Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Involvement of nitric oxide (NO) in cough reflex sensitivity between non-sensitized and OVA-sensitized guinea pigs. | Hori et al. Cough 2011 7 5 http content 7 1 5 RESEARCH Cough Open Access Involvement of nitric oxide NO in cough reflex sensitivity between non-sensitized and OVA-sensitized guinea pigs Akihiro Hori Masaki Fujimura Noriyuki Ohkura and Akira Tokuda Abstract Background Exhaled nitric oxide ENO is elevated in bronchial asthma patients and inhaled corticosteroid therapy lowers the elevated ENO levels in such patients. ENO appears to be an inflammatory marker but its role in the pathophysiology of cough remains unclear. This study aimed to elucidate the relationship between NO and increased cough reflex sensitivity induced by allergic airway reactions. Methods Cough reflex sensitivity to inhaled capsaicin was observed under NO depletion caused by NO synthase NOS inhibitors in non-sensitized and ovalbumin OVA -sensitized guinea pigs. The bronchoalveolar lavage fluid BALF was analyzed in an NO depletion setting using the inducible NOS iNOS inhibitor ONO1714 in OVA-sensitized guinea pigs. Results NO depletion by the non-selective NOS inhibitor L-NAME suppressed cough reflex sensitivity in nonsensitized guinea pigs and OVA-induced increase in cough reflex sensitivity in sensitized guinea pigs however iNOS inhibition caused by ONO1714 partially suppressed the OVA-induced increase in cough reflex sensitivity but not the normal cough response in non-sensitized guinea pigs. ONO1714 did not change BAL cell components in OVA-sensitized guinea pigs. Conclusions The results suggest that NO may be involved not only in the normal cough reflex circuit but also in the OVA-induced increase in cough reflex sensitivity possibly via a different mechanism of action. Further studies are needed to clarify the precise mechanism. Background Nitric oxide NO may play an essential role in regulating airway function and in the pathophysiology of inflammatory airway diseases 1 . NO is generated by NO synthase NOS from L-arginine in vivo 2 . NOS has three isoforms namely neuronal
