Effects of bronchial vascular engorgement on airway dimensions.
Wagner, Elizabeth M., Wayne Mitzner.
Divisions of Pulmonary and Critical Care Medicine and Physiology,
The Johns Hopkins University, Baltimore, Maryland
APStracts 3:0116A, 1996.
Airway vascular engorgement has been suggested to cause lumenal
narrowing and airflow obstruction. To determine the extent to which
changes in bronchial vascular volume could influence airway
dimensions, we studied the effects of left atrial pressure elevation
on airway morphometry in sheep(n=17). The bronchial branch of the
bronchoesophageal artery was cannulated and perfused with autologous
blood (0.6 ml/min/kg). A balloon-tip catheter was inserted into the
left atrial appendage to elevate left atrial pressure by 10mmHg, and
papaverine was infused into the bronchial artery to eliminate airway
smooth muscle tone. Morphologic measurements were made from rapidly
frozen lungs excised in vivo. Left atrial pressure elevation caused a
79% increase in total vascular area(p=0.0002). Average airway lumenal
area was significantly decreased from 86% to 71% of the airways
maximal area(p<0.0001). Noteworthy were the prominent bronchial
vessels located within mucosal folds. However, when papaverine was
infused during left atrial pressure elevation, despite a comparable
total vascular area, lumenal narrowing did not occur and remained at
87% of the maximal area(p=0.6267). In conclusion, we found that
engorgement of the bronchial vasculature leads to an increase in the
vascular area in regions inside and outside the smooth muscle layer.
The associated decrease in lumen area only occurs in the presence of
airway smooth muscle tone. This suggests a reflex effect on the
airway caused by the vascular engorgement. We conclude that vascular
engorgement of the airway wall per se has a negligible effect on
airway obstruction.
Received 22 June 1995; accepted in final form 7 February 1996.
APS Manuscript Number A668-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96