Visual disturbances in man as a result of experimental and occupational exposure to dimethylethylamine.
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Experimental exposure of four volunteers to 40-50 mg/m3 of dimethylethylamine (DMEA) for eight hours caused irritation of the mucous membrane of their eyes, subjective visual disturbances (haze), and slight oedema of the corneal epithelium. The thickness of the cornea showed a slight but consistent increase in all four subjects at these exposures and in two subjects exposed to 10 mg/m3. Concentrations of 80 and 160 mg/m3 for 15 minutes caused eye irritation but no visual disturbances or corneal oedema. Occupational exposure for eight hours to about 25 mg/m3 of DMEA (with peaks above 100 mg/m3) was also associated with eye irritation, haze, and corneal oedema. The divergence between our findings and other reports in which visual disturbances occurred at lower concentrations during occupational exposure may be due to peak concentrations. (+info)
Contact lens-induced edema in vitro. Pharmacology and metabolic considerations.
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The effects of physiologic and pharmacologic manipulations on contact lens-induced edema were studied. In isolated superfused rabbit corneas bathed in Ringer's solution and covered with large-diameter polymethylmethacrylate (PMMA) lenses, corneal swelling rates of 17-26 microns/hr (versus -5-5 microns/hr in paired controls) were observed. Neither the calcium antagonist diltiazem (10(-4) M), the glucocorticoid dexamethasone (10(-7) M), the glucose substitute fructose (20 mM), nor 0.5 mM adenosine and 0.3 mM reduced glutathione mitigated the edema. Lens-induced edema was 25 microns/hr in corneas bathed at pH 8.2 and decreased to 9 microns/hr at pH 7.0. In corneas without lenses, however, decreasing the pH from 7.4-7.0 caused significant swelling (P less than 0.05). The pyruvate dehydrogenase stimulant sodium dichloroacetate (3.2 mM) on the tears side ameliorated the edema, and its congener, 3.2 mM 2-chloropropionate, was less effective. These latter agents are known to relieve lactic acidosis systemically and had no significant effect on corneas without lenses. In tissues bathed with 20 mM lactate Ringer's, normal thickness was maintained in both control and PMMA-treated corneas throughout the 3-hr period. These findings suggest that the contact lens-induced edema does not involve the acute cytotoxic mechanisms seen in severe tissue ischemia or hypoxia. The edema appears to result in part from acidosis but mainly from stromal lactate accumulation. (+info)
Bilateral reversible corneal edema associated with amantadine use.
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Recurrent corneal oedema following late migration of intraocular glass.
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This is a report of very late complications following intraocular penetration of numerous fragments of glass as a result of a test tube explosion. Fifteen years after the initial injury glass splinters began to migrate from the vitreous into the anterior chamber, causing acute episodes of corneal oedema. Four such episodes occurred over the past nine years, the corneal oedema each time disappearing within a few days following surgical extraction of the glass splinters. The literature on intraocular glass and its movement within the eye is reviewed. (+info)