Biomedical subjects

M O Tso

Publications and source records attributed to M O Tso.

At least 127 records · Page 7Linked to original sources

PubMed1985

Drusen of the optic nerve associated with retinitis pigmentosa.

Globular excrescences of the optic nerve associated with retinitis pigmentosa have been interpreted as drusen or as astrocytic hamartomas. The histopathologic and ultrastructural findings of globular excrescences of the peripapillary region of the optic nerve associated with retinitis pigmentosa were described in a 22-year-old patient who died in a car accident. From our findings we conclude that the globular excrescences of the optic nerve associated with retinitis pigmentosa are definitely drusen and not astrocytic hamartomas.

Adult↗

PubMed1985

Cellular mechanisms of resolution of drusen after laser coagulation. An experimental study.

Naturally occurring drusen in two eyes of a rhesus monkey resolved after the application to the retina of mild laser coagulation. Clinically, resolution took place approximately nine days following treatment. The cellular mechanism for resolution was observed by light and electron microscopy over a time period of three days to six weeks after treatment. A previously unidentified phagocytic cell, probably derived from the pericyte of the choriocapillaris, was observed to remove drusenoid material after laser photocoagulation. The cell appeared to be analogous to the mesangial cell of the renal glomerulus.

Animals↗

PubMed1985

Fundus lesions in malignant hypertension. I. A pathologic study of experimental hypertensive choroidopathy.

Experimental hypertensive choroidopathy was studied in 29 eyes from 15 monkeys in which accelerated renovascular systemic hypertension developed after a modified Goldblatt procedure. We followed up the animals from five days to 21 months to examine clinically and histopathologically the spectrum of the pathologic process. The pathologic features of hypertensive choroidopathy in our animals may be categorized into three phases: (1) Acute ischemic phase: The initial change in the choroidal vasculature was constriction of arterioles, which leads to focal necrosis of the choriocapillaris and the retinal pigment epithelium and focal subretinal exudate. (2) Chronic occlusive phase: Occlusive changes involving arteries, arterioles, and choriocapillaris occurred later. (3) Chronic reparative phase: With time, recanalization took place at all levels of the choroidal vasculature. The subretinal fluid was reabsorbed, leaving diffuse patchy depigmentation of the retinal pigment epithelium, which followed lobular arrangement of the choriocapillaris. Arteriolization of the choriocapillaris developed; this seems to be a defense mechanism to withstand the elevated systemic blood pressure.

Animals↗

PubMed1985

Fundus lesions in malignant hypertension. II. A pathologic study of experimental hypertensive optic neuropathy.

Accelerated renovascular hypertension produces optic nerve changes ranging from optic disc edema to optic atrophy. To elucidate the pathogenesis of hypertensive optic neuropathy, the optic nerves from 12 monkeys (23 eyes) with accelerated renovascular systemic hypertension were studied by electron and light microscopy. Within 21 months, the animals demonstrated the entire spectrum of pathologic changes. In the optic nerves with optic disc edema, the prelaminar optic nerve exhibited vasoconstriction with subsequent axonal hydropic swelling, axolemma disruption, and glial swelling. In retrolaminar myelinated optic nerve, vasoconstriction was more severe, with endothelial swelling and pericytic degeneration resulting in intramyelinic vacuoles and glial swelling. Optic disc edema appeared to result from axonal hydropic swelling secondary to ischemic infarct, followed by loss of axons and gliosis in the prelaminar optic nerve. The retrolaminar myelinated nerve showed prominent microglial reaction and eventual atrophy of axons and glia. Ischemia seemed to play a major role in hypertensive optic neuropathy, which represents anterior ischemic optic neuropathy.

Animals↗

PubMed1985

Phacoanaphylactoid reaction in persistent hyperplastic primary vitreous.

Three cases of persistent hyperplastic primary vitreous (PHPV) showing a ruptured lens capsule and a phacoanaphylactoid reaction are presented. In two cases, there was evidence that the lens had been clinically clear in the presence of a ruptured capsule and posterior cortical granulomatous reaction. The capsular rupture and granulomatous reaction can begin in utero, as shown by the third case, a premature who died at one day of age. It is suggested that a phacoanaphylactoid reaction can contribute to the lens swelling, cataract, and anterior chamber narrowing which often initiate the downhill course in eyes with PHPV. The immunological implications of this reaction are discussed.

