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急性肺损伤患者肺水肿液中硝酸盐和表面活性蛋白a硝化水平升高。

Increased levels of nitrate and surfactant protein a nitration in the pulmonary edema fluid of patients with acute lung injury.

作者信息

Zhu S, Ware L B, Geiser T, Matthay M A, Matalon S

机构信息

Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama 35249-0006, USA.

出版信息

Am J Respir Crit Care Med. 2001 Jan;163(1):166-72. doi: 10.1164/ajrccm.163.1.2005068.

Abstract

Levels of nitrite (NO2-) and nitrate (NO3-) were measured in pulmonary edema fluid and plasma from 34 patients with early acute lung injury (ALI) and 20 patients with hydrostatic pulmonary edema. Pulmonary edema fluid from patients with ALI had significantly higher levels of NO2- + NO3- compared with pulmonary edema fluid from patients with hydrostatic pulmonary edema (108 +/- 13 microM versus 66 +/- 9 microM; means +/- SEM; p < 0.05). In addition, patients with shock had higher plasma NO2- + NO3- levels than those without shock (79 +/- 11 microM versus 53 +/- 12 microM, p < 0.05). Acidemia and increased anion gap, markers of systemic hypoperfusion, were also associated with twofold higher plasma NO2- + NO3- levels (p < 0.01). Increased levels of NO2- + NO3- in edema fluid samples were associated with slower rates of alveolar fluid clearance. Nitrated pulmonary surfactant protein A (SP-A) was also detected in the edema fluid of patients with ALI after immunoprecipitation with a specific antibody against this protein. Previously, we have shown that nitration of SP-A impairs its host- defense properties. In aggregate, the results of this study indicate that reactive oxygen-nitrogen species may play a role in the pathogenesis of human ALI.

摘要

对34例早期急性肺损伤(ALI)患者和20例静水压性肺水肿患者的肺水肿液和血浆中的亚硝酸盐(NO2-)和硝酸盐(NO3-)水平进行了测量。与静水压性肺水肿患者的肺水肿液相比,ALI患者的肺水肿液中NO2- + NO3-水平显著更高(108±13微摩尔/升对66±9微摩尔/升;均值±标准误;p<0.05)。此外,休克患者的血浆NO2- + NO3-水平高于无休克患者(79±11微摩尔/升对53±12微摩尔/升,p<0.05)。作为全身低灌注标志物的酸血症和阴离子间隙增加也与血浆NO2- + NO3-水平升高两倍相关(p<0.01)。水肿液样本中NO2- + NO3-水平升高与肺泡液体清除率降低有关。在用针对该蛋白的特异性抗体进行免疫沉淀后,在ALI患者的水肿液中也检测到了硝化的肺表面活性物质蛋白A(SP-A)。此前,我们已经表明SP-A的硝化会损害其宿主防御特性。总体而言,本研究结果表明活性氧氮物质可能在人类ALI的发病机制中起作用。

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