Citation

Feng ZM. Zhonghua Zheng Xing Shao Shang Wai Ke Za Zhi 1989; 5(2): 130-3, 160.

Copyright

(Copyright © 1989, Chinese Academy of Medical Sciences)

DOI

unavailable

PMID

2509042

Abstract

In this study, lung Schiff Base was used as a measure indicating the lung injury induced by free radicals, and lung water, lung vascular permeability, blood gases levels as well as pulmonary pathomorphological change (IM) as measures denoting extents of lung injury after inhalation injury. Experiment was performed on rats and observed for a period of 12 hr post smoke inhalation. In addition, control studies were also achieved on normal rats, and rats depleted from leukocytes by cyclophosphamide prior to the experiments. The results were: 1. The lung Schiff bases were generally higher than that of the control through the whole observation period and two peaks were demonstrated at 30' and 6 hr (56.2% and 31.4% higher than controls respectively) indicating that free radicals played a significant role on lung damage in smoke inhalation injury. 2. Lung Schiff bases of rats depleted from leukocytes revealed a 33.7% and a 50.3% reduction respectively at 30' and 6 hr after injury. It seems that leukocytes lead a more important position at 6 hr than at 30' after injury. 3. The reduction rates of peripheral leukocytes, lung Schiff bases and lung water content were not identical in rats depleted from leukocyte after inhalation injury. There were 94.3%, 50.3% and 42.6% reduction respectively at 6 hr after injury. Correlations among them were not significant. These data suggest that after smoke inhalation injury leukocyte is not the only source of free radicals and also the free radicals are not the only means which leukocyte rely upon to cause lung injury.

Language: zh