Biochemical reaction products of nitric oxide as quantitative markers of primary pulmonary hypertension
Biochemical reaction products of nitric oxide as quantitative markers of primary pulmonary hypertension
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DOI：
10.1164/ajrccm.158.3.9802066
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发表时间：
1998-09-01
影响因子：
24.7
通讯作者：
Erzurum, SC
中科院分区：
文献类型：
--
作者：
Kaneko, FT;Arroliga, AC;Erzurum, SC
原发性肺动脉高压（PPH）是一种病因不明的罕见和致命的疾病。炎性氧化剂机制和一氧化氮（NO）缺乏与肺动脉高压的发病机制有关。为了研究PPH患者体内氧化剂和抗氧化剂的异常，我们研究了PPH患者（n = 8）和健康对照组（n = 8）肺内NO水平、NO生化反应产物和抗氧化剂（谷胱甘肽[GSH]、谷胱甘肽过氧化物酶[GPx]和超氧化物歧化酶[SOD]）。在支气管镜检查时采集肺内气体和液体样本。通过右心导管检查确定肺动脉高压。PPH患者肺组织中NO及NO生化反应产物均较健康对照组减少（气道气体中NO [ppb]：对照组，8 +/- 1; PPH，2.8 +/- 0.9; p = 0.016;支气管肺泡灌洗液[BALF]中NO产物[μ M]：对照组，3.3 +/- 1.05; PPH，0.69 +/- 0.21; p = 0.03）。然而，PPH患者肺中的GSH高于对照组（BALF中的GSH [μ M]：0.55 +/- 0.04; PPH，0.9 +/- 0.1; p = 0.015）。两组SOD、GPx活性相似（p ≥ 0.50）。NO的生化反应产物与肺动脉压（R = -0.713; p = 0.047）和诊断PPH后的年数（R = -0.776; p = 0.023）呈负相关。NO反应产物是通过氧化剂和NO之间的相互作用形成的，反应的最终产物取决于两种类型分子的相对水平。因此，研究结果表明，肺中的NO和氧化反应与PPH中肺动脉压升高有关。
Primary pulmonary hypertension (PPH) is a rare and fatal disease of unknown etiology. inflammatory oxidant mechanisms and deficiency in nitric oxide (NO) have been implicated in the pathogenesis of pulmonary hypertension. In order to investigate abnormalities in oxidants and antioxidants in PPH, we studied intrapulmonary NO levels, biochemical reaction products of NO, and antioxidants (glutathione [GSH], glutathione peroxidase [GPx], and superoxide dismutase [SOD]) in patients with PPH (n = 8) and healthy controls (n = 8). Intrapulmonary gases and fluids were sampled at bronchoscopy. Pulmonary hypertension was determined by right-heart catheterization. NO and biochemical reaction products of NO in the lung were decreased in PPH patients in comparison with healthy controls (NO [ppb] in airway gases: control, 8 +/- 1; PPH, 2.8 +/- 0.9; p = 0.016; and NO products [mu M] in bronchoalveolar lavage fluid [BALF]: control, 3.3 +/- 1.05; PPH, 0.69 +/- 0.21; p = 0.03). However, GSH in the lungs of PPH patients was higher than in those of controls (GSH [mu M] in BALF: 0.55 +/- 0.04; PPH, 0.9 +/- 0.1; p = 0.015). SOD and GPx activities were similar in the two groups (p greater than or equal to 0.50). Biochemical reaction products of NO were inversely correlated with pulmonary artery pressures (R = -0.713; p = 0.047) and with years since diagnosis of PPH (R = -0.776; p = 0.023). NO reaction products are formed through interactions between oxidants and NO, with the end products of reaction dependent upon the relative levels of the two types of molecules. The findings of the study therefore show that NO and oxidant reactions in the lung are related to the increased pulmonary artery pressures in PPH.