Ventilatory changes associated with changes in pulmonary blood flow in dogs.

To examine the influence of pulmonary blood flow (Qp) on spontaneous ventilation (VE), we isolated the systemic and pulmonary circulations and controlled the arterial blood gases and blood flow (Q) in each circuit as we measured VE. Each dog was anesthetized with ketamine and maintained with halothane. Systemic Q was drained from the right atrium and pumped through an oxygenator and heat exchanger and returned to the aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and pumping it to the pulmonary artery. The heart was fibrillated, all cannulas were brought through the chest wall, and the median sternotomy was closed. The dog was then allowed to breathe spontaneously. The arterial O2 partial pressure (PO2) of both circuits was maintained greater than 300 Torr. Systemic Q was maintained at 0.080 l X min-1 X kg-1. Initially the arterial CO2 partial pressure (PCO2) of both circuits was set at 40 Torr as Qp was varied randomly between approximately 0.025 and 0.175 l X min-1 X kg-1. The average VE-Qp relationship was linear with a slope of 1.45 (P less than 0.0005). Increasing the arterial PCO2 of both circuits to 60 Torr elevated VE an average of 0.37 l X min-1 X kg-1 at each level of Qp (P less than 0.0005). Vagotomy abolished the effect of Qp on VE. Increasing Qp affected the systemic arterial PCO2-VE response curve by shifting it upward without altering its slope. These results demonstrate that increases in Qp are associated with increases in VE. This phenomenon may contribute to exercise hyperpnea.