Background: During exercise and recovery the transient and steady-state changes in autonomic activity regulating lower airway blood flow and dimensions are unknown. The aim of this study was to define changes in bronchial blood flow (Qbr) and dimensions during moderate and strenuous exercise, and to analyse the role of vagal and sympathetic nerves. Methods: Nine ewes (34–44 kg) underwent left thoracotomy during general anaesthesia (thiopentone/isoflurane) and either (5 sheep = Group 1) a pulsed Doppler transducer was placed on the bronchial artery, or (4 sheep = Group 2) a pulsed Doppler transducer was placed on the bronchial artery, and transit-time and single crystal sonomicrometers were mounted on the left main bronchus. These measured continuously Qbr, bronchial circumference (Circbr) and wall thickness (Thbr). Aortic pressure (Pa) and central venous pressure catheters were placed in the superficial cervical artery and vein. Trained sheep exercised on a horizontal treadmill, i.e. Group 1, moderate exercise 2.2 mph over 1.6, 6 min recovery, for analysis of changes in Qbr before and after cholinoceptor blockade; Group 2, strenuous exercise 4.4 mph over 2, 10 min recovery for analysis of changes in Qbr and airway dimensions, before and after cholinoceptor plus α1-, α2-adrenoceptor blockade. β-adrenoceptor systems were intact. Results: In Group 1 during moderate exercise Pa and heart rate (HR) rose. Qbr and blood flow conductance (Cbr) fell immediately to 83% (P<0.001) before returning toward resting levels, but fell when exercise ceased to 89% (P<0.01) before recovering. Prior cholinoceptor blockade abolished the immediate fall in Qbr and Cbr, but not the recovery vasoconstriction. Later in recovery the bronchial bed dilated progressively over 6 min (P<0.05). In Group 2 during strenuous exercise Pa and HR rose substantially. Qbr and Cbr fell to 68% and 54% (P<0.001), respectively, and there was early vasoconstriction in recovery. Circbr fell immediately and remained at 93% (P<0.01), and did not recover fully when exercise ceased. Thbr did not change during or after exercise. Prior cholinoceptor plus α-adrenoceptor block caused Pa and Qbr to fall slightly during exercise, but the bronchovascular constriction during and after exercise was abolished, as was circumferential shortening in the airway. Conclusions: At exercise onset and steady-state, resetting the arterial baroreflex upward in sheep increases parasympathetic cholinergic vasoconstrictor activity and causes bronchial wall and bronchovascular smooth muscle contraction in concert with sympathetic adrenergic constriction of systemic vascular beds. Whether the known sigmoid baroreflex control of tracheal smooth muscle tension at rest is extended to tracheobronchial smooth muscle and its circulation during exercise is yet to be determined.
Pulmonary Pharmacology and Therapeutics Vol. 20, Issue 2, p. 190-199