The Effect of Ranitidine Administration Time to Axon Degeneration due to Optic Nerve Neuropathy

Abstract

Background: Formic acid is the end product of methanol metabolism that can damage the axons of the optic nerve. Previous studies have suggested that, besides ethanol and fomepizole, ranitidine can inhibit the formation of this formic acid. However, the timing of administration of ranitidine in acute methanol intoxication is unknown. The study aim to determine the effect of ranitidine administration time to degeneration of axon optic nerve in the incidence of acute methanol intoxication. Method: The study used 4 groups with 6 rats in each group. Two treatment groups and the positive control group were given methanol 14 g/kg BW, the first treatment group was given ranitidine 30 mg/kgBW right after administration of methanol and second group 30 minutes after methanol administration. Meanwhile, the negative control group was given oral aquadest, then rats were terminated after 8 hours Results: Histological examination of optic nerve with H&E showed the administration of ranitidine right after methanol administration can inhibit optic nerve degeneration significantly (p<0.05). Meanwhile, the administration of ranitidine after 30 minutes had not been able to inhibit optic nerve degeneration significantly (p>0.05) Conclusion: Ranitidine administration right after acute methanol intoxication can prevent optic nerve degeneration significantly. Further research is needed to investigate the effect of ranitidine dose on the degeneration rate of the axons of the optic nerve Keyword: axon degeneration, methanol, neuropathy, optic nerve, ranitidine