TY - JOUR
T1 - Effects of infusion of human methemoglobin solution following hydrogen sulfide poisoning
AU - Chenuel, B.
AU - Sonobe, T.
AU - Haouzi, Philippe
N1 - Funding Information:
The authors would like to thank Nicole Tubbs for her skillful technical assistance, and Dr. Bogdan Prokopczyk and Neil Trushin from the Department of Pharmacology at Penn State University College of Medicine for their expertise in the determination of H 2S using HPLC. This work was supported by the CounterACT Program, National Institutes of Health Office of the Director (NIH OD), and the National Institute of Neurological Disorders and Stroke (NINDS), Grant Number 5R21NS080788-02.
Funding Information:
Dr. B. Chenuel is supported by a scholarship from “Association des Chefs de Service du CHU de Nancy ” and “Association Nanc é ienne pour l ’ Encouragement à la Recherche Physiologique.”
Publisher Copyright:
© 2015 Informa Healthcare USA, Inc.
PY - 2015/2/1
Y1 - 2015/2/1
N2 - 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.
AB - 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.
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U2 - 10.3109/15563650.2014.996570
DO - 10.3109/15563650.2014.996570
M3 - Article
C2 - 25634666
AN - SCOPUS:84923044413
SN - 1556-3650
VL - 53
SP - 93
EP - 101
JO - Clinical Toxicology
JF - Clinical Toxicology
IS - 2
ER -