Communications; the role of ascorbic acid in corneal vascularization.

Introduction ALTHOUGH the cornea normally has no blood vessels, yet, under certain conditions, new vessels freely enter the substa-nce of the cornea from the limbal plexus. To explain this invasion many theories have been advanced. In riboflavin deficiency there is corneal vascularization. Since riboflavin is part of an oxidation enzyme system, Bessey and Wolbach (1939), and Johnson and Eckardt (1940), believe that anoxia is a stimulus for corneal vascularization. Campbell and Michaelson (1949) brought forward evidence that injury to the cornea close to the limbus sets free a humoral substance which then diffuses to the limbal vessels to stimulate new vessel formation. Julianelle and Lamb (1934) injected an antigen into the cornea of a sensitized animal. This evoked evascularization of the cornea.