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R L Radius

Publications and source records attributed to R L Radius.

At least 37 records · Page 2Linked to original sources
PubMed1981

Pressure-induced optic nerve axonal transport interruption in cat eyes.

After intravitreal injection of tritiated leucine, optic nerve axonal transport was studied in 30 cat eyes by tissue radioautography. Twenty-five experimental eyes were examined after four hours of acute pressure elevation with perfusion pressures maintained at 20 to 70 mm Hg. In five control specimens, intraocular pressures were maintained at 10 mm Hg for the four-hour interval. The extent of leucine accumulation, as seen by radioautographs, was inversely proportional to the perfusion pressure. Accumulation was limited to the region fo the lamina cribrosa. The anatomic distribution and pressure response of this transport interruption were similar to those seen in primate eyes studied under similar conditions.

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PubMed1981

Morphology of axonal transport abnormalities in primate eyes.

The ultrastructure of the retina and optic nerve head was studied in primate eyes after central retinal artery occlusion. Within 2 hours of the vascular occlusion the inner retinal layers undergo watery (isosmotic) swelling. This watery swelling of axons and astroglia extends into the nerve head as far back as the anterior boundary of the scleral lamina cribrosa. The swelling is increased 4 hours after the occlusion, and by 24 hours disintegration has occurred. At the optic nerve head mitochondria and vesicles of smooth endoplasmic reticulum begin to accumulate within 2 hours. The accumulation increases at 4 hours and persists to 24 hours. The watery swelling seems characteristic of ischaemic axons. Membranous organelles accumulate at the boundary of an ischaemic zone when material carried by axonal transport is brought via the healthy axon segment to the boundary, but they cannot proceed further into the ischaemic zone. Such accumulation is typical of locations where rapid orthograde axonal transport or retrograde axonal transport is blocked. In contrast, when slow axonal flow is impaired, the swelling is characterised by an excess of cytoplasmic gel without a marked accumulation of organelles. Rapid orthograde transport and retrograde transport seem to be closely related to one another, while slow axoplasmic flow seems fundamentally different. From morphological findings we suspect that, in experimental glaucoma, intraocular pressure first affects the intracellular physiological process of rapid orthograde and retrograde axonal transport. Watery swelling may not occur unless the ischaemic injury to cell metabolism is more advanced. In contrast, in experimental papilloedema, the swelling results predominantly from impaired slow axoplasmic flow.

Animals↗
PubMed1981

Anatomy of the retinal nerve fiber layer.

Anatomy of the retinal nerve fiber layer in rabbit eyes is studied by light microscopy, transmission electron microscopy, and scanning electron microscopy. It is demonstrated that retinal striations noted ophthalmoscopically in these eyes represent individual fiber bundles, Axon bundles are compartmentalized within tissue tunnels comprised of elongated processes of glial cell origin.

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PubMed1980

Thickness of the retinal nerve fiber layer in primate eyes.

Thickness of the retinal nerve fiber layer is studied in the eyes of three primate species. Measurements are made at various points throughout the fundus, including the peripapillary, arcuate, macular (area centralis), equatorial, and peripheral parts of the retina. Anatomic findings are compared with the clinical appearance of retinal light reflexes in these way. It is proposed that the nature of this light reflex is, in part, determined by the thickness of the retinal nerve fiber layer.

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PubMed1980

Optic nerve fast axonal transport abnormalities in primates. Occurrence after short posterior ciliary artery occlusion.

Fast axonal transport abnormalities in primate (Aotus trivirgatus) optic nerve were studied in ten eyes at various intervals after occlusion of the lateral short posterior ciliary circulation. Evidence of focal axonal ischemia, as indicated by swelling of mitochondria and dissolution of cytoplasmic detail, was noted as early as one hour after occlusion. Accumulation of mitochondria, microvesicles, and dense bodies, indicating focal interruption of axonal transport mechanisms, was noted in eyes examined at 2, 4, and 6 hours. This accumulation of organelles was limited to the region of the lamina cribrosa. Nerve head abnormalities were not seen in two eyes studied at two weeks.

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PubMed1980

Aqueous humor changes after experimental filtering surgery.

We studied aqueous humor of rhesus and owl monkeys for its effect on the growth of subconjunctival fibroblasts in tissue culture. Aqueous humor samples obtained before glaucoma surgery inhibited the initiation of growth of fibroblasts. However, postoperative aqueous humor samples supported growth of fibroblasts. The change in aqueous humor physiology lasted for up to two months after glaucoma surgery. Our study indicated that possibly material added to the postoperative aqueous humor inactivates an inhibitor normally present in primary aqueous humor. An alternative explanation would be that primary aqueous humor, in contrast to secondary aqueous humor, lacks sufficient nutrient material to support fibroblast growth in tissue culture.

Animals↗
PubMed1980

Histopathology in the iris-nevus (Cogan-Reese) syndrome.

A 23-year-old-woman had iris-nevus (Cogan-Reese) syndrome characterized by unilateral glaucoma with peripheral anterior synechiae, multiple iris nodules, and ectopic Descemet's membrane. A surgical specimen excised from the involved eye was examined by light and electron microscopy. A cuticular membrane covered both the anterior and posterior surfaces of the iris in this specimen. On the anterior surface of the iris, many projections of apparently normal iris stroma pierced or were surrounded by this membrane. On the posterior surface of the iris, this membrane was associated with a monolayer of cuboidal cells.