Child↗

PubMed1985

Pathogenetic factors of aging macular degeneration.

In order to explore the pathogenetic factors of aging macular degeneration, risk factors from epidemiologic studies and causative factors from clinical and laboratory studies were reviewed. From the epidemiologic studies, the risk factors of senile macular degeneration included: personal characteristics such as age, sex, race, height, family history, and strength of hand grip; ocular characteristics such as hyperopia, color of iris and senile cataract; and systemic diseases and environmental exposure such as cardiovascular diseases, smoking, lung infections, and chemical exposures. The causative factors suggested from clinical and laboratory studies include: drusen, choroidal vascular diseases, photic injury, and vitamin C deficiency. It is postulated that aging macular degeneration is a multifactorial syndrome. Different etiologic factors may inflict damaging effect on the macula, resulting in a common set of clinical manifestations that are interpreted as aging macular degeneration.

Aged↗

PubMed1985

Cellular deposits on intraocular lenses.

We examined cellular deposits on 14 intraocular lenses (IOL) that were removed after implantation for a variety of clinical reasons. Five of the lenses were cultured to evaluate the growth potential of preexisting cells on the IOLs. The most common cells found were iris pigment epithelial cells. The thickest membranes were probably formed by iris stromal cells. Other cellular deposits included macrophages, multinucleated foreign body giant cells, lens epithelial cells, squamous epithelial ingrowth, red blood cells, uveal melanocytes, and vitreous strands. Cells around the IOL had only limited growth in tissue culture. We propose that a continuous influx of inflammatory cells in conjunction with a disruption of the blood-aqueous barrier may be an important pathogenetic mechanism for the production of thick secondary membranes around an IOL.

Anterior Chamber↗

PubMed1985

The pathophysiology of experimental insulin-deficient diabetes in the monkey. Implications for pancreatic transplantation.

In an 11-year study of experimental insulin-deficient diabetes (IDDM) induced in rhesus monkeys by streptozotocin or total pancreatectomy, the authors have found that pathophysiologic changes occur in eye and kidney, which closely resemble the early stages of human insulin deficient diabetes mellitus (IDDM). In addition, morphologic changes of thickening of glomerular capillary basement membrane and expansion of mesangial matrix (by light microscopy) appear within 3 years of onset of hyperglycemia. However, progression to irreversible complications of advanced diabetic nephropathy or proliferative retinopathy, have not occurred. This animal model resembles human disease in that the animals tend to become ketotic unless maintained with exogenous insulin; C-peptide production is low to absent, and large amounts of glycosylated hemoglobin develop within a month of onset. The monkeys differ from humans in the absence of hypertension and hyperlipidemia. The authors suggest that the abnormalities in basement membrane form and function caused by hyperglycemia form the necessary background upon which other factors, such as hypertension and hyperlipidemia, then act to cause irreversible complications. The role of pancreatic transplantation is in prevention of these background changes.

Animals↗

PubMed1985

The protective effect of ascorbate in retinal light damage of rats.

Cyclic light and dark-reared rats were exposed to intense visible light for various periods and then rhodopsin-measured following recovery in darkness for up to 14 days. Animals were injected with ascorbic acid or ascorbate derivatives at various doses prior to light exposure in green Plexiglas chambers. The results show that ascorbic acid administration elevates retinal ascorbate and reduces the loss of rhodopsin and photoreceptor cell nuclei resulting from intense light. When given in comparable doses, L-ascorbic acid, sodium ascorbate, and dehydroascorbate were equally effective in preserving rhodopsin. The ascorbate protective effect in the retina is also dose dependent in both cyclic light and dark-reared rats and exhibits a requirement for the L-stereoisomer of the vitamin. Ascorbic acid is effective when administered before, but not after, light exposure, suggesting that protection from light damage in the retina occurs during the light period. In some experiments, rod outer segments were isolated from rats immediately after light exposure, lipids extracted, and fatty acid composition determined. As judged by the preservation of rod outer segment docosahexaenoic acid in rats given ascorbate, the vitamin may act in an antioxidative fashion by inhibiting oxidation of membrane lipids during intense light.

