To explore the mechanisms of neurogenic inflammation and airway hyperresponsiveness of rat by inhaled sulfur.
- Author:
Han-Jun LIN
1
;
Hao-Wen QI
;
Li-Ping FANG
;
Shu-Jun LI
;
Zhi-Chao LI
;
Bai-Mei XIE
Author Information
- Publication Type:Journal Article
- MeSH: Air Pollutants; adverse effects; Animals; Asthma; chemically induced; Bronchi; drug effects; innervation; physiopathology; Bronchial Hyperreactivity; chemically induced; physiopathology; Bronchitis; chemically induced; Bronchoalveolar Lavage Fluid; cytology; Male; Nerve Fibers; drug effects; physiology; Neurogenic Inflammation; chemically induced; physiopathology; Random Allocation; Rats; Rats, Sprague-Dawley; Substance P; blood; Sulfur Dioxide; adverse effects
- From: Chinese Journal of Applied Physiology 2009;25(1):113-116
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2).
METHODSSixteen SD male rats were divided randomly into 2 groups (n = 8): the control group and SO2 group. The control group was exposed o pure air. SO2 group was exposed to SO2 of the content 1.0 mg/(m(3) x h) 6h daily for consecutive 3 d. At 4th day, we determined the airway responsiveness, collected the bronchoalveolar lavage fluid (BALF), plasma and lung tissue. Then we counted the total cellular score in BALF, measured the plasma SP content and made the immunohistochemistry staining on the lung tissue (HE and SP methods).
RESULTSCompared with the control group, the total cellular score in BALF and plasma SP content in SO2 group's increased significantly ( P < 0.01). HE staining showed there were a great deal of inflammatory cells infiltration under the tunica mucosa bronchiorum; and SP immunohistochemistry staining indicated there were significant changes in numbers of SP-IR positive fibers of SO2group.
CONCLUSIONExposure to low concentration of SO2 would injure healthy rat's airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critical pathophysiological mechanisms.
