摘要
目的:探讨大鼠吸入低浓度SO_2后引起气道损伤以及气道反应性的变化与相关的病理生理机制。方法: SD雄性大鼠16只,随机分为2组(n=8):对照组和SO_2组。对照组暴露于正常空气中。SO_2组暴露于含量为1.0 mg/(m^3·h)的SO_2室内空气中,每天6 h,连续3 d,第4 d测大鼠气道反应性,采集血清、收集支气管肺泡灌洗液(BALF),留取肺组织。分别进行BALF细胞计数,测血清中P物质(SP)的含量,作肺组织病理切片行HE及SP免疫组化染色。结果:SO_2组与对照组比较,大鼠的气道反应性增高(P<0.01),BALF中细胞总数明显升高(P<0.01);血清SP含量显著增加(P<0.01)。肺组织病理切片UE染色显示SO_2组支气管粘膜下有大量炎性细胞浸润;免疫组化染色提示SO_2组SP免疫阳性神经纤维数量明显增加(P<0.05)。结论:吸入SO_2诱发大鼠出现气道高反应性,气道内感觉神经源性炎症是其重要的病理生理机制之一。
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 to pure air. SO2 group was exposed to SO2 of the content 1.0 mg/（ m3.h）, 6 h dail 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 immtmohistochemistry 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 inflannnatory cells infiltration under the tunica mucosa bronchiorum; and SP immunohis- tochemistry, staining indicated there were significant changes in numbers of SP-IR positive fibers of SO2 group. Conclusion： Exposure to low concentration of SO2 would injure healthy rat＇ s airway, and induce airway hyperresponsiveness, neurogenic inflammation is one of its critica pathophysiological mechanisms
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2009年第1期113-116,共4页
Chinese Journal of Applied Physiology
关键词
二氧化碳
气道高反应
感觉神经
SP
sulfur dioxide
airway responsiveness
sensory nerves
substance P
