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Biomedical subjects

B D Srinivasan

Publications and source records attributed to B D Srinivasan.

34 records · Page 2Linked to original sources

Polymorphonuclear leukocyte response. Inhibition following corneal epithelial denudation by steroidal and nonsteroidal anti-inflammatory agents.

Topically administered nonsteroidal anti-inflammatory drugs (NSAID), indomethacin (0.5%), flurbiprofen (0.01%), and aspirin (0.5%), as well as the steroidal anti-inflammatory drug 1% prednisolone acetate but not dexamethasone (0.1%) or fluorometholone (0.1%) inhibited the acute polymorphonuclear leukocyte (PMN) response following partial and complete corneal de-epithelialization. Intraperitoneal doses of indomethacin (100 mg/kg), flurbiprofen (100 mg/kg), and aspirin (600 mg/kg) inhibited the PMN response after partial de-epithelialization, but only indomethacin (100 mg/kg) inhibited the PMN response following complete corneal de-epithelialization. Conjunctival prostaglandin biosynthesis was inhibited effectively at these doses by indomethacin and flurbiprofen. These results suggest that indomethacin is more consistent than either flurbiprofen or aspirin in blocking the PMN response following partial or complete epithelial denudation. However, topical applications of flurbiprofen is 50 times more potent than indomethacin in blocking the PMN response and partial corneal denudation.

Administration, Topical↗

Anti-inflammatory effects of betamethasone phosphate, dexamethasone phosphate and indomethacin on rabbit ocular inflammation induced by bovine serum albumin.

Following the induction of immunogenic uveitis betamethasone and dexamethasone reduced conjunctiva and iris hyperemia and aqueous flare. Indomethacin reduced iris hyperemia, but potentiated conjunctival hyperemia. All three agents inhibited the increase in the protein content of the aqueous that follows induction of immunogenic uveitis. Betamethasone was slightly more potent than dexamethasone and indomethacin. White cell entry into the aqueous was inhibited by betamethasone and dexamethasone. Paradoxically, however, indomethacin significantly potentiated the number of polymorphonuclear leukocytes (PMNs) entering the aqueous. The anti-inflammatory effects of steroidal agents may be due to the inhibition of the release of arachidonic acid (AA) which is a precursor of both lipoxygenase and cyclooxygenase products. The potentiation of the PMN response by indomethacin in immunogenic uveitis may be due to an inhibition of cyclooxygenase product formation and a facilitation of lipoxygenase products (which are potent chemotactic agents) from AA.

Animals↗

The effect of steroidal and nonsteroidal anti-inflammatory agents on corneal re-epithelialization.

Topical 0.5% indomethacin, 0.01% flurbiprofen, 1% prednisolone acetate, 0.1% dexamethasone, or 0.1% fluorometholone pretreatment and daily instillation did not affect the course of re-epithelialization after partial corneal epithelial denudation. However, topical 1% prednisolone acetate, 0.1% dexamethasone, and 0.1% fluorometholone--but not 0.5% indomethacin and 0.01% flurbiprofen--significantly retarded re-epithelialization after complete corneal denudation.

Animals↗

The role of arachidonic acid metabolites in the mediation of the polymorphonuclear leukocyte response following corneal injury.

The immediate polymorphonuclear leukocyte (PMN) response in the tear fluid was investigated following five different types of corneal injury. All injuries produced significant amounts of PMNs in the tear fluid within the first 6 hr of injury. Histological examination of injured corneas demonstrated that PMNs were attached to the denuded surface but were unable to attach to intact epithelium. Topical arachidonic acid, prostaglandin (PG) PGE1 and PGE2, and prostacyclin (PGI2) induced the arrival of PMNs into the tear fluid of normal rabbit eyes, but topical PGF2 alpha, PG-6-keto-PGF1 alpha, and thromboxane did not elicit a PMN response from normal conjunctiva. Tear fluid samples 2 to 4 hr following corneal epithelial denudation demonstrated PGE-type activity. Pretreatment with topical (0.05% and 0.5%) and intraperitoneal (i.p.) indomethacin (100 mg/kg) markedly inhibited the PMN response following partial corneal epithelial denudation. However, an i.p. dose of 5 mg/kg indomethacin potentiated the tear fluid PMN response following corneal injury. The inhibition of the PMN response by indomethacin suggested that arachidonic acid metabolites may be involved in the mediation of PMN chemotaxis following corneal injury.

