Inhibition of baroreceptor and chemoreceptor reflexes on heart rate by afferents from the lungs.

Brief stimuli were delivered to the carotid baroreceptors or chemoreceptors in dogs anaesthetized with chloralose and paralysed with D-turbocurarine. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml or air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0.2-0.5 ml of warmed CO2-equilibrated saline into the external carotid artery. Observations were made during periods of temporary cessation of artificial ventilation. 2. When the volume of the lungs was not changing, prompt decreases in heart rate were evoked by chemoreceptor or baroreceptor stimuli except when these were delivered during the inspiratory phase of breathing (as judged from the records of phrenic nerve activity). 3. No changes in heart rate were evoked when these stimuli were timed to occur during expansion of the lungs in response to a rapid increase in intratracheal pressure (6-10 mmHg in 1-2 sec). Decreases in heart rate were evoked when the stimuli occurred during slower inflations of the lungs. 4. Both stimuli regained their effectiveness on heart rate with time after inflations of the lung when the lungs were held inflated. Both stimuli evoked large decreases in heart rate when delivered during deflations of the lung. 5. The effects of lung inflation on the effectiveness of both cardiodepressor reflexes were abolished by surgical denervation of the lungs.