Mechanism of exogenous nitric oxide in attenuating endotoxin-induced increase of rat pulmonary microvascular permeability
- VernacularTitle:外源性一氧化氮抗内毒素致肺微血管高通透性的作用机制初探
- Author:
Yanmei LIU
;
Dianhua WANG
;
Yiling LING
;
Junlan ZHANG
- Publication Type:Journal Article
- Keywords:
Nitric oxide;
Endotoxins;
Lung;
Capillary permeability;
Neutrophils;
Rats
- From:
Chinese Journal of Pathophysiology
1986;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM and METHODS: The animal model of acute lung injury (ALI) caused by intratracheal instillation of lipopolysaccharides(LPS) in vivo and human peripheral blood polymorphonuclear neutrophil (PMN) in vitro were used to study the effects of sodium nitroprusside (SNP), nitric oxide (NO) donor, on LPS-induced PMN accumulation, microvascular permeability and PMN apoptosis. RESULTS: ① In vivo , PMN accumulation in lung, the protein content in bronchoalveolar lavage fluid (BALF) and the Evans blue dye and monastral blue dye extravasation in lung tissue of LPS group were markedly higher than those of both sham operation group and LPS+SNP group. ② In vitro, the apoptotic percentage of SNP group was much higher than that of control group, while compared with LPS group, SNP+LPS group has significantly higher apoptotic percentage. CONCLUSIONS: SNP intratracheal instillation attenuated LPS-induced microvascular permeability and alleviated ALI. PMN apoptosis induced by SNP may be one of the potential mechanisms underlying the decrease of PMN accumulation in lung tissue.
