Featherstone R L, Parry J E, Evans D M, Jones D M, Olsson H, Szelke M, Church M K
Immunopharmacology Group, Southampton General Hospital, United Kingdom.
Lung. 1996;174(4):269-75. doi: 10.1007/BF00173141.
It has been suggested that bradykinin may play a role in stimulating cough in at least one pathological condition in humans. We have employed an animal model to investigate the possible role of this peptide in irritant-induced cough. The kinin antagonist Hoe 140 and codeine both produced dose-related inhibition of cough responses to inhalation of citric acid or bradykinin aerosols by conscious guinea pigs. The selective tissue kallikrein inhibitor CH694 inhibited cough caused by citric acid but not by bradykinin. Indomethacin pretreatment attenuated the responses to both stimuli as did phosphoramidon. It is concluded that cough produced by citric acid inhalation may be mediated, at least in part, by generation of kinins; secondary to this, a release of prostanoids also appears to participate in the response.
有人提出，缓激肽可能至少在人类的一种病理状况下刺激咳嗽中发挥作用。我们采用了一种动物模型来研究这种肽在刺激性咳嗽中的可能作用。激肽拮抗剂Hoe 140和可待因均对清醒豚鼠吸入柠檬酸或缓激肽气雾剂引起的咳嗽反应产生剂量相关的抑制作用。选择性组织激肽释放酶抑制剂CH694抑制柠檬酸引起的咳嗽，但不抑制缓激肽引起的咳嗽。吲哚美辛预处理可减弱对两种刺激的反应，磷酰胺也有同样作用。得出的结论是，吸入柠檬酸引起的咳嗽可能至少部分由激肽的生成介导；其次，前列腺素的释放似乎也参与了该反应。
