracranial balloons. Autoradiographic studies of the optic nerve head showed that six hours after intravitreous injection of the isotope the fast component of axoplasmic transport accumulated in the regions of the lamina choroidalis and lamina scleralis. The slow component arrived at the optic nerve head two to four days after injection, and the swollen axons of the entire optic nerve head were filled with radioactive isotopes. Twelve days after injection of isotope, the axons in the optic nerve head were still diffusely labeled. Disturbance of axoplasmic transport was one of the primary events resulting in swelling of axons in papilledema. The pattern of axoplasmic disturbances in papilledema secondary to raised intracranial pressure was similar to that observed in papilledema secondary to ocular hypotony or increased intraocular pressure. Ocular hypotony, raised intracranial pressure, and increased intraocular pressure appear to share a final common pathway. All these conditions apparently converge into this final common pathway of disturbance of axoplasmic transport to give rise to papilledema.
 ...
PMID:Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema. 7 Feb 1

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.
 ...
PMID:An evaluation of anticoagulation in glaucoma therapy. 7 Oct 7

An electron-microscopic investigation was conducted to determine the distribution of extracellular materials in the rhesus monkey outflow apparatus at various maintained levels of intraocular pressure. Intraocular pressure was maintained at either 0,8, 15, 22, 30, or 50 mm Hg, by an intracameral needle attached to a reservoir system for a period of 1 h. Thereafter the eyes were fixed either by intracameral perfusion of glutaraldehyde at the appropriate pressure level, or by carotid perfusion of the fixative, or by rapid enucleation and immersion fixation. The electron-dense cationic stains, colloidal thorium and colloidal iron were used to indicate the presence of carbohydrate-rich extracellular materials in the drainage tissues. In the control tissue (15 mm Hg), heavy concentrations of stain were detected within the cores of the trabeculae and in the extracellular spaces of the endothelial meshwork. With pressure elevation there was a progressive decrease in the surface staining on the meshwork cells, an increase in staining intensity within the trabecular cores, and a 'washout' of extracellular materials from the spaces of the endothelial meshwork. The washout was thought to occur via giant vacuoles up to 30 mm Hg, but at 50 mm Hg the process was accelerated by loss of association between the cells of the canal endothelial monolayer. Over the entire pressure range 0 to 50 mm Hg, there was an increase in the staining on the apical surface of the canal endothelium which was associated with a decrease in the incidence of micropinosomes.
 ...
PMID:Pressure effects on the distribution of extracellular materials in the rhesus monkey outflow apparatus. 7 8

The anterior optic nerve and the macular region of the retina of glaucomatous eyes of five rhesus monkeys (Macaca mulatta) have been examined by light and electron microscopy. The experimental glaucoma had been induced by argon laser treatment of the anterior chamber angle. The eyes were examined 3 to 11 weeks after the onset of sustained elevation of intraocular pressure above 20 mm Hg. Severe degenerative changes were seen in eyes with higher intraocular pressure and longer duration of glaucoma. Eyes with a lesser elevation of intraocular pressure and shorter duration of glaucoma showed changes sharply localized to the axon bundles in the scleral lamina cribrosa. Accumulation of mitochondria and dense bodies occurred anterior and posterior to collagenous septae. The location of these changes is in agreement with the localization of block of axoplasmic transport identified by autoradiographic studies. It is speculated that these cytologic changes reflect blockage of axoplasmic flow in the optic nerve of eyes with glaucoma.
 ...
PMID:Axoplasmic flow during chronic experimental glaucoma. 1. Light and electron microscopic studies of the monkey optic nervehead during development of glaucomatous cupping. 8 Nov 92

After acute intraocular pressure (IOP) elevation, an induced disturbance of rapid axonal transport at the optic nerve head began within three hours at the IOP levels tested. The accumulation of radioactive label at the scleral lamina cribrosa increased with time of IOP elevation. There was a 60% decrease in the amount of transported material in the optic nerve, tract, and lateral geniculate body (LGN). Detailed analysis suggests that this decrease is not due to a simple slowdown of transport, but results from a total block of rapid transport in some axons, with no impairment in other axons. This total blockade of rapid transport by elevated IOP in involved axons differs from the apparent slowdown of transport in experimental papilledema, and the difference may explain the response of ganglion cells to the two conditions.
 ...
PMID:Blockade of rapid axonal transport. Effect of intraocular pressure elevation in primate optic nerve. 8 62


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>