Gas Exchange, Acid-Base Balance, and the Oxygen Supply to the Tissues During a Molt of the Blue Crab Callinectes Sapidus

At temperatures compatible with molting the hemocyanin in the blood of an intermolt stage C blue crab transports all but a very small fraction of the oxygen consumed. A number of previous investigations suggest that the respiratory mechanisms permitting the oxygen carrier to function at such a high level during stage C are perturbed during a molt. Many of these suggestions prove to be correct. The uptake of water and the apparent decrease in net hemocyanin synthesis during stages D3 through A result in the virtual loss of the hemocyanin-oxygen transport system. A pronounced premolt alkalosis compensates for a concomitant hypercapnia. During exuviation lactate frequently accumulates in the blood, which presumably results from the inadequacy of gas exchange and aerobic metabolism at this time. When the molt is successful, however, the blood becomes only slightly acidotic, if at all, and the acidosis rapidly disappears. The changes in net metabolism of hemocyanin do not entail shifts in the composition of functionally distinct subunits that might permit an adaptation of the oxygen transport system to altered operating conditions in the blood during the early postmolt. There is, however, an increase in oxygen permeability of the general body surface, which becomes a site of oxygen uptake from the medium directly into the metabolically activated epidermis and also into the blood. In animals that survive a molt, including groups exposed to moderately hypoxic as well as normoxic water, there is no sign of tissue hypoxia and total O2 uptake actually increases during the early postmolt. The critical role of these compensatory mechanisms is indicated by severe acidosis and tissue hypoxia prior to mortality in cases of aborted molts and molts that result in morphological aberrations. Later in the postmolt period the decrease in blood calcium that accompanies hardening of the new skeleton lowers hemocyanin-oxygen affinity, permitting the carrier to function at elevated blood PO2.