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Biomedical subjects

S J Ryan

Publications and source records attributed to S J Ryan.

At least 199 records · Page 11Linked to original sources
PubMed1982

Subretinal neovascularization. Natural history of an experimental model.

The disciform response is characterized bu its many manifestations determined by subretinal neovascularization. Many advances have been made clinically and with histopathologic correlation, but a clear understanding of the pathogenesis of subretinal neovascularization has not yet been achieved at the basic level. The need to determine the pathogenesis and understand the rationale for therapy argues strongly for the development of a suitable experimental model of subretinal neovascularization. The macula is much more predisposed to the development of subretinal neovascularization than is the area nasal to the nerve head or the periphery. Spontaneous hemorrhages in experimentally induced subretinal neovascularization occurred, underscoring the clinical relevance of this model system. The delineation of the natural history in this report provides the basis for future morphologic correlations and subsequent manipulations of this model system.

Animals↗
PubMed1982

Blood-retinal barrier after blunt trauma to the eye.

The competence of blood retinal barrier at the level of retinal pigment epithelium (RPE) and retinal capillaries was studied 30 min, 24 h, 3 days, and 7 days after experimental blunt eye injury in the pig, using horseradish peroxidase (HRP). Leakage of HRP into the outer retinal layers was observed in association with disrupted RPE in the first three days after injury. No HRP leakage was seen 7 days after the trauma and the retinal vessels remained competent throughout the study. It is suggested that extracellular edema occurs in the early stages of commotio retinae due to the disruption of blood retinal barrier at the level of the RPE.

Animals↗
PubMed1982

A comparison of different cellular inocula in an experimental model of massive periretinal proliferation.

We modified a preexisting experimental model of massive periretinal proliferation by injecting cells of differing origins into the rabbit vitreous cavity. These cells included autologous and homologous fibroblasts, homologous chondrocytes, homologous retinal pigment epithelial cells, heterologous bovine endothelial cells, and heterologous murine embryonal cells. All cell injections caused vitreous and retinal membrane formation that resulted in a process similar to massive periretinal proliferation. Clinically the character of the membranes formed and the time course in the development of traction retinal detachments was similar for all the different cell types. The initial cell dosage injected was the critical factor in determining the severity of the traction retinal detachments leading to massive periretinal proliferation.

Animals↗
PubMed1982

The role of cellular proliferation in an experimental model of massive periretinal proliferation.

Transplantation of from 10,000 to 750,000 autologous and homologous dermal fibroblasts into the vitreous cavity of rabbit eyes resulted in identical clinical findings leading to massive periretinal proliferation. A dose-response relationship between the number of cells injected and the extent of retinal traction that developed was established. The second phase of the experiment evaluated the effects of formalin and cobalt irradiation on the fibroblasts' ability to cause traction retinal detachment. Cell proliferation or the attainment of a critical mass of living cells was necessary for the development of traction retinal detachment.

Animals↗
PubMed1982

Combined posterior contusion and penetrating injury in the pig eye. II. Histological features.

The main histological features observed after an experimental posterior contusion injury in the pig eye were haemorrhage from the choroidal vessels into the subretinal space and into the vitreous, uveal vessel dilatation, and an inflammatory reaction. These changes resolved during the first 2 weeks, and the subretinal haemorrhage was replaced by a fibrocellular membrane. The addition of a posterior penetrating injury resulted in fibrocellular proliferation at the wound site 6 days after injury and in formation of vitreoretinal traction membranes and subsequent traction retinal detachment. Posterior vitreous separation did not occur.

Animals↗
PubMed1982

Vascular casts of experimental subretinal neovascularization in monkeys: a preliminary report.

Experimental subretinal neovascularization (SRN) was produced in rhesus monkeys by laser burn and its vascular casts were examined with the scanning electron microscope (SEM). The results showed a vascular pattern similar to that seen in fluorescein angiography, but provided a three-dimensional vascular architecture, which is not detectable by angiography. The SRN represents an ingrowth of new vessels into the subretinal space from the choroid through each burn site. Special attention was given to the afferent and efferent vessels of the SRN frond. The frond was supplied by the choroidal arteriole and the routes of egress from the frond to the choriocapillaris were observed. These observations suggest the uniformity of this experimental SRN, i.e., arteriolar supply to the frond and drainage to the choriocapillaris around the burn sites.

Animals↗
PubMed1982

Pars plana vitrectomy entry sites.

The histological features of vitrectomy entry sites were studied in a group of monkeys following pars plana vitrectomy for experimental posterior penetrating injury. The extent of fibrocellular proliferation and vitreo-retinal complications arising from the vitrectomy wounds were compared to the proliferation from a much larger penetrating trauma site after complete and partial (core) vitrectomies. Although scarring and complications were more severe following core vitrectomy, there was little difference on histological examination between fibrocellular proliferations from the vitrectomy entry sites and from the penetrating wound.

Animals↗
PubMed1981

Vitrectomy in penetrating eye injury. Results of a controlled trial of vitrectomy in an experimental posterior penetrating eye injury in the rhesus monkey.

A controlled trial of pars plana vitrectomy for posterior penetrating eye injury was done in rhesus monkeys. After standard injury, each eye was allocated randomly into a treatment or control group. Treatment groups (ten eyes each) had vitrectomy at 1, 14, or 70 days after injury. The control group had 15 eyes. The same techniques were employed as in human eyes. Surgical objectives were lensectomy, then complete posterior vitrectomy and excision of the anterior vitreous to within 1 or 2 mm of the surface of the peripheral retina and pars plana. Results from this controlled trial provide strong support for the effectiveness of vitrectomy techniques in managing selected posterior penetrating injuries in human eyes and in preventing the complication of traction retinal detachment.

