Right ventricular pressure and ventilatory responses to pulmonary gas embolism

This study was designed to test the hypothesis that changes in right ventricular pressure (PRV) are responsible in part for the altered breathing frequency (f) during pulmonary gas embolism (PGE). PGE was induced by infusing air into the femoral vein of alpha-chloralose anesthetized dogs. Respiratory flow pattern was recorded and analyzed in relation to PRV changes induced resulting from PGE. The rise of PRV, whether induced by PGE, by pulmonary artery occlusion, or by acute elevation of pulmonary arterial blood flow, was consistently associated with increased f. Breathing frequency rose principally through reduction of expiratory duration (TE). The inspiratory duration (TI) was shortened somewhat and the fractional inspiratory cycle, TI/(TE + TI), increased. The relationships between PRV and f were altered by changes of PRV resulting from the administration of histamine antagonist, by beta-adrenergic blockade, beta-adrenergic stimulation, and by changing pulmonary arterial blood flow. The responses did not occur after bilateral cervical vagotomy. These results demonstrate that f during PGE is partially regulated in response to changes in PRV and is mediated through the vagal afferent.