Ventilation in Pacific hagfish (Eptatretus stoutii) during exposure to acute hypoxia or hypercapnia

A technique was developed to measure ventilation in unrestrained Pacific hagfish (Eptatretus stoutii) by inserting and fastening into the nostril a flexible tube fitted with an ultrasonic flow probe. This technique permitted the continuous measurement of ventilation (respiratory) frequency (fR), stroke volume and minute ventilation (.V(E)) in real time in fish exposed to acute hypoxia or hypercapnia. Exposing fish to acute hypoxia (final PW(O2)=21.0 +/- 3.4 mm Hg) caused hypoxaemia and a marked increase in .V(E) of 350+/-71 ml min(-1)kg(-1) (from 235 to 585 ml min(-1)kg(-1)) owing exclusively to an increase in fR of 44+/-7 min(-1) (from 19 to 63 min(-1)). Because O(2) consumption (approximately 0.4 mmol kg(-1)h(-1)) was unaltered during hypoxia, there was an associated marked increase in the ventilation convection requirement from 36.7 to 81.8l mmol(-1). Injecting the O(2) chemoreceptor stimulant NaCN into inspired water (external CN-) or pre-branchial blood (internal CN-) evoked ventilatory responses that were similar to those observed during hypoxia although of a lesser magnitude. With external CN(-), V (E) increased maximally by 146+/-46 ml min(-1)kg(-1) and fR increased by 20+/-2 min(-1). With internal CN-, the maximal increase in .V(E) was 93+/-30 ml min(-1)kg(-1) and fR increased maximally by 19+/-6 min(-1). Exposure to acute hypercapnia (final PwC=7.0+/-0.2 mmHg) caused an increase in V (E) of 169+/-60 ml min(-1)kg(-1). These results provide compelling evidence for chemoreceptor-mediated control of breathing in hagfish and suggest that ventilatory responses to environmental hypoxia and hypercapnia in the vertebrates arose in the myxine lineage.