Interaction between airway edema and lung inflation on responsiveness of individual airways in vivo

被引:26
作者
Brown, RH
Mitzner, W
Wagner, EM
机构
[1] JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT MED,DIV PULM & CRIT CARE MED,BALTIMORE,MD 21205
[2] JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT RADIOL,BALTIMORE,MD 21205
[3] JOHNS HOPKINS UNIV,SCH HYG & PUBL HLTH,DEPT ANESTHESIOL & CRIT CARE MED,BALTIMORE,MD 21205
关键词
bradykinin; high-resolution computed tomography; hyperresponsiveness; hyperreactivity; methacholine;
D O I
10.1152/jappl.1997.83.2.366
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Inflammatory changes and airway wall thickening are suggested to cause increased airway responsiveness in patients with asthma. In five sheep, the dose-response relationships of individual airways were measured at different lung volumes to methacholine (MCh) before and after wall thickening caused by the inflammatory mediator bradykinin via the bronchial artery. At 4 cmH(2)O transpulmonary pressure (Ptp), 5 mu g/ml MCh constricted the airways to a maximum of 18 +/- 3%. At 30 cmH(2)O Ptp, MCh resulted in less constriction (to 31 +/- 5%). Bradykinin increased airway wall area at 4 and 30 cmH(2)O Ptp (159 +/- 6 and 152 +/- 4%, respectively; P < 0.0001). At 4 cmH(2)O Ptp, bradykinin decreased airway luminal area (13 +/- 2%; P < 0.01), and the dose-response curve was significantly lower (P = 0.02). At 30 cmH(2)O, postbradykinin, the maximal airway narrowing was not significantly different (26 +/- 5%; P = 0.76). Bradykinin produced substantial airway wall thickening and slight potentiation of the MCh-induced airway constriction at low lung volume. At high lung volume, bradykinin increased wall thickness but had no effect on the MCh-induced airway constriction. We conclude that inflammatory fluid leakage in the airways cannot be a primary cause of airway hyperresponsiveness.
引用
收藏
页码:366 / 370
页数:5
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