[To explore the mechanisms of neurogenic inflammation and airway hyperresponsiveness of rat by inhaled sulfur].

AIM: To explore the physiopathological mechanisms of airway injury and the effect on the airway responsiveness of rat by inhaled sulfur dioxide(SO2). METHODS: Sixteen 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). RESULTS: Compared 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. CONCLUSION: Exposure to low concentration of SO2 would injure healthy rat's airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critical pathophysiological mechanisms.

[Respiratory syncytial virus infection enhances airway hyperresponsiveness in guinea pigs and the underlined mechanism].

AIM: To study the relation between Respiratory Syncytial Virus infection and asthma development by measuring airway responsiveness (AR) and M2R function. METHODS: Guinea pigs (n = 34) were randomly divided into 4 groups: Hep-2/NS group (group A, n = 9), RSV/NS group (group B, n =9), Hep-2/OVA group (group C, n = 8) and RSV/OVA group(group D, n = 8). On day 21 after infection we tested AR and M2R. Then counted eosinophils in BALF and observed pathological change. RESULTS: Intraairway pressure(IP mmH20) of group B had no significant difference with group A(P > 0.01), and the extent of IP decrease also had no difference between groups A and B (P > 0. 05), but IP of C group were much higher than group A (P<0.05), with extent of IP decrease lower than group A (P < 0.05). And IP of group D were higher than group C (P < 0.01), with the extent of IP decrease much lower than group C (P < 0.05). CONCLUSION: RSV infection could enhance OVA-induced M2R dysfunction, then develop AHR.