【摘要】 目的:通过检测气道反应性和M2受体功能,研究呼吸道合胞病毒（RSV）感染与哮喘发病的关系及机制。方法:34只豚鼠随机分为4组:Hep-2滴鼻+生理盐水雾化（Hep-2/NS,A）组,RSV滴鼻+生理盐水雾化（RSV/NS,B）组,Hep-2滴鼻+鸡卵蛋白（OVA）雾化（Hep-2/OVA,C）组和RSV滴鼻+OVA雾化（RSV/OVA,D）组,其中A和B组各9只,C和D组各8只,以A组为对照组。21 d通过电刺激迷走神经检测各组气道反应性和M2受体功能,行嗜酸性粒细胞计数以及病理学观察。结果:B组气道内压力（mmH₂O）与A组无明显差异（P>0.05）,给予匹罗卡品,IP下降幅度高于A组,但差别无显著性（P>0.05）。C组IP明显高于A且（P<0.05）,且给予匹罗卡品,IP下降幅度明显低于A组,差别有显著性（P<0.05）。D组IP明显高于C组（P<0.05）,给予匹罗卡品后IP下降幅度明显低于C组（P<0.05）。结论:RSV感染可促进过敏原引起的M2R功能障碍,从而促进AHR发生。更多还原

【Abstract】 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 mmH₂ O）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.更多还原