Proceedings of The Physiological Society
University of Leeds (2002) J Physiol 544P, S004
Distension of the main pulmonary artery stimulates vagal afferent activity in anaesthetized dogs
J.P. Moore, R. Hainsworth and M.J. Drinkhill
Institute for Cardiovascular Research, University of Leeds, Leeds LS2 9JT, UK
Previously we have reported that distension of the main pulmonary artery by pressures in excess of 30 mmHg leads to an increase in systemic vascular resistance (McMahon et al. 2000). These pressures are higher than those normally observed in the pulmonary circulation, indicating that physiological pressures may not elicit this response. However, this failure to observe a pressor response at pressures below 30 mmHg might also reflect the effects of general anaesthesia on autonomic reflex mechanisms. The aim of the present study, therefore, was to determine whether or not vagal afferent fibres respond to physiological changes in pressure in this reflexogenic region.
Dogs were anaesthetized with α-chloralose (100 mg kg-1 I.V.) and artificially ventilated. A cardiopulmonary bypass was established that received blood from the right atrium and inferior vena cava. A pouch consisting of the entire extrapulmonary parts of the pulmonary arteries and the trunk was created and this was independently perfused with venous blood from a pressurized reservoir. The cephalic and subdiaphragmatic circulations were perfused with oxygenated blood. Afferent activity was recorded from single units or small multi-units in slips dissected from the left or right cervical vagi. The animals were humanely killed at the end of each experiment.
An increase in pulmonary pouch pressure from 5.0 ± 2.0 to 46.0 ± 4.5 mmHg elicited an increase in activity from 12.0 ± 4.1 to 40.3. ± 7.6 impulses s-1 (means ± S.E.M., P < 0.05, paired t test, n = 9). At a mean pulmonary pressure of 20.5 ± 1.0 mmHg, activity was significantly increased by 7.0 ± 2.5 impulses s-1 (P < 0.05), representing 25 % of the overall response. In additional experiments, the chest cavity was resealed and ventilation was simulated by application of a pulsatile negative pressure (approximately 8 mmHg) to the thoracic cavity at a frequency of 0.3 Hz. The mean pulmonary arterial pressure corresponding to 50 % of the overall response was lower during simulated ventilation than in its absence (21.7 ± 2.2 versus 16.8 ± 2.4 mmHg, P < 0.05, n = 7). We conclude that afferent activity from baroreceptors located in the extrapulmonary pulmonary arteries does increase to distension of this region. This response is enhanced by changes in intrathoracic pressure during ventilation. It is likely, therefore, that the vagal afferents attached to these receptors contribute to normal circulatory control.
This work was supported by the British Heart Foundation.
All procedures accord with current UK legislation.
Where applicable, experiments conform with Society ethical requirements