THE EFFECTS OF ALTERED AQUATIC AND AERIAL RESPIRATORY GAS CONCENTRATIONS ON AIR-BREATHING PATTERNS IN A PRIMITIVE FISH (AMIA-CALVA)

The mechanisms and physiological control of air-breathing were investi gated in an extant halecomorph fish, the bowfin (Amia calva). Air flow during aerial ventilation was recorded by pneumotachography in undist urbed Amia calva at 20-24-degrees-C while aquatic and aerial gas conce ntrations were independently varied. Separation of aquatic and aerial gases was used in an attempt to determine whether Amia calva monitor a nd respond to changes in the external medium per se or to changes in d issolved gases within the body. Air flow measurements revealed two dif ferent types of ventilatory patterns: type I air-breaths were characte rized by exhalation followed by inhalation; type II air-breaths, which have not been described previously in Amia calva, consisted of single inhalations with no expiratory phase. Expired volume (V(exp)) for typ e I breaths ranged from 11.6 +/- 1.1 to 26.7 +/- 2.9 nil kg - 1 (95 % confidence interval; N=6) under normoxic conditions and was unaffected by changes in aquatic or aerial gases. Gas bladder volume (V(B)), det ermined in vitro, was 80 ml kg - 1; the percentage of gas exchanged fo r type I breaths ranged from 14 to 33 % of V(B) in normoxia. Fish expo sed to aquatic and aerial normoxia (P(O2)=19-21 kPa), or aerial hyperc apnia (P(CO2)=4.9 kPa) in normoxic water, used both breath types with equal frequency. Aquatic or aerial hypoxia (P(O2)=6-7 kPa) significant ly increased air-breathing frequency in four of eight fish and the ven tilatory pattern changed to predominantly type I air-breaths (75-92 % of total breaths). When fish were exposed to 100 % 02 in the aerial ph ase while aquatic normoxia or hypoxia was maintained, air-breathing fr equency either increased or did not change. Compared with normoxic con trols, however, type II breaths were used almost exclusively (more tha n 98 % of total breaths). Type I breaths appear to be under feedback c ontrol from O2-sensitive chemoreceptors since they were stimulated by aquatic or aerial hypoxia and were