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Research Article Free access | 10.1172/JCI118155
Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Find articles by Freed, A. in: JCI | PubMed | Google Scholar
Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Find articles by Omori, C. in: JCI | PubMed | Google Scholar
Department of Environmental Health Sciences, Johns Hopkins University, Baltimore, Maryland 21205, USA.
Find articles by Schofield, B. in: JCI | PubMed | Google Scholar
Published September 1, 1995 - More info
We examined the effect of bronchial blood flow (BBF) on hyperpnea-induced airway obstruction (HIAO) in dogs. HIAO in in situ isolated pulmonary lobes with or without BBF was monitored via a bronchoscope. An intravascular tracer in conjunction with morphometric analysis was used to document the efficacy of our occlusion technique. We found that (a) Occlusion of the bronchial artery abolished bronchovascular leakage, but did not alter HIAO; (b) HIAO occurred in postmortem dogs, and was attenuated by cooling; (c) absence of BBF did not cause mucosal damage, although hyperpnea-induced injury was enhanced in airways lacking BBF; (d) BBF did not affect either goblet/ ciliated cell ratios or hyperpnea-induced goblet cell degranulation; (e) ligation of the bronchial artery and hyperpnea each caused mast cell degranulation, and these effects were additive; (f) hyperpnea-induced leukocyte infiltration was reduced in the absence of BBF; and (g) ligation of the bronchial artery and hyperpnea with dry air each increased airway vessel diameter, and these effects were additive. We conclude that either impairment or absence of BBF abolishes bronchovascular leakage and increases hyperpnea-induced mucosal injury, but fails to affect HIAO. Based on these results we speculate that bronchovascular leakage protects the bronchial mucosa from excessive losses of heat and water, and inhibits mucosal damage.