Animals↗

PubMed1985

Amelioration of photic injury in rat retina by ascorbic acid: a histopathologic study.

It has been postulated that ascorbic acid may help to protect the retina from oxidative insult by light. To confirm this hypothesis, the authors compared light-damaged retinas of rats with or without ascorbate supplement by morphologic and morphometric studies at different time periods after light exposure. No dramatic morphologic differences were observed in the photoreceptor-retinal pigment epithelium complex between the two groups six hr after light exposure to 200 to 250-foot candles of visible light. Six to 13 days after 24 hr of exposure, the retina of rats that received ascorbate supplement showed significantly less severe damage than the retina of unsupplemented rats. The superior and temporal quadrants of the retina appeared to be most susceptible to the light damage when comparing rats with or without ascorbate supplement. These findings suggested that ascorbate ameliorates the photic injury in rat retina.

Animals↗

PubMed1984

Argon laser-induced cataract. A clinicopathologic study.

A patient with diabetic retinopathy and senile anterior cortical and nuclear cataract was treated with argon laser photocoagulation of the fundus. During the treatment, white ovoid opacities appeared in the lens cortex, extending into the nucleus. They remained nonprogressive for five weeks, when cataract extraction was performed. The lens was studied by light and electron microscopy. The lenticular opacities contained rows of damaged, spindle-shaped lens fibers, with laminated cellular debris and clear spaces. We compared the unique features of the laser-induced lenticular lesions with the senile cataractous changes in the same crystalline lens.

Argon↗

PubMed1984

Vitrectomy and Whipple's disease.

We diagnosed Whipple's disease from the vitreous aspirate of two patients who underwent vitrectomies . In one case, the vitrectomy specimen would have indicated the diagnosis three years before the jejunal biopsy was performed had the appropriate PAS stain been used. In the second case, the PAS-positive macrophages were identified at the time of surgery.

Biopsy↗

PubMed1984

Coloboma of optic nerve associated with serous maculopathy. A clinicopathologic correlative study.

A rhesus monkey with a congenital coloboma of the optic nerve head associated with serous macular detachment underwent intravenous (IV), intrathecal, and retrobulbar fluorescein angiography. No fluorescein leaked beneath the serous detachment after IV or intrathecal injection, although the retrobulbar injection caused a bolus to extravasate from the margin of the optic nerve coloboma, drifting toward the macular region temporally. Histopathologically, glial tissue replaced optic nerve axonal bundles in the temporal coloboma. The intermediary tissue of Kuhnt was disrupted, and fluid from the retrobulbar space diffused into the subretinal space temporally, where a localized retinal detachment extended from the optic nerve to the macula. Subretinal fluid in the macula associated with optic nerve coloboma might derive from (1) fluid perfusing into the retrobulbar space from surrounding orbital tissue, (2) peripapillary choriocapillaris, or (3) CSF.

Animals↗

PubMed1984

Effects of chronic intracameral injections of chondroitin sulfate on cat eyes.

The effect of chondroitin sulfate on the metabolism of trabecular meshwork was studied by repeatedly injecting a chondroitin sulfate solution into the anterior chamber of cat (experimental) eyes for 28-29 weeks. The aqueous humor of the opposite (control) eyes were similarly replaced with a phosphate-buffered saline-glucose solution. The intraocular pressure of the experimental eyes was increased 4-7 mm Hg above that of the control eyes for a prolonged period of time. In addition, collagen fibers, elastic fibers, and basement membrane-like material were moderately increased in the trabecular meshwork of experimental eyes. Three forms of thickened basement membranes of endothelial cells were observed. The compact multilaminated basement membrane was formed concentrically around some of the trabecular beams. The discontinuous, thin basement membrane was seen among bundles of coarse collagen in association with long spacing collagen fibers. Also, fine filaments were noted streaming from the plasma membrane and basement membrane of endothelial cells of angular aqueous veins. Chondroitinase ABC was able to remove ground substance in the elastic fiber of the trabecular meshwork. Biochemically, the chamber angle tissues from these eyes showed a higher synthetic activity of glycosaminoglycans and proteins. Chondroitin sulfate appears to have a direct effect on trabecular meshwork and can influence the physiologic function of these cells.

