Non-equilibrium acid-base status in C. productus: role of exoskeletal carbonate buffers.

Hemolymph acid-base variables (pH, PCO2 and CCO2), hemolymph Ca2+ and Na+ concentrations, and osmolality were measured in unrestrained crabs, Cancer productus, before, during and following 4 hr emersion and 43 hr hyperoxia (460-510 Torr), both at 10 degrees C. Emersion and hyperoxia provoked an acidosis associated with elevation of hemolymph CCO2 and PCO2, yet attempts to calculate PCO2 from measured pH and CCO2 always resulted in values greater than those measured directly. This discrepancy between measured and calculated PCO2, was associated with base excess, and was eliminated upon in vitro equilibration of the hemolymph and more slowly in vivo, suggesting that metabolic compensation for the acidosis occurred more rapidly than could acid-base equilibration. During emersion, increases of CCO2 and [Ca2+] provide evidence that the internal CaCO3 stores, possibly from the exoskeleton, were mobilized during acid-base compensation. Hyperoxia provoked no such increase in Ca2+, and branchial uptake of HCO3- may make a major contribution to the elevation of CCO2 during hyperoxia. It is suggested that shell buffering by aquatic crustaceans provides a means of compensation for acidosis under conditions during which branchial function is impaired.