Crustacean gills function in gas exchange, ion transport, and immune defense against microbial pathogens. Hemocyte aggregates that form in response to microbial pathogens become trapped in the fine vasculature of the gill, leading to the suggestion by others that respiration and ion regulation might by impaired during the course of an immune response. In the present study, injection of the pathogenic bacterium Vibrio campbellii into Callinectes sapidus, the Atlantic blue crab, caused a dramatic decline in oxygen uptake from 4.53 to 2.56 micromol g-1 h-1. This decline in oxygen uptake is associated with a large decrease in postbranchial PO2, from 16.2 (+/-0.46 SEM, n=7) to 13.1 kPa (+/-0.77 SEM, n=9), while prebranchial PO2 remains unchanged. In addition, injection of Vibrio results in the disappearance of a pH change across the gills, an indication of reduced CO2 excretion. The hemolymph hydrostatic pressure change across the gill circulation increases nearly 2-fold in Vibrio-injected crabs compared with a negligible change in pressure across the gill circulation in saline-injected, control crabs. This change, in combination with stability of heart rate and branchial chamber pressure, is indicative of a significant increase in vascular resistance across the gills that is induced by hemocyte nodule formation. A healthy, active blue crab can eliminate most invading bacteria, but the respiratory function of the gills is impaired. Thus, when blue crabs are engaged in the immune response, they are less equipped to engage in oxygen-fueled activities such as predator avoidance, prey capture, and migration. Furthermore, crabs are less fit to invade environments that are hypoxic.

Upon exposure to air (emersion), the purple sea urchin Strongylocentrotus purpuratus releases an "emersion fluid" from its esophagus. Release of this fluid causes air to appear within the test (or calcareous theca), most likely inside the intestine. The air space is large, occupying 33.5% of the volume of the intrathecal space. The intestine containing air forms a facultative lung and contributes to the oxygenation of the perivisceral coelomic fluid (PCF) during emersion. During emersion, the mean partial pressure of oxygen (PO(2)) of the PCF declined from 56 to 24 torr (1 torr = 0.1333 kPa) after 2 h, remained relatively unchanged after 4 h, and rose to 39 torr after 8 h. The partial pressure of carbon dioxide (PCO(2)) rose from 2.6 to 3.8 torr after 2 h, remained unchanged after 4 h, and declined to 2.7 after 8 h. Due to the elevation of PCO(2) PCF pH declined from 7.41 to 7.17. PCF osmotic concentration, calcium ion concentration, chloride ion concentration, ammonium ion concentration, and protein concentration were unchanged by air exposure. Lactate levels in the PCF were undetectable. S. purpuratus was an osmoconformer and a chloride ion conformer at salinities down to 20.9 ppt. Below this salinity, the sea urchins died. The respiratory acidosis resulting from air exposure was uncompensated, supporting the hypothesis that compensation for a respiratory acidosis induced by air exposure does not occur in organisms that are unable to regulate ions in a dilute environment. We suggest that the facultative lung ensures a minimal PO(2) in the PCF, which may be especially important when the intrathecal space is full of ripe gonads, allowing the gonads to be more reliant on aerobic metabolism.