Abstract
The high dissolved gas tensions required for the secretion of gases into deep-sea fish swimbladders are thought to be produced in the rete mirabile by a countercurrent multiplication mechanism, the capacity of which is theoretically limited by the physical characteristics of the rete and by the magnitudes of minute gas solubility changes in the blood plasma. These gas solubility changes are presumably induced through the salting-out effect following the addition of lactic acid to rete venous blood as it circulates through the gas gland. In order to estimate the maximum swimbladder gas pressures attainable by this mechanism, the effects of lactic acid on N2 and Ar solubilities in water were determined at 5 and 25°C with a new volumetric method. The results show that the salting-out effect with lactic acid is much smaller than with NaCl, and that the agreement between predicted and observed swimbladder gas pressures is more critically dependent on the physical properties of the rete vasculature than indicated by previous theoretical treatments. When augmented by the release of hemoglobin-bound O2, the salting-out effect with lactic acid appears large enough to account for the production of even the highest swimbladder O2 pressures, provided the rete characteristics lie within certain reasonable limits. However, successful theoretical explanation of observed swimbladder N2 pressures in some deep-sea species will require rigorous attention to such theoretically neglected factors as dissolved gas backdiffusion along the rete and the unequal size and number of the rete arterial and venous capillaries.
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