[Pathobiochemical aspects of corneal neovascularization]

Natural inflammatory compounds were implanted in the corneas of rabbits to clarify the question whether corneal neovascularization is induced by stromal edema alone, or by neovascular mediators. It could be demonstrated that prostaglandin E1 and E2 have an angiogenic capacity, whereas their precursor (arachidonic acid) as well as PGA1, A2, B2, I2 and thromboxane A2 were inactive in this regard. Histology showed that corneal neovascularization is always accompanied by the invasion of polymorphonuclear leukocytes. Corneal edema in the beginning of angiogenesis can be explained by the activities of PGE's (vasodilation, increase of vascular permeability). The implantation of lipoxygenase-dependent arachidonic acid compounds (5-HETE, leukotriene B4) demonstrated that these mediators share in the process of neovascularization by inducing the chemotaxis.