Metabolic factors of vasomotor regulation of the inner retina

Abstract

Lactic acid, the end metabolic product of anaerobic glycolysis is probably the mediator of the hypoxia induced vasodilation on retinal arterioles. In this study we explored the mechanisms of the retinal vasomotor effect of this metabolite by performing preretinal juxtaarteriolar pulsatile pressure microinjections on the intact eye of anesthetized and artificially ventilated miniature pigs. Microinjections of the levorotatory isomer L-lactic acid (pH: 2) induced a local maximal dilation of retinal arterioles. This vasodilator effect, like that of systemic hypoxia, was not mediated by the release of prostaglandins. Preretinal pulsatile pressure juxtaarteriolar microinjections of neutral-pH solution of L-lactic acid also induced a segmental retinal arteriolar dilation. In contrast, microinjections of the dextrorotatory isomer D-lactic acid (pH: 2, solution), which is not produced by the retina, did not affect significantly the arteriolar diameter. Consequently, the vasodilator effect of lactic acid does not depend on periarteriolar pH modification and probably interferes with retinal metabolism since only the natural levorotatory metabolite is recognized.