Elevation of temperature from 20 to 30 °C, increased the pulmonary ventilation and pulmonary oxygen consumption (from 0·18 to 0·43 ml O2.kg−1. min−1). The total CO2 excretion also rose, but branchial ventilation and branchial oxygen consumption did not change significantly.

The blood pH dropped quickly when temperature was elevated, with a slope (dpH/dT°) of −0·015, but the OH−/H+ ratio did not change significantly. This change in pH resulted from an elevation in arterial ⁠, without any concomitant change in plasma HCO3−. Arterial per se was probably not actively regulated, but rose passively as a consequence of the gar’s utilization of the lung for increased oxygen uptake, and the inefficiency of the lung in CO2 exchange. The lung had an exchange ratio (R) of about 0·1.

Temperature change produced no significant alteration in the net acid excretion from either the kidney or the gills, despite an increased ammonia excretion rate at 30 °C. The urine formation rate was very low (74 μl. 100 −1.h− 1) which imposed a limitation on the importance of the kidney in acid-base regulation.

Hypercapnia produced a respiratory acidosis which was partially compensated by an elevation in blood HCO3− after 24 h of exposure. The gill ventilation rose only slightly, and later fell as compensation proceeded. Air-breathing frequencies were not greatly affected by hypercapnia.

© 1982 by Company of Biologists
1982
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