The effect of nitric oxide on acute lung injury following ischemia/reperfusion of hind limbs in the rat.
- Author:
Xiu-Hong YANG
1
;
Lian-Yuan ZHANG
;
Shu-Xun SUN
;
Shu-Yun DONG
;
Xiu-Li MEN
;
You-Ling JING
;
Yi-Bing ZHANG
Author Information
1. Department of Pathophysiology, North China Coal Medical College, Tangshan 063000, China. zhangly@ncmc.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Hindlimb;
Lung Diseases;
etiology;
metabolism;
pathology;
Male;
Nitric Oxide;
metabolism;
physiology;
Nitric Oxide Synthase;
metabolism;
Rats;
Rats, Wistar;
Reperfusion Injury;
metabolism
- From:
Acta Physiologica Sinica
2002;54(3):234-238
- CountryChina
- Language:Chinese
-
Abstract:
On a model of reperfusion after ischemia in the hind limbs (LIR) of rats, we used aminoguanidine (AG) which inhibits nitric oxide synthase (NOS) and L-arginine (L-Arg), one of the substrates in the process of nitric oxide synthesis, to observe the changes in NO, NOS, malondialdehyde (MDA), myeloperoxidase (MPO) and wet/dry ratio (W/D) in both skeletal muscles and the lung as well as the changes in phosphatidyl choline (PC) of lung surfactant. The morphologic changes were observed with microscopy. It was observed that the values of NOS, MPO, MDA of the muscle and lung in LIR group increased significantly and the content of PC decreased obviously compared with those of the normal control. Pulmonary observation revealed that after LIR leucocyte assembling and infiltration took place, which was dominated by polymorphocytes with broadened pulmonary interstitial tissue. In LIR+L-Arg group the above changes were reversed, and in LIR+AG group the injuries became more serious. The results obtained suggest that the activity of NOS and the production of NO following ischemia/reperfusion of hind limbs increased significantly, and that the endogenous NO may play a protective role during the early stage of acute lung injury after LIR.
