Odontobuthos doriae, a native scorpion in southern tropical parts of Iran, can cause serious health threats and wide ranges of pharmacological disturbances. α-toxins in its venom cause prolongation of Na+ channels activity. In this study, reversing effects of lidocaine, as a Na+-channel blocker, was studied on mice following exposure to venom. Lidocaine (up to 500 mg/kg) and O. doriae crude venom (up to 12 μg/mice) was used in a 14-day acute toxicity test, to yield LD50s of 110mg/kg and 10μg/mice, respectively. Afterward, different sub-acute amounts of lidocaine (25%, 50% and 80% of LD50) were used in the presence of venom (80%, 100% and 120% of LD50). Our results show 80% LD50 of lidocaine, and not higher concentrations, could cause 50% reduction in lethality rate induced by O. doriae venom at LD50 concentration, showing the Na+-channel function in this event. Reducing the amount of lidocaine to safer doses show no significant effect in this aspect. Finally, lidocaine (80% LD50) can partially decrease the O. doriae venom mortality. However, due to some other systemic dangerous lidocaine adverse effects, it is doubtful that it can be a relevant life-saving agent in this case. Further to lidocaine failure in reversing the complete venom toxicity, it would be explained that high Na+ current induced by venom might prevent lidocaine effect at above doses, while higher concentrations also can cause lidocaine toxicity, which restricts our further investigation. Preferably, it would be suggested to use other medical approaches and medication to save the envenomed victim’s life.