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Journal of Experimental Biology 96,295-306 (1982)
Published by Company of Biologists 1982

Respiration and Acid-Base Physiology of the Spotted Gar, A Bimodal Breather : III. Response to a Transfer from Fresh Water to 50% Sea Water, and Control of Ventilation

NEAL J. SMATRESK ¹ and JAMES N. CAMERON ²

¹ Departments of Zoology and Marine Studies, The University of Texas at Austin, Port Aransas Marine Laboratory, Port Aransas, Texas 78373, U.S.A.; Present address: University of Pennsylvania, School of Medicine, Department of Physiology, Philadelphia, PA 19104, U.S.A.
² Departments of Zoology and Marine Studies, The University of Texas at Austin, Port Aransas Marine Laboratory, Port Aransas, Texas 78373, U.S.A.

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.

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