No abstract

The physical variables which directly affect organisms inhabiting desert ephemeral pools were examined in four pools in southeastern Utah . During the day, pools were hyperoxic (240 torr) and hypocapnic (0 .07 ton) while pH and temperature increased (7 .5-9 .0 & 17-35 °C respectively) . Conversely, predawn pool measurements were hypoxic (40 torr) and hypercapnic (3 torr) . While TA increased throughout the season (from 0 .4 to 1 .43 meq 1-1 ), due largely to increased bicarbonate concentration (from 0 .5 to 1 .4 mmol 1 -1 ), water osmolarity remained relatively constant . These desert ephemeral systems represent unique environmental habitats where organisms experience both diurnal and seasonal changes in numerous physical variables over short time frames .

We hypothesized that aggregation of bacteria and hemocytes at the gill, which occurs as part of the shrimp's antibacterial immune defenses, would impair normal respiratory function and thereby disrupt aerobic metabolism. Changes in oxygen uptake and lactate accumulation were determined in Litopenaeus vannamei, the Pacific white shrimp, following injection with either saline (control) or a strain of the gram-negative bacterium Vibrio campbellii that is pathogenic in crustaceans. The rate of oxygen uptake was determined during the first 4 h after injection and after 24 h. Injection of bacteria decreased oxygen uptake by 27% (from 11.0 to 8.2 micromol g-1 h-1) after 4 h, while saline-injected shrimp showed no change. Decreased oxygen uptake persisted 24 h after Vibrio injection. In well-aerated water, resting whole-animal lactic acid levels increased in shrimp injected with bacteria (mean=2.59 micromol lactate g-1+/-0.39 SEM, n=8) compared to saline-injected control shrimp, but this difference did not persist at 24 h. Exposure to hypercapnic hypoxia (PCO2=1.8 kPa, PO2=6.7 kPa) also resulted in significant whole-body lactic acid differences (mean=3.99 and 1.8 micromol g-1 tissue in Vibrio and saline-injected shrimp, respectively). Our results support the hypothesis that the crustacean immune response against invading bacteria impairs normal metabolic function, resulting in depression of oxygen uptake and slightly increased anaerobic metabolism.

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.

A regulated decrease in internal body temperature (Tb) appears to play a protective role against metabolic disruptions such as exposure to ambient hypoxia. This study examined the possibility that Tb depression is initiated when low internal oxygen levels trigger the release of adenosine, a neural modulator known to influence thermoregulation. We measured selected Tb of Anolis sagrei in a thermal gradient under varied ambient oxygen conditions and following the administration of the adenosine receptor antagonist 8-cyclopentyltheophylline (CPT). The average decrease in Tb observed following exposure to hypoxia (<10% O2) and following exhaustive exercise were 5 degrees and 3 degrees C, respectively, suggesting a role of oxygen availability on initiation of regulated hypothermia. When A. sagrei were run to exhaustion and recovered in hyperoxic (>95% O2) conditions, exercise-induced Tb depression was abolished. Administration of CPT similarly abolished decreased Tb due to both exercise and hypoxia. Trials using Dipsosaurus dorsalis indicate that elevated ambient oxygen during exercise does not influence blood pH or lactate accumulation, suggesting that these factors do not initiate changes in thermoregulatory setpoint following exhaustive exercise. We suggest that when oxygen is limiting, a decrease in arterial oxygen may trigger the release of adenosine, thereby altering the thermoregulatory setpoint.