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首页> 外文期刊>American Journal of Physiology >Erythrocytes of humans with cystic fibrosis fail to stimulate nitric oxide synthesis in isolated rabbit lungs.
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Erythrocytes of humans with cystic fibrosis fail to stimulate nitric oxide synthesis in isolated rabbit lungs.

机译：患有囊性纤维化的人的红细胞无法刺激离体兔肺中一氧化氮的合成。

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摘要

Erythrocytes (red blood cells) of either rabbits or healthy humans are required to demonstrate the participation of nitric oxide (NO) in the regulation of pulmonary vascular resistance in the isolated rabbit lung. The property of the erythrocyte that is responsible for the stimulation of NO synthesis was reported to be the ability to release ATP in response to physiological stimuli, including deformation. Moreover, a signal transduction pathway that relates mechanical deformation of erythrocytes to ATP release has been described, and the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) is a component, i.e., erythrocytes of individuals with CF do not release ATP in response to deformation. Here, we investigated the hypothesis that, in contrast to those of healthy humans, erythrocytes of humans with CF fail to stimulate endogenous NO synthesis in the isolated rabbit lung. We report that CFTR is a component of the membranes of both rabbit and human erythrocytes. The addition of the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 muM) produced increases in vascular resistance in isolated rabbit lungs perfused with physiological salt solution (PSS) containing erythrocytes of healthy humans, but L-NAME was without effect when the lungs were perfused with PSS alone or PSS containing erythrocytes of CF patients. These results provide support for the hypothesis that, in CF, a defect in ATP release from erythrocytes could lead to decreased endogenous pulmonary NO synthesis and contribute to pulmonary hypertension.
机译：要求兔子或健康人的红细胞（红细胞）表现出一氧化氮（NO）参与离体兔肺中肺血管阻力的调节。据报道，负责刺激NO合成的红细胞的性质是响应生理刺激（包括变形）释放ATP的能力。而且，已经描述了将红细胞的机械变形与ATP释放相关的信号转导途径，并且囊性纤维化（CF）跨膜电导调节剂（CFTR）是一个成分，即具有CF的个体的红细胞不响应于形变。在这里，我们调查的假说，与健康的人相反，患有CF的人的红细胞不能刺激离体兔肺中的内源性NO合成。我们报道CFTR是兔和人类红细胞膜的一个组成部分。 NO合酶抑制剂N（ω）-硝基-L-精氨酸甲酯（L-NAME，100μM）的添加增加了灌注了含有健康人红细胞的生理盐溶液（PSS）的离体兔肺的血管阻力，但是当肺部单独灌注PSS或CF患者含有PSS的红细胞时，L-NAME无效。这些结果为以下假设提供了支持：在CF中，红细胞释放的ATP缺陷可能导致内源性肺NO合成减少，并导致肺动脉高压。

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