Hydrogen sulfide oxidation and the arterial chemoreflex: Effect of methemoglobin
Hydrogen sulfide oxidation and the arterial chemoreflex: Effect of methemoglobin
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DOI：
10.1016/j.resp.2011.04.025
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发表时间：
2011-08-15
影响因子：
2.3
通讯作者：
Philmon, Maeve
中科院分区：
文献类型：
--
作者：
Haouzi, Philippe;Bell, Harold;Philmon, Maeve
内源性H（2）S被认为是缺氧对颈动脉体（CB）的影响。为了验证这一假设，我们通过在自主呼吸的麻醉绵羊中注射250 mg亚硝酸钠诱导类似于10%高铁血红蛋白血症的方法，为内源性产生的H（2）S创建了一个汇。高铁血红蛋白血症已被证明可以催化血液和组织中大量硫化物的氧化。我们发现，metHb的存在下完全取消了10毫克NaHS（i. v.）诱导的兴奋。其在对照条件下模拟呼吸6-7潮气量的氮气的作用，证实了血液对硫化物的氧化能力的显著增加。metHb对低氧（10%O（2））、氮和高氧的兴奋性反应无抑制作用。我们的结果表明，在存在高硫氧化能力的情况下，通气化学反射不会受到抑制，并挑战了H（2）S转导CB中缺氧效应的观点。(C)2011爱思唯尔有限公司版权所有。
Endogenous H(2)S has been proposed to transduce the effects of hypoxia in the carotid bodies (CB). To test this hypothesis, we created a sink for endogenously produced H(2)S by inducing similar to 10% methemoglobinemia via the injection of 250 mg of sodium nitrite in spontaneously breathing anaesthetized sheep. Methemoglobinemia has been shown to catalyze the oxidation of large quantities of sulfide in the blood and tissues. We found that the presence of metHb completely abolished the ventilatory stimulation induced by 10 mg NaHS (i.v.). which in control conditions mimicked the effects of breathing 6-7 tidal volumes of nitrogen, confirming the dramatic increase in the oxidative power of the blood for sulfide. The ventilatory responses to hypoxia (10% O(2)), nitrogen and hyperoxia were in no way depressed by the metHb. Our results demonstrate that the ventilatory chemoreflex is not depressed in the presence of a high oxidative capacity for sulfide and challenge the view that H(2)S transduces the effects of hypoxia in the CB. (C) 2011 Elsevier B.V. All rights reserved.