Effects of infusion of human methemoglobin solution following hydrogen sulfide poisoning.

Effects of infusion of human methemoglobin solution following hydrogen sulfide poisoning.
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DOI:
10.3109/15563650.2014.996570
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发表时间:
2015-02
期刊:
Clinical toxicology (Philadelphia, Pa.)
影响因子:
--
通讯作者:
Haouzi P
Haouzi P
中科院分区:
其他
文献类型:
--
作者:
Chenuel B;Sonobe T;Haouzi P

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我们最近报道,在暴露于硫化氢的过程中,输注含有高铁血红蛋白(MetHb)的溶液导致血液中可溶性/扩散性H2S的浓度迅速大幅下降。然而,由于溶解的H2S池在H2S暴露后很快消失,因此尚不清楚MetHb在血液中“捕获”硫化物的能力在硫化物中毒的治疗中是否具有任何临床意义和相关性。在麻醉大鼠中,重复短期高水平H2S输注,以使缺氧快速发展。在H_2S中毒结束后1.5分给予含高铁血红蛋白(600 mg/kg)或其溶剂的溶液。高铁血红蛋白溶液的注射几乎立即将高铁血红蛋白血症增加至约6%,但不能降低在输注时已经消失的可溶性H2S的血液浓度,也不能增加结合H2S。此外,H2S诱导的O2不足和乳酸产生以及颈动脉血流量和血压的恢复在治疗组或对照组动物中相似。我们的研究结果不支持这样的观点,即在镇静大鼠严重H2S中毒后的恢复阶段给予MetHb或药物诱导的高铁血红蛋白血症可以恢复细胞的氧化代谢,因为接触MetHb的可扩散硫化物池在H2S暴露后迅速从血液中消失。
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. In anesthetized rats, repetition of short bouts of high level of H2S infusions were applied to allow the rapid development of an oxygen deficit. A solution containing methemoglobin (600mg/kg) or its vehicle was administered one minute and a half after the end of H2S intoxication. The injection of methemoglobin solution increased methemoglobinemia to about 6%, almost instantly, but was unable to decrease 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 or control animals. 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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