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Journal of Applied Physiology, Vol 80, Issue 1 341-344, Copyright © 1996 by American Physiological Society
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M. Scuri, V. McCaskill, A. D. Chediak, W. M. Abraham and A. Wanner
Division of Pulmonary Disease, University of Miami School of Medicine at Mount Sinai Medical Center, Florida 33140, USA.
The reported effects of cholinergic agonists on bronchial blood flow (Qbr) have been inconsistent. The aim of the present study was to determine whether the inconsistency could be due to the mode of agonist administration (systemic vs. aerosol) or the anatomic site of blood flow in the bronchus (mucosal vs. deep wall). In 10 anesthetized mechanically ventilated adult sheep, we measured Qbr in main bronchi by color-coded microspheres, systemic and pulmonary arterial pressures, cardiac output, and lung resistance (RL) before and after acetylcholine (ACh) administered either as an aerosol (nebulized dose 100 micrograms) or as an intravenous bolus (2 micrograms/kg). Before drug administration, 72% of mean Qbr was distributed to the bronchial mucosa and the remainder was distributed to the deep bronchial wall. For a comparable increase in mean RL (150% for intravenous ACh and 205% for aerosol ACh), mean total Qbr normalized for systemic arterial pressure increased by 291% after intravenous ACh (P < 0.05) and decreased by 9% after aerosol ACh (not significant). Mucosal and deep wall Qbr increased proportionally. Atropine (0.2 microgram/kg) prevented the changes in Qbr and RL after intravenous ACh. Thus intravenous but not aerosol ACh increased blood flow in the mucosa and deep wall of extrapulmonary bronchi. This suggests that the muscarinic receptors mediating vasodilation are more accessible to intravascular than intrabronchial ACh.
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