APPS November 2002 Meeting Abstract 2427


Saxon White, Stephen McIlveen, Robert Bishop, Anthony Quail, David Cottee, Gibbe Parsons, Robert Gunther, Jessica Davis, Linda Talken, Human Physiology and Hunter Heart-Lung Research Guild, University of Newcastle, NSW, 2308, Australia, and Departments of Pulmonary and Critical Care Medicine, and Surgery, University of California Davis, Davis, CA, 95616, USA.

Bronchial blood flow (Qbr) is postulated to rise during and after exercise and may be associated with mechanisms of asthma syndromes. However, the true bronchovascular events and underlying mechanisms are unknown. Eight sheep were instrumented at thoracotomy under thiopentone sodium/isoflurane anaesthesia with pulsed Doppler flow probes on the bronchial artery, and aortic and central venous catheters were inserted in transcapular vessels. Sheep exercised on a horizontal treadmill at 0.8, 1.6, 2.2, 1.6, 0.8 mph over 5 min, or intensively at 4.4 mph over 2 min. They were followed after both protocols for 10 min. Aortic pressure (AoP) and heart rate (HR) rose, and Qbr did not change or fell. In 4 sheep, at 4.4 mph, AoP rose 118%. Qbr and bronchial flow conductance (Cbr) fell to 65% and 56%, respectively. Analysis over 1.5 min at 2.2 mph and for 5.5 min post-exercise for alpha-1,-2 adrenoceptor and cholinoceptor mechanisms was carried out in 4 other sheep using phentolamine mesylate and methscopolamine bromide, respectively. Exercise onset caused a rise in AoP and HR, and a fall in Qbr at 10-16s to 93%, and conductance to 89% (P=0.01). Both flow and conductance returned to pre-exercise levels at 1 and 1.5 min, respectively. At 24s post-exercise, aortic pressure and heart rate returned toward resting, but bronchial flow and conductance fell to new nadirs of 90% and 86% (P=0.01), respectively, before returning to resting at 5.5 min. Either alpha-1,-2 adrenoceptor or cholinoceptor antagonists attenuated vasoconstrictor responses during and post-exercise. Thus in normal sheep exercising, sympathetic and parasympathetic nerves interact to maintain or lower Qbr and Cbr during and after exercise. If a rise in Qbr is associated with bronchial obstruction in asthma syndromes of exercise, these mechanisms normally limit airway hyperaemia, a rise in bronchovascular capillary pressure, and airway oedema, in achieving airway homeostasis.

Supported in part by Ramaciotti Foundation (Australia)

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