The histopathology of corneal neovascularization. Inhibitor effects.
With the use of a previously described model of corneal neovascularization induced by thermal cautery, we examined the effects of inhibitors on both the incidence of corneal neovascularization and the degree of inflammatory cell response. Three known inhibitors of corneal neovascularization, 1% prednisolone acetate, indomethacin, and 0.3% flurbiprofen, were studied and the results were compared with those in saline-treated controls. As expected, corneal neovascularization, preceded by conjunctival and corneal polymorphonuclear leukocyte (PMNL) infiltration, occurred in all control animals. Corneal neovascularization did not occur in any of the inhibitor-treated eyes. Histopathologically, both conjunctival and corneal PMNL counts in the treated eyes were markedly reduced compared with controls. These findings are consistent with the hypothesis that inflammatory cells, particularly PMNLs, are closely associated with the initiation of corneal neovascularization.
Robin
J B
JB
Regis-Pacheco
L F
LF
Kash
R L
RL
Schanzlin
D J
DJ
D000818:Animals; D002634:Chemotaxis, Leukocyte; D003315:Cornea / Q000098:blood supply*; D065306:Corneal Injuries; D004195:Disease Models, Animal; D004564:Electrocoagulation; D005260:Female; D005480:Flurbiprofen / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology*; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D009504:Neutrophils; D011239:Prednisolone / Q000494:pharmacology*; D011422:Propionates / Q000494:pharmacology*; D011817:Rabbits
D011422:Propionates; D005480:Flurbiprofen; D011239:Prednisolone; D007213:Indomethacin