The purpose of this study is to compare the effects of
vitamin E (VE) on corneal neovascularization induced by linoleic acid
hydroperoxide (LHP) between the normal rabbits and the hyperglycemia one. (T.Ueda, Angiogenesis 1: 174-184, 1997 ). Rabbits
were divided into 4 groups, C; New Zealand rabbits (NZ) as control (n=5), C+E;
NZ with VE treatment (n=3), HG; hyperglycemia above 200 mg/dl by 80 mg/kg
alloxan i.v.(n=10) and HG+E; HG with VE treatment (n=3). One week after HG
condition, rabbits were fed chow (RC4; Oriental Yeast Co., Ltd., Tokyo) with or
without 0.02% VE for 3 wks. Next, 10μl of LHP (40 mM) synthesized from lipoxygenase was injected with a
30 ga needle positioned under a
Zeiss operating microscope. Vessel growth area from the limbal
vasculature was measured over a period of 2 wks. Neovascularization was
observed in the superior segment of the cornea and grew towards the injection
site. At 14 days post-injection, the longest vessel length were 1.17±0.09 mm in
C, 1.07±0.24 mm in C+E, 1.92±0.31 mm in HG, 1.40±0.14 mm in HG+E. VE inhibited
LHP-induced corneal neovascularization. The LHP-induced neovascular response
was markedly enhanced in the high
glucose animals. These data suggest that hyperglycemia sensitizes corneal and
endothelial cells, probably by glucose derived radicals, which enhance
production of additional LHP and angiogenìc cytokines through more rapid
propagation reactions, raising the concentration levels to induce an enhanced,
sustained neovascularization.