The role of N-acetylcysteine against the injury of pulmonary artery induced by LPS.
- Author:
Xin-li HUANG
1
;
Yi-ling LING
;
Tie-nian ZHU
Author Information
- Publication Type:Journal Article
- MeSH: Acetylcysteine; pharmacology; Animals; Endothelium; metabolism; pathology; ultrastructure; Lipopolysaccharides; adverse effects; Malondialdehyde; metabolism; Microscopy, Electron, Scanning; Nitric Oxide; metabolism; Pulmonary Artery; metabolism; pathology; ultrastructure; Rabbits; Superoxide Dismutase; metabolism
- From: Chinese Journal of Applied Physiology 2002;18(4):370-373
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo investigate the alleviating effect of N-acetylcysteine (NAC) on lung injury induced by lipopolysaccharides (LPS) and its mechanism.
METHODSThe effects of NAC on changes of the pulmonary arterial reactivity and the ultrastructure of pulmonary arterial endothelium induced by LPS were observed with the isolated artery ring technique and scanning electron microscope (SEM). Malondialdehyde (MDA), nitric oxide (NO) contents and superoxide dismutase (SOD) activity of pulmonary artery tissues were detected.
RESULTSThe exposure of pulmonary artery to LPS (4 microg/ml, 7 h) led to reduction of endothelium-dependent relaxation response to acetylcholine (ACh), which was reversed by the concomitant exposure to NAC (0.5 mmol/L, 7 h), whereas NAC itself had no effect on the response. Significant structural injury were observed under SEM in LPS group and alleviated the changes in LPS + NAC group. The MDA, NO contents increased but SOD activity decreased in LPS group, which were reversed by the concomitant exposure to NAC.
CONCLUSIONNAC protects pulmonary artery endothelium and enhances endothelium-dependent relaxation response of pulmonary artery by antioxidation effect, which may be one of the mechanisms of its reversing pulmonary artery hypertension and following lung injury induced by LPS.
