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Journal of Applied Physiology, Vol 76, Issue 4 1624-1629, Copyright © 1994 by American Physiological Society
ARTICLES |
S. Blosser, W. Mitzner and E. M. Wagner
Division of Pulmonary and Critical Care Medicine and Physiology, Johns Hopkins University, Baltimore, Maryland 21224.
It has been suggested that airway obstruction may be mediated in part by airway vascular engorgement or airway wall edema. However, there are few data that support this conjecture. In this study we examined the effects of increased bronchial blood flow (Qba) on airway wall dimensions, conducting airway resistance, peripheral airway resistance, and airway reactivity assessed by methacholine aerosol challenge. The bronchial artery was perfused with autologous blood (control Qba = 0.6 ml.min-1.kg-1) in anesthetized ventilated sheep. The artery was perfused at either control (C) Qba or at high (H) Qba (300% of C Qba) for 3 h. Morphometry showed a doubling of the vascular area in airways exposed to H Qba (n = 4) compared with C Qba (n = 4). However, the significant increase in wall area could be accounted for only partially by the vascular changes, with edema fluid accumulation accounting for the major increase. Despite these changes, baseline airway resistance (n = 16) and peripheral airway resistance were both unaltered. Airway reactivity to methacholine before and after H Qba was also examined (n = 12). The 3 h of H Qba had no effect on airway reactivity regardless of whether challenge occurred with C or H Qba. The lack of effect of vascular engorgement on airway resistance or reactivity does not support a primary role for these factors in mediating airway obstruction.
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