Effects of infusion of human methemoglobin solution following hydrogen sulfide poisoning

Rationale. We have recently reported that infusion of a solution containing methemoglobin (MetHb) during exposure to hydrogen sulfide results in a rapid and large decrease in the concentration of the pool of soluble/diffusible H²S in the blood. However, since the pool of dissolved H²S disappears very quickly after H²S exposure, it is unclear if the ability of MetHb to "trap" sulfide in the blood has any clinical interest and relevance in the treatment of sulfide poisoning. Methods. In anesthetized rats, repetition of short bouts of high level of H²S infusions was applied to allow the rapid development of an oxygen deficit. A solution containing MetHb (600 mg/kg) or its vehicle was administered 1 min and a half after the end of H²S intoxication. Results. The injection of MetHb solution increased methemoglobinemia to about 6%, almost instantly, but was unable to affect the blood concentration of soluble H²S, which had already vanished at the time of infusion, or to increase combined H²S. In addition, H²S-induced O² deficit and lactate production as well as the recovery of carotid blood flow and blood pressure were similar in treated and control animals. Conclusion. Our results do not support the view that administration of MetHb or drugs-induced methemoglobinemia during the recovery phase following severe H²S intoxication in sedated rats can restore cellular oxidative metabolism, as the pool of diffusible sulfide, accessible to MetHb, disappears rapidly from the blood after H²S exposure.