Prostaglandins and inflammation in the eye.

Traumatic injury of the eye promotes the release of prostaglandins E2 and F2alpha from the iris and other tissues. These induce vasodilation, increased capillary permeability and an increase in protein content of the aqueous. They are leukotactic. With an influx of leukocytes PGE1 appears in the aqueous having been synthesized by these cells. Infectious agents also attract leukocytes and sensitized lymphocytes characterize inflammation of both allergic and infectious origin. The cascade of molecular and cellular events seen in ocular inflammation of various origin seem ultimately to result in a reaction largely mediated by prostaglandins. Effective therapy should be directed at preventing their synthesis (synthetase inhibitors), interferring with their action once synthesized (receptor blockers), and inhibiting the migration of leukocytes into the eye.