N. nigricollis venom caused transient corneal oedema, extensive chemosis and pupillary dilation when applied topically to the corneas of albino and pigmented rabbits. After 1 month, permanent corneal scarring, neovascularization and deepithelialization was noted in albino eyes, whereas minimal scarring or deepithelialization occurred in pigmented eyes. In contrast, mydriasis and cycloplegia occurred initially in the pigmented eye, with the pupil remaining fixed and dilated for more than 7 days. The albino pupil, however, returned to normal within 2-3 days. Preliminary penetration studies using labelled venom revealed that N. nigricollis venom was mainly bound in the corneal stroma of the albino eye and showed poor penetration, whereas minimal corneal binding and poor penetration was noted in the pigmented eye. It appears that the high initial corneal edema may result from the intrinsic release of histamine and acetylcholine. The progression of corneal edema to liquefaction and opacification is probably due to the release of an endogenous corneal damaging factor by the venom presumably a collagenase or proteinase. Treatment with corticosteroids significantly increased the severity of the keratoconjunctivitis and deepithelialization, whereas treatment with heparin significantly reduced the keratoconjunctivitis and prevented further opacification. It is postulated that heparin might act through its chelating effect on ions necessary for the action of the proteolytic enzymes.