Journal of Applied Physiology, Vol 56, Issue 5 1418-1422, Copyright © 1984 by American Physiological Society
Mechanism of hyperpnea induced by changes in pulmonary blood flow
J. F. Green and N. D. Schmidt
Increases in pulmonary blood flow can elicit hyperpnea. To examine the
mechanisms responsible, we surgically isolated the systemic and pulmonary
circulations in six dogs and independently controlled PCO2, PO2, and blood
flow in each circuit. Anesthesia was induced with ketamine and maintained
with halothane. Systemic venous return was drained from the right atrium
and passed through a membrane oxygenator and heat exchanger; blood was
returned to the ascending aorta (Qs). An identical bypass was established
for the pulmonary circulation, draining blood from the left atrium and
returning it to the pulmonary artery (Qp). The lungs were initially
ventilated with room air. Qs and systemic arterial CO2 gas tension were
maintained at approximately 0.080 1 X min-1 X kg-1 and 40 Torr,
respectively. Pulmonary arterial CO2 gas tension was set near 55 Torr, and
Qp varied. Ventilatory drive was assessed by minute integration (MI) of the
activity recorded from the central end of the left C5 root of the phrenic
nerve. MI increased as much as 160% above control as Qp was increased over
the range of 0.025 (control) to 0.175 1 X min-1 X kg-1. When pulmonary CO2
gradients were eliminated by a rebreathing technique, MI was independent of
Qp. These results suggest that CO2-sensitive pulmonary receptors respond to
the change in pulmonary PCO2 gradients which occur when Qp is elevated
(breathing room air) augmenting ventilation.
