Reflex interactions between aerial and aquatic gas exchange organs in larval bullfrogs.

The interaction between lung and gill ventilation was investigated in unanesthetized Rana catesbeiana larvae (stage XVII-XIX) in hypoxic (PO2 = 80 +/- 1 Torr), normoxic (PO2 = 142 +/- 1 Torr), and hyperoxic (PO2 = 580 +/- 23 Torr) water. Lung inflation with N2, air, or O2 initially reduced the frequency (fG) and buccal pressure amplitude (PBC) of the following gill ventilation cycles. However, 65 s after lung inflation fG was significantly greater for N2 inflation than for air inflation, whereas fG after O2 inflation was significantly lower. In further experiments, the effects of lung inflation and gaseous PO2 on gill ventilation were dissociated. Flow of N2, air, or O2 was established through the lungs of tadpoles in hypoxic water. Flow of N2 produced a significant rise in fG and flow of O2 a significant fall compared with airflow. Regardless of the PO2 of the gas, subsequent lung inflation produced by occlusion of the outflow cannula caused a fall in fG and PBC from the preestablished flow value. We conclude that lung inflation per se and the resulting increase in PO2 both contribute to the suppression of gill ventilation following spontaneous air breathing, which serves to limit O2 loss of the gills in aquatic hypoxia.