Animals↗
PubMed1981

Traction retinal detachment. A cell-mediated event.

In posterior-segment penetrating injuries, the role of cellular and extracellular structures for the development of fraction retinal detachment is a matter of controversy. With the use of immunofluorescence techniques, we studied the cellular components of intravitreal membranes, with particular attention to the presence of intracellular contractile proteins. Our results demonstrate increasing concentrations of intracellular actin filaments in 12- to 21-day-old membrane specimens at the time when traction retinal detachment is most likely to occur in the rabbit eye. The sequence of events reflects the same process that occurs in the wound-healing response throughout the body. The specialized anatomy of the eye, particularly the vitreoretinal relationship at the vitreous base, accounts for the disastrous consequence of fraction retinal detachment.

Actins↗
PubMed1981

Mechanisms in traction retinal detachment.

We have developed a reproducible model of traction retinal detachment in the rhesus monkey secondary to a penetrating eye injury. The model is characterized histologically by intravitreal fibroblastic proliferation and by epiretinal and by retroretinal membranes. Cells proliferating within the vitreous and in the epiretinal membranes have the ultrastructural characteristics of myofibroblasts. The presence of these contractile cells suggests that vitreous traction and the contraction of epiretinal membranes may be cell mediated. Our findings suggest that the pathophysiology of traction retinal detachment has many features in common with the normal process of wound healing and in particular with the mechanisms responsible for wound contraction and cicatrization.

Animals↗
PubMed1980

Bright-flash electroretinography and vitreous hemorrhage. An experimental study in primates.

Serial, bright-flash electroretinograms (ERGs) were recorded from rhesus monkey eyes before and after a standard posterior penetrating ocular injury and injection of 0.5 mL of blood into the vitreous. This procedure resulted in a progressive depression to virtual nonrecordability of the ERG during a period of several weeks, owing to a combined progressive increase in optical density and loss of retinal function. The ERG depression, however, was reversible, showing a remarkable recovery during the subsequent four to eight weeks. These findings suggest that in the presence of a recent, massive vitreous hemorrhage, a nonrecordable bright-flash ERG does not necessarily indicate a permanent loss of retinal function.

Animals↗
PubMed1980

The disciform response: an historical perspective.

This paper is a survey of the literature in an attempt to provide the basis for our current understanding of the disciform process. Particular emphasis is placed on its pathogenesis and the role of subretinal neovascularization. No two lesions appear exactly alike because of the many stages and combinations possible. Gass (1967) has delineated the broad spectrum with the many different clinical manifestations of this disease process. Verhoeff and Grossman (1937) provided the histopathologic basis for our understanding of the disciform process. The histologic correlation of the clinical "predisciform" state would seem to offer the most promising information for understanding the pathogenesis of the disciform process (Frank et al. 1973; Green and Key 1977; Kornweig 1967; Sarks 1973 and 1976; Small et al. 1976; Zauberman 1970). It is hoped that this literature review has sufficiently emphasized the inherent deficiencies of strictly clinical studies and the need for an appropriate experimental animal model (Ryan 1979).

Aged↗
PubMed1980

Enzymatic and mechanically induced subretinal neovascularization.

Mechanical and enzymatic disruption of Bruch's membrane and induction of subretinal neovascularization in an experimental primate model have produced limited success. The methods and results are reported here to identify some problems encountered in methodology and to detail the results of this approach to subretinal neovascularization.

Animals↗
PubMed1980

Subretinal neovascularization after argon laser photocoagulation.

An investigation has been conducted to test different theories relating to the pathogenesis of the disciform response. Considered an important first step in this systematic study, a reproducible model of subretinal neovascularization in an experimental primate model has been developed. The following report describes the methodology, clinical appearances, and results including histopathologic and electron microscopic correlation. This experimental model has served as a useful mechanism for testing the roles of breaks in Bruch's membrane, ischemia, hemorrhage, the inflammatory response, and position in relation to the center of the vascular free zone as important factors in the development and evolution of subretinal neovascularization.

Animals↗
PubMed1980

Birdshot retinochoroidopathy.

Thirteen patients had a new syndrome and entity in intraocular inflammation called birdshot retinochoroidopathy, which was characterized by a white, painless eye with minimal anterior segment inflammation but particulate debris in the anterior and posterior vitreous. There was profuse retinal vascular leakage with resultant retinal, macular, and disk edema, which are the primary causes of the decreased vision in this syndrome. Long-term follow-up (mean of ten years) revealed that only two patients seemed to respond to anti-inflammatory therapy (systemic corticosteroids) and five patients progressed to 6/60 (20/200) or less visual acuity in at least one eye.

Adrenal Cortex Hormones↗
PubMed1980

Ultrastructure of traction retinal detachment in rhesus monkey eyes after a posterior penetrating ocular injury.

We studied the ultrastructural characteristics of an experimental model of traction retinal detachment secondary to a penetrating eye injury in the rhesus monkey. Cells with the characteristics of myofibroblasts were present in the intravitreal fibrous tissue and in epiretinal membranes. These cells were probably derived from many sources, and were capable of contraction through the mechanism of intracytoplasmic contractile proteins such as actin or myosin. The morphologic observations supported our hypothesis that traction retinal detachment is a cell-mediated event analogous to the processes of wound healing and wound contraction. The force of contraction is mediated by cell-to-cell and cell-to-vitreous connections and by glial bridges that connect epiretinal membranes to the retina. These ultrastructural studies, which provide insight into the pathogenesis of traction retinal detachment in the experimental animal model, may well have significant clinical relevance.

Animals↗