Animals↗

Giant papillary conjunctivitis with ocular prostheses.

In seven patients who each had either a methyl methacrylate corneal shell, a postenucleation ocular prosthesis, or a keratoprosthesis, giant papillary conjunctivitis of the tarsus of the upper lids developed after prolonged wear. These cases expand the spectrum of disease that was initally described in wearers of hard and soft contact lenses. The papillary changes in prostheses wearers did not always produce symptoms and were not readily reversible. Basophils and mast cells characterized the inflammatory infiltrate, suggestng an antigen-antibody mechanism underlying the response. Increased production of epithelial mucin, in contrast to goblet cell mucin, may play a role in producing symptoms in this syndrome.

Adolescent↗

Vitreous wick syndrome.

A 67-year-old man had vitreous wick syndrome after an uncomplicated intracapsular cataract extraction with a sector iridectomy in the left eye. The intraocular infection cleared with antibiotic therapy including intravitreal antibiotic injection, but a residual anterior cyclitic membrane and shallow anterior chamber persisted. An anterior vitrectomy was performed later in the course of treatment after the intraocular infection subsided, to relieve the shallow anterior chamber, prolonged hypotony, and ciliary body detachment. Final visual acuity was 6/15+(20/50+) in the left eye.

Aged↗

Recurrent herpetic angular blepharitis in an adult.

A 36-year-old man had several episodes of left angular blepharoconjunctivitis associated with upper respiratory infections, herpes labialis, or emotional stress. The clinical diagnosis had always been a blepharitis of bacterial origin. During the last attack, cytologic examination of a scraping obtained from an eyelid pustule vesicle revealed multinucleated keratinocytes, diagnostic of a herpetic infection. Virologic studies proved that herpes simplex virus type 1 was the causal agent.

Adult↗

Epibulbar mucogenic subconjunctival cysts.

Two patients had freely movable epibulbar subconjunctival cysts that occurred in the absence of trauma, inflammation, and infection. Histopathologic examination of these cysts revealed them to be linked by nonkeratinizing epithelial cells and goblet cells. The cysts had little or no stroma and contained PAS-positive mucoid material. Electron microscopy of adjacent conjunctiva indicated that the epithelial cells were actively producing mucous granules and did not form many hemidesmosomes. The mechanical displacement of epithelial cells, as well as their mucous-producing ability, probably contribute to cyst formation. The relative lack of hemidesmosomes may explain why these cysts are freely movable.

Aged↗

Electron microscopy of epithelial downgrowth.

Four cases of epithelial downgrowth following cataract surgery were studied by electron microscopy. The invading epithelium was excised by posterior keratectomy, iridectomy, and vitrectomy. Diagnostic photocoagulation on the iris was performed before the operations in all cases. Multilayered epithelium on these tissues showed ultrastructural features similar to conjunctival epithelium, and in the cornea no intact endothelial cells were identified. A subepithelial connective tissue of varying grades of development was present between the downgrowth epithelium and Descemet's membrane. The basal epithelial cells on the vitreous contained numerous dense granules, and a thick basement membrane-like layer was found underneath. Changes attributable to photocoagulation included partial replacement of the iris pigment epithelium with macrophages, degeneration of blood vessels, and marked swelling and dissociation of collagen fibrils in the iris stroma due to splitting into longitudinal filamentous components. Identical changes of collagen fibrils could be reproduced in the rabbits iris after experimental photocoagulation.

Aged↗

Ultrastructural variation in granular dystrophy of the cornea.

Corneal deposits of granular dystrophy were studies in six corneas from five patients. Two additional corneas from two patients with lattice dystrophy were used for comparison. The diagnoses were confirmed by light and electron microscopy. Three types of ultrastructural features were distinguished in the electron-dense rod-shaped deposits of granular dystrophy, i.e., Type 1 with homogenous structure, Type 2 with fibrillar constituents, and Type 3 with a moth-eaten or sponge-like appearance. In polarization microscopy of Congo-red stained sections, the Type 2 tended to show an increased birefringence without green dichroism, while the other types were less birefringent than the stroma. Three different components were found immediately around the deposits, i.e., 1. normal collagen fibrils, 2. finely filamentous substance, and 3. areas of thin fibrils (70-100 A in diameter). While the second component appeared non-specific, the third component was found only in two corneas, superimposed on the lesions of granular dystrophy, and showed light and electron microscopic characteristics of the lesions of amyloid as well as of lattice dystrophy.

Aged↗