Ventilatory response to hypercapnia in the larger spotted dogfish Scyliorhinus stellaris.
Dogfish were exposed to sudden changes of Pco2 in inspired seawater. During hypercapnia breathing frequency remained constant, but gill ventilation was transiently increased to about 140% of control levels in the 1st h. O2 uptake was significantly increased also, but returned to the initial level before nomalization of gill ventilation. In contrast to the transient rise in gill ventilation and O2 uptake, arterial Po2 was increased for the whole period of hypercapnia. Hypercapnia results in a marked fall in pHa which returned to the initial value in 4-5 h even though hypercapnia is maintained. This rise in pHa with little change in PaCO2 was associated with an increase in plasma bicarbonate concentration. The increase of plasma bicarbonate was in part due to compensatory bicarbonate uptake from the seawater across the gills and in part was effected by transfer between intracellular tissue compartments and extracellular spaces. The compensatory bicarbonate exchange mechanism in the gills seems to have a delay both after onset and termination of hypercapnia.
Ventilatory response to hypercapnia in the larger spotted dogfish Scyliorhinus stellaris. Dogfish were exposed to sudden changes of Pco2 in inspired seawater. During hypercapnia breathing frequency remained constant, but gill ventilation was transiently increased to about 140% of control levels in the 1st h. O2 uptake was significantly increased also, but returned to the initial level before nomalization of gill ventilation. In contrast to the transient rise in gill ventilation and O2 uptake, arterial Po2 was increased for the whole period of hypercapnia. Hypercapnia results in a marked fall in pHa which returned to the initial value in 4-5 h even though hypercapnia is maintained. This rise in pHa with little change in PaCO2 was associated with an increase in plasma bicarbonate concentration. The increase of plasma bicarbonate was in part due to compensatory bicarbonate uptake from the seawater across the gills and in part was effected by transfer between intracellular tissue compartments and extracellular spaces. The compensatory bicarbonate exchange mechanism in the gills seems to have a delay both after onset and termination of hypercapnia.