Adult↗
PubMed1980

Failure of unilateral carotid artery ligation to affect pressure-induced interruption of rapid axonal transport in primate optic nerves.

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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PubMed1980

Fast axonal transport in early experimental disc edema.

Previous work has documented impairment of slow axonal transport in papilledema, but the abnormalities in rapid transport were less certain. Therefore fast axonal transport was studied in 19 primate eyes subjected to ocular hypotony for 6 to 72 hr following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling was apparent. These changes in fast transport mechanisms in cases of nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Furthermore, since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema and, moreover, since previous data shows a "slowdown" rather than complete blockade of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete flock of axonal transport. Therefore we hypothesize that the swelling results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.

Animals↗
PubMed1980

Breakdown of the normal optic nerve head blood-brain barrier following acute elevation of intraocular pressure in experimental animals.

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.

Animals↗
PubMed1980

Distribution of albumin in the normal monkey eye as revealed by Evans blue fluorescence microscopy.

Since intravenously injected Evans blue binds irreversibly to serum albumin, its distribution reflects albumin exchange between the intravascular and extravascular tissue compartments. In histologic specimens examined by fluorescence, microscopy, extravasated Evans blue--albumin complex was identified within the ciliary body and trabecular meshwork of normal monkey eyes. In eyes fixed by intra-arterial perfusion of fixative, no dye was identified in the choroid, retina, or optic nerve. With immersion fixation, however, some extravasation was seen in the choroid and adjacent optic nerve. In some specimens, the optic nerve was stained not only with material apparently leaking from the choroid but also from a breakdown of the blood-brain barrier in the major disc vasculature during the interval before fixative penetrates into the tissue. Perfusion fixation must be used to avoid this artifact, and freezing techniques would be even better.

Animals↗
PubMed1979

The mechanism of disc pallor in experimental optic atrophy. A fluorescein angiographic study.

Ascending optic atrophy was produced in 13 eyes of owl monkeys (Aotestrivirgatus) by retinal photocoagulation. Color fundus photography and fluorescein angiography were used to study and document the evolution of nerve head abnormalities. The optic nerve heads were also studied histopathologically. Except in certain instances of early transient (relative) filling defects, normal disc fluorescent patterns were preserved, despite clinically apparent optic nerve head pallor. Sectorial defects did not persist into the later phases of the angiogram. These findings may suggest a reduced blood flow, but neither angiographic nor histopathologic studies detected a reduced vascularity in the atrophic optic nerve. Pallor of the optic nerve head seems to result from alterations in the tissue reflectance and translucency following axonal loss and glial reorganization rather than from a decreased microvascular bed.

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PubMed1979

The histology of retinal nerve fiber layer bundles and bundle defects.

The fiber bundle striations recognized clinically in normal monkey eyes appear to be bundles of axons compartmentalized within glial tunnels formed by Müller's-cell processes, when viewed histologically. The dark boundaries that separate individual bundles are the broadened foot endings of these cells near the inner surface of the retina. Within one week after focal retinal photocoagulation, characteristic fundus changes could be seen in experimental eyes. In histologic sections of the involved retina, there was marked cystic degeneration of the retinal nerve fiber layer. Within one month, atrophy of distal axon segments was complete. With the drop-out of damaged axons and thinning of individual fiber bundles, retinal striations became less prominent. The resulting fundus picture in these experimental eyes is similar to fiber bundle defects that can be seen clinically in various neuro-ophthalmic disorders.

Animals↗
PubMed1979

The course of axons through the retina and optic nerve head.

By identifying degenerating axons in tissue specimens from 22 primate eyes, it was possible to demonstrate the normal course of axon fibers. Nerve fiber bundles from a group of retinal ganglion cells travel together with little tendency to disperse laterally. In addition, axons are stratified such that processes from more central ganglion cells are successfully added to the inner strata of the retinal nerve fiber layer. Within and behind the lamina cribrosa, areas of degeneration following retinal photocoagulation were well circumscribed and confined to a group of adjacent axon bundles. This degree of retinotopic organization of axons within the nerve head and retinal fiber layer is believed to be consistent with the premise that isolated lesions within the lamina cribrosa could cause well-organized paracentral scotomas such as those characteristic of early glaucoma.

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PubMed1978

Timolol. A new drug for management of chronic simple glaucoma.

Timolol maleate, a potent beta-adrenergic antagonist, reduces intraocular pressure in rabbits. With topical application in one eye, a significant reduction in pressure is seen in the contralateral, untreated eye also. When used in conjunction with timolol, other adrenergic amines, such as norepinephrine and epinephrine, produce an additional hypotensive response. On the other hand, pretreatment with timolol does inhibit the ocular hypotensive response to topically applied albuterol. No further reduction in pressure is seen after application of this beta-adrenergic agonist to eyes pretreated with timolol. In a double-blind study with patients who had previously been receiving various medications for control of elevated intraocular pressures, timolol was as effective as pilocarpine in reducing intraocular tension. Many common complaints associated with pilocarpine therapy, including miosis, ocular irritation, and blurred vision, were not encountered with timolol therapy.

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