Distension of the main pulmonary artery results in an increase in systemic vascular resistance (McMahon et al. 2000). However, significant vasoconstriction is not observed until the distension pressure is above 30 mmHg, which is higher than that normally observed in the pulmonary circulation. Recently we reported that afferent activity from pulmonary arterial baroreceptors is enhanced and that the ‘set point’ of this response is decreased when the chest is closed and phasic negative intrathoracic pressure is applied (Moore et al. 2002). The aim of this present study, therefore, was to re-examine the systemic vascular response to pulmonary artery distension, and to determine if this is altered by phasic intrathoracic pressure changes.

Eight dogs were anaesthetized with α chloralose (100 mg kg^-1 I.V.) and artificially ventilated. The carotid sinuses were vascularly isolated and perfused at controlled pressures. A cardiopulmonary bypass was established that received blood from the left atrium and inferior vena cava, oxygenated it, and pumped it to a pressurized reservoir connected to cannulae inserted into the central and distal ends of the thoracic aorta. The subdiaphragmatic circulation was perfused at constant flow, and systemic perfusion pressure (SPP) provided an index of vascular resistance. 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 another pressurized reservoir. Strapping the ribs and sternum together and then suturing the overlying muscle and skin tightly together resealed the chest cavity. The animals were humanely killed at the end of each experiment.

With intrathoracic pressure at atmospheric, the pulmonary arterial pressure (PAP) at the threshold for the response, which was taken to a 5 % increase in SPP from baseline, was 31.2 ± 5.5 mmHg (mean ± S.E.M.). Simulation of physiological thoracic pressure changes by applying phasic negative intrathoracic pressure (minus 10 mmHg at 0.3 Hz) decreased the PAP at threshold to 21.2 ± 4.1 mmHg (t test, P < 0.05). The ‘set point’ of the stimulus-response curve was also significantly reduced, from 38.2 ± 4.5 mmHg to 25.5 ± 4..3 mmHg (P < 0.05).

We conclude that with physiological intrathoracic pressures, normal levels of pulmonary artery pressure induce reflex vasoconstriction and that pulmonary arterial baroreceptors are likely to have a role in circulatory control.

This work was supported by the British Heart Foundation.