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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A nitric oxide processing defect of red blood cells created by hypoxia: deficiency of S-nitrosohemoglobin in pulmonary hypertension.
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A nitric oxide processing defect of red blood cells created by hypoxia: deficiency of S-nitrosohemoglobin in pulmonary hypertension.

机译：由缺氧引起的红细胞一氧化氮处理缺陷：肺动脉高压中S-亚硝基血红蛋白缺乏。

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摘要

The mechanism by which hypoxia [low partial pressure of O(2) (pO(2))] elicits signaling to regulate pulmonary arterial pressure is incompletely understood. We considered the possibility that, in addition to its effects on smooth muscle, hypoxia may influence pulmonary vascular tone through an effect on RBCs. We report that exposure of native RBCs to sustained hypoxia is accompanied by a buildup of heme iron-nitrosyl (FeNO) species that are deficient in pO(2-)governed intramolecular transfer of NO to cysteine thiol, yielding a deficiency in the vasodilator S-nitrosohemoglobin (SNO-Hb). S-nitrosothiol (SNO)-deficient RBCs produce impaired vasodilator responses in vitro and exaggerated pulmonary vasoconstrictor responses in vivo and are defective in oxygenating the blood. RBCs from hypoxemic patients with elevated pulmonary arterial pressure (PAP) exhibit a similar FeNO/SNO imbalance and are thus deficient in pO(2)-coupled vasoregulation. Chemical restoration of SNO-Hb levels in both animals and patients restores the vasodilator activity of RBCs, and this activity is associated with improved oxygenation and lower PAPs.
机译：缺氧[O（2）（pO（2））的低分压]引发信号以调节肺动脉压的机制尚不完全清楚。我们考虑了除了对平滑肌的影响外，缺氧还可能通过对RBC的影响来影响肺血管张力。我们报告说，天然红细胞暴露于持续的缺氧伴随着血红素亚硝基（FeNO）物种的积累，这些物种在pO（2-）控制的分子内从NO转移到半胱氨酸硫醇中不足，从而导致血管扩张剂S-亚硝基血红蛋白（SNO-Hb）。缺乏S-亚硝基硫醇（SNO）的RBC在体外产生受损的血管舒张反应，在体内产生过度的肺血管收缩反应，并且在充氧血液方面存在缺陷。低氧血症患者肺动脉高压（PAP）的RBC表现出相似的FeNO / SNO不平衡，因此在pO（2）耦合的血管舒张功能不足。动物和患者体内SNO-Hb水平的化学恢复均可恢复RBC的血管舒张活性，而这种活性与氧合改善和PAP降低有关。

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