Ventilatory and Cardiac Reflex Responses to Hypoxia and NaCN in Lepisosteus osseus, an Air-breathing Fish

The hypoxic depression of gill ventilation, along with other ventilatory and cardiovascular responses to hypoxia, were studied in the bimodal breather, Lepisosteus osseus. Air-breathing frequency increased hyperbolically as water Po2 declined. The response of gill ventilation to changes in water Po2 was complex. Opercular pressure initially increased as Po2 fell, reaching maximal levels between 75 and 125 torr Po2. As the Po2 fell further, opercular pressure fell to about 50% of its maximal level. Heart rate rose as Po2 fell. Gill ventilation frequency did not change significantly with hypoxia. A 1/1 coupling between heart rate and gill ventilation was observed in four of nine fish in which heart rate was measured, during normoxia only. The Po2 in the dorsal aorta (DA) fell with hypoxia but did not change significantly in the ventral aorta (VA) at any level of aquatic hypoxia. External administration of NaCN had a large stimulatory effect on air-breathing frequency but did not significantly affect gill ventilation. Internal injections of NaCN into either the DA or VA produced a prolonged stimulation of gill ventilation and transiently stimulated air breathing, but the response to VA injections was much quicker. Heart rate was not significantly affected by NaCN. These data suggest that air breathing is initiated on stimulation of external chemoreceptors located in or near the gills, while gill ventilation is controlled by internal chemoreceptors. The depression of gill ventilation seen during hypoxia, contrasted to the exclusively stimulatory effects of the NaCN, further suggests that the internal chemoreceptors are positioned where they are able to sense the increased flow of oxygenated pulmonary blood during intense air breathing.