CONTROL OF RESTING BRONCHIAL HEMODYNAMICS IN THE AWAKE DOG

In the resting awake dog a continuous-wave Doppler flow transducer on the right bronchoesophageal artery inscribes a sharp early systolic sp ike and low flow in late systole and throughout diastole, indicating a highly resistive bed. An analysis of autonomic factors using intraven ous, cumulative, and randomly applied cholinoceptor, beta1- and beta2- adrenoceptor, and alpha1- and alpha2-adrenoceptor antagonists indicate s that the low vascular conductance is due to cholinoceptor and alpha1 - and alpha2-adrenoceptor effects in a ratio 3.6:1. No beta-adrenocept or tone is present. Sighing behavior invokes a transient (<2 s) fall i n intrapleural pressure (and thus rise in bronchovascular transmural p ressure) of 10-30 mmHg, which is followed by a two- to threefold incre ase over 30 s in bronchial flow and conductance, an effect simulated i n 50% of dogs when bronchovascular transmural pressure is acutely rais ed and maintained over 40-60 s by inflating an intra-aortic balloon di stal to the origin of the bronchial artery. Autonomic blockade has no effect on bronchovascular dilatation evoked either by sighing or by ba lloon inflation. It is concluded that, in the resting bronchial circul ation, there exists strong cholinoceptor and alpha-adrenoceptor-based vasoconstrictor activity which can be overpowered by strong nonadrener gic noncholinergic local vasodilator reflexes evoked by sudden changes in intrathoracic transmural pressure possibly acting on stretch-sensi tive sensory nerve endings containing substance P, calcitonin gene-rel ated peptide, and neurokinins. The tonic vasoconstrictor but not the s igh-evoked vasodilator effects are sensitive to pentobarbital sodium a nesthesia.