Animals↗

PubMed1984

Effects of chondroitin sulfate on trabecular meshwork in rabbit eyes: an electron microscopic study.

The intraocular pressure of four New Zealand albino rabbit eyes was elevated when we replaced the aqueous humor of these eyes repeatedly with a chondroitin sulfate solution. Seen by electron microscopy, the trabecular meshwork of these eyes showed moderately increased collagen fibers, elastic fibers, and fine fibrils, and thickening of basement membrane. The amount of extracellular material present was markedly increased when compared with control eyes. Three types of basement membranes were noted. Compact multilaminated basement membrane and placoid accumulations of filamentous material with a granular background were found adjacent to the endothelial cells of the trabecular meshwork, and fine fibrils were observed around the angular aqueous veins. The ultrastructural alterations we observed were similar to those seen in some human glaucoma cases. The metabolism of trabecular meshwork cells may be affected by the long-term chondroitin sulfate treatment. As a result, extracellular matrix material appears to be accumulated in the trabecular meshwork, which may then contribute to an increased outflow resistance and a mild intraocular pressure elevation.

Animals↗

PubMed1984

Effects of chondroitin sulfate on metabolism of trabecular meshwork.

Glycosaminoglycans are believed to play a role in the physiological functions of trabecular meshwork. The effects of chondroitin sulfate on the metabolism of trabecular meshwork were studied by replacing the aqueous humor in the right eye (experimental eye) of 12 albino rabbits with 0.3 ml of chondroitin-4-sulfate solution (10 mg ml-1 in glucose-supplemented phosphate buffered saline). The aqueous humor in the left eye (control eye) was replaced with the phosphate buffered saline-glucose solution in the same manner. The intracameral procedures were performed twice a week for four weeks (initial injection period), and then discontinued for another four weeks (resting period). No significant or prolonged increase in the intraocular pressure was observed during either period in any eyes. Subsequent intracameral injections performed after the resting period, however, caused an intraocular pressure elevation in 10 of the 12 experimental eyes. During this second injection period, the injections were carried out whenever the intraocular pressure of experimental eyes dropped to the control value. The pressure generally remained 5-10 mmHg above that of the control eyes for periods ranging from two days to four weeks. In the eyes with elevated intraocular pressure, light microscopy showed that the trabecular beams were compact and sclerotic and the intertrabecular spaces were narrower. Chamber angle tissues obtained from the eyes with elevated intraocular pressure incorporated more radioactive precursors into glycosaminoglycans than those from the control eyes. The synthesis of glycosaminoglycans and the metabolism of trabecular meshwork seemed to be modified by the long-term chondroitin sulfate treatment.

Animals↗

PubMed1984

Animal modeling of cystoid macular edema.

Primate models of cystoid macular edema (CME) were developed along four sets of presumed primary causative factors: 1) disruption of the blood-retinal barrier at the retinal vasculature and the retinal pigment epithelium; 2) ischemic tissue injury with cyst formation; 3) intraocular events frequently observed in patients with CME, such as inflammation, ocular hypotony, and vitreous traction; and 4) the probable additive effect on the macula by systemic diseases such as diabetes mellitus and systemic hypertension. While each experiment produced some aspects of CME in the human, none gave the complete picture. It is concluded that CME is the final common pathway of a multifactorial syndrome.

Animals↗

PubMed1984

Chronic lead administration in neonatal rats: electron microscopy of the retina.

The morphologic effects on the retina resulting from chronic lead exposure were assessed in neonatal rats. Newborn rats nursed from dams were given a low (0.115%) or a high (4.5%) concentration of lead in their diet. At day 21 the pups were weaned to the mother's diet. The retinas of the pups were studied by electron microscopy at various ages up to day 60. High and low lead concentrations produced necrosis of photoreceptor cells and cells of the inner nuclear layer. The high lead concentration, in addition, was associated with swelling of endothelial cells of the retinal vessels and narrowing of the lumen. Increased permeability of the retinal vessels and pigment epithelium to horseradish peroxidase was also observed under the high-dose condition. The authors conclude that lead can produce direct neuronal damage and, at high doses, produces retinal vascular lesions and alteration of the blood-retinal barrier.

Animals↗