ABSTRACT
Transfer from fresh water to 50% sea water (SW) at 26 °C increased the blood osmolarity of spotted gar (Lepisosteus oculatus) from 275 to 310 mosmol during the first 24 h. It then returned slowly to freshwater levels by 5 days after the transfer. The arterial pH dropped sharply, from 7·69 in fresh water to 7·46 in 50% SW, as a result of a small elevation in the blood CO2 partial pressure, and a marked metabolic acidosis. The respiratory (CO2) portion of the acidosis appeared to be a result of the reduction in branchial ventilation, and possibly permeability as well. The metabolic portion of the acidosis was not due to the accumulation of lactic acid, but probably involved a disruption of the extracellular strong ion difference in the saltier medium. The metabolic acidosis did not diminish during 5 days.
The rate of air breathing rose from 7 to 20 bph during 50% SW exposure. The control of pulmonary ventilation was directly responsive to the availability of O2, in general increasing when O2 was limiting (e.g. 50% SW transfer, hypoxia) and decreasing in hyperoxia. CO2 had no affect on the rate of air breathing. Withdrawal from 5–20% of total lung volume elicited an immediate air breath during hypoxia, but the response was inconsistent in normally aerated water. Lung inflation with O2 prolonged the interval between air breaths, but inflation with N2 did not change the rate of air breathing. Thus, pulmonary ventilation was secondarily controlled by lung volume. Gill ventilation frequency fell in 50 % SW, despite a respiratory and metabolic acidosis, while gill ventilation increased in response to treatment with acetazolamide. Hyperoxia caused a marked depression of gill ventilation, despite a respiratory acidosis. The gill ventilation rate appears to be most closely linked to oxygen, but may be affected indirectly by CO2 through the Root or Bohr effects.
