Evidence for pulmonary CO2 chemosensitivity: effects on ventilation

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Abstract
To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (.ovrhdot.VE), the systemic and pulmonary circulations were separated and partial pressure of CO2 (PCO2) was controlled independently in each circuit under hyperoxic conditions and .ovrhdot.VE was measured. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l.cntdot.kg-1.cntdot.min-1. Systemic PCO2 (PsCO2) was held constant at 3 different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between .apprx. 7-85 torr. With PsCO2 at 43.5 .+-. 0.4 torr, .ovrhdot.VE increased 2.67 .+-. 0.061 l.cntdot.min-1 as PpCO2 was varied between these limits. With PsCO2 at 63.8 .+-. 2.5 torr, .ovrhdot.VE increased 3.95 .+-. 0.73 l.cntdot.min-1 over these same limits of PpCO2. With PsCO2 < 25-30 torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on .ovrhdot.VE was abolished by vagotomy. These resuls suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of .ovrhdot.VE.