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A. Bringmann, O. Uckermann, T. Pannicke, I. Iandiev, A. Wolf, F. Kutzera, A. Reichenbach, S. Wolf, P. Wiedemann; Triamcinolone Acetonide Inhibits Hypotonic Glial Cell Swelling in the Rat Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5322.
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Purpose: Anti–inflammatory corticosteroids such as triamcinolone acetonide are commonly used to treat macular edema during ischemic and inflammatory eye diseases. Beside the leakage of blood–retinal barriers that causes extracellular edema, swelling of Muller glial cells (cytotoxic edema) may contribute to the formation of cystoid macular edema. In the postischemic retina of the rat, hypotonic stress (that resembles hypoxia–induced cytotoxic edema in the brain) induces Muller cell swelling (Pannicke et al., 2004, Mol. Cell. Neurosci., 26:493–502). However, it is not known whether swelling occurs also during intraocular inflammation. Therefore, we investigated in a rat model whether ocular inflammation (endotoxin–induced uveoretinitis) alters the swelling characteristics of Muller cells, and whether triamcinolone may inhibit hypotonic Muller cell swelling. Methods: Transient retinal ischemia was induced in one eye of adult rats by elevating the intraocular pressure for 60 min. Ocular inflammation was induced by intravitreal application of lipopolysaccharide (LPS). At different stages (up to seven days) after treatment, the swelling of Muller cell somata upon hypotonic stress was recorded in retinal slices. Triamcinolone was applied simultaneously with the hypotonic solution. The plasma membrane K+ conductance of Muller cells was investigated in isolated cells, and retinal slices were immunostained against Kir4.1 protein. Results: At three and seven days after LPS treatment, hypotonic stress induced swelling of Muller cells that was not observed in non–treated control eyes. In slices of control retinas, acute application of arachidonic acid or of prostaglandin E2 rapidly induced Muller cell swelling during hypotonic stress. Muller cells of LPS–treated eyes displayed a downregulation of the plasma membrane K+ conductance that was accompanied by decreased expression of Kir4.1 protein in retinal slices. Acute application of triamcinolone (100 µM) fully inhibited the glial cell swelling in slices of postischemic retinas and from LPS–treated eyes. Conclusions: Acute application of triamcinolone rapidly inhibits the hypotonic glial cell swelling that is a characteristic feature of retinas of the rat during ischemia–reperfusion and inflammation. The inhibiting effect on the cytotoxic Muller cell swelling may contribute to the edema–resolving action of triamcinolone observed in human subjects.
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