Dynamic changes of microscopical structure and NOS expression in rat lung tissues under simulated weightlessness

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WANG De-sheng(Department of Pathophysiology,College of Veterinary Medicine,China Agricultural University,Beijing 100094,China)
YUAN Ming()
LI Zhi-li()
WANG Hui-juan()
LI Tian-zhi()
LIU Chang-ting()
QIAO Jian(Department of Pathophysiology,College of Veterinary Medicine,China Agricultural University,Beijing 100094,China)
Journal Title:
Volume 14, Issue 01, 2008
Key Word:
Weightlessness simulation;Lung;Pathology;Nitricoxide synthase

Abstract: Objective To observe dynamic changes of microscopical structure and nitric oxide synthase(NOS) expression in rat lung tissues under simulated weightlessness,and to collect the data for studies of the adaptive mechanism of local regulation in lung tissues. Methods Wistar male rats were -30° tail suspended to simulate the physiological effects of weightlessness. The microscopical structure,constitutive NOS(cNOS)and inducible NOS(iNOS)expression of rat lung tissues in control group(Con),7-day tail suspension group(TS7) and 14-day tail suspension group(TS14) were respectively observed with routine microscope and immunohistochemistry. Results The solid edema of lungs appeared in TS7 rats,accompanied with lymphocyte soakage in bronchial mucous membranes,red blood cells in alveolus and alveolar amalgamation. The pathological change was more obvious in the TS14 group than that in TS7 group,accompanied with more alveolar amalgamation,more red blood cells in alveolus and thicker alveolar walls. The cNOS expression regions of lung tissues in three groups were mostly the bronchial epithelium,vascular endothelial cells and vascular smooth muscle cells,but there were no significant differences among all groups. The iNOS expression of the TS7 and TS14 rat lung tissues increased significantly as compared with Con rats,which was more obvious in vascular endothelial cells of TS14 than TS7.Conclusion The morphological changes in lung tissues induced by simulated weightlessness are mainly due to the up-regulation of iNOS expression in pulmonary circulation.

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