Nitric oxide and [beta]-adrenergic agonist-induced bronchial
arterial vasodilation.
Charan, Nirmal B., Shane R. Johnson, S. Lakshminarayan, William H.
Thompson, Paula Carvalho.
Pulmonary Research Laboratory, VA Medical Center, Boise, Idaho
83702 and Division of Pulmonary/Critical Care Medicine, Department of
Medicine, University of Washington, Seattle, Washington 98195
APStracts 3:0489A, 1996.
In anesthetized sheep, we measured bronchial blood flow (QBR) by an
ultrasonic flow probe to investigate the interaction between inhaled
nitric oxide (NO, 100 ppm) given for 5 min, and 5 ml of aerosolized
isoetharine (1.49X10-2M concentration). NO and isoetharine increased
QBR from 26.5+/-6.5 (mean+/-SEM) to 39.1+/-10.6 and 39.7 ml/min
respectively (n=5). Administration of NO immediately following
isoetharine further increased QBR to 57.3+/-15.1 ml/min. NO synthase
inhibitor, N_-nitro-L-arginine methyl ester hydrochloride (L-NAME, 30
mg/kg, in 20 ml saline given intravenously), decreased QBR to 14.6+/
-2.6 ml/min. NO given 3 times alternately with isoetharine,
progressively increased QBR from 14.6+/-2.6 to 74.3+/-17.0 ml/min,
suggesting that NO and isoetharine potentiate vasodilator effects of
each other. In three other sheep, following L-NAME, three sequential
doses of isoetharine increased QBR from 10.2+/-3.4 to 11.5+/-5.7,
11.7+/-4.7 and 13.3+/-5.7 ml/min respectively indicating that
isoetharine's effects are predominantly mediated through synthesis of
NO. When this was followed by three sequential administrations of NO,
QBR increased by 146%, 172%, and 185% respectively. Thus, in the
bronchial circulation, there seems to be a close interaction between
cAMP and cGMP mediated vasodilatation.
Received 29 July 1996; accepted in final form 15 October 1996.
APS Manuscript Number A715-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996