Vasodynamic and angiogenic effects of eicosanoids in the eye.

In the eye, the main vascular response to PGs is vasodilation. Although its effect has not been studied in detail, TxA2 can be expected to cause vasoconstriction in the eye, as it does in other tissues. When applied in high doses, PGs also increase the permeability of the microvasculature in the anterior segment, especially in rabbits. This may contribute to protein leakage associated with disruption of the BAB. The peptidoleukotrienes seem to reduce blood flow in the anterior segment, although more data will be required to substantiate this observation. It has been suggested over the years that PGs have a physiologic role in the autoregulation of the retinal blood flow. It has also been hypothesized that PGs, particularly those of the E series, play an important role in corneal neovascularization. The evidence obtained thus far in support of such hypothesis is not conclusive. It is possible that in the course of corneal vascularization or its induction, PGs are released, together with other mediators such as lipoxygenase products, but the pathophysiologic mechanisms are poorly understood. The role of eicosanoids in CME remains speculative. It is possible that other compounds in the cyclooxygenase pathway such as thromboxane and prostacyclin or some lipoxygenase products play a more important role in CME than the classical PGs, but, there is insufficient data so far to implicate any one eicosanoid or any other autacoids in the initiation of the vascular changes that are associated with CME.