High-Resolution Topography-Following Chemical Mapping of Ocean Hypoxia by Use of an Autonomous Underwater Vehicle: The Santa Monica Basin Example

This paper reports on the execution of a combined chemical sensing/high-resolution terrain-following autonomous underwater vehicle (AUV) survey to explore the fine structure and functional boundaries of the Santa Monica Basin suboxic zone and its relationship to topography. An AUV mapping vehicle is used in a novel configuration—combining the mapping vehicle tail section, with precision inertial navigation and acoustic communications systems, with CTD/O2, NO3 sensing, and Gulper water sampling systems. The challenge was to perform a long-distance near-bottom physical/chemical survey in deep water without any intermediate surfacing to disrupt the survey or require the vehicle to surface in areas of heavy ship traffic. Some 210 km of AUV cruise track at ≈10 m above bottom were accomplished during a 3-day survey. The dissolved oxygen concentration [O2] data are combined with temperature T, salinity S, and hydrostatic pressure P to produce maps of oxygen partial pressure pO2 that help define the limits at which the oceanic supply of O2 can match the O2 demands required to sustain various forms of marine life. The chemical NO3 sensing was included to define the critical pO2 boundary at which NO3 reduction occurs. The combination of a high-resolution terrain-following AUV with chemical sensors is important for a diverse array of investigations, including the study of vent sites, and for locating the source of chemical signals originating from the seafloor. The hypoxic basin example here permits better discrimination between general climate/circulation controls on hypoxia and more specific point-source-driven processes.

Acid-base and respiratory responses to hypoxia in the grasshopper Schistocerca americana.

How do quiescent insects maintain constant rates of oxygen consumption at ambient PO2 values as low as 2-5 kPa? To address this question, we examined the response of the American locust Schistocerca americana to hypoxia by measuring the effect of decreasing ambient PO2 on haemolymph acid-base status, tracheal PCO2 and CO2 emission. We also tested the effect of hypoxia on convective ventilation using a new optical technique which measured the changes in abdominal volume during ventilation. Hypoxia caused a progressive increase in haemolymph pH and a decrease in haemolymph PCO2. A Davenport analysis suggests that hypoxia is accompanied by a net transfer of base to the haemolymph, perhaps as a result of intracellular pH regulation. Hypoxia caused a progressive increase in convective ventilation which was mostly attributable to a rise in ventilatory frequency. Carbon dioxide conductance ( micromol h-1 kPa-1) across the spiracles increased more than threefold, while conductance between the haemolymph and primary trachea nearly doubled in 2 kPa O2 relative to room air. The rise in trans-spiracular conductance is completely attributable to the elevations in convective ventilation. The rise in tracheal conductance in response to hypoxia may reflect the removal of fluid from the tracheoles described by Wigglesworth. The low critical PO2 of quiescent insects can be attributed (1) to their relatively low resting metabolic rates, (2) to the possession of tracheal systems adapted for the exchange of gases at much higher rates during activity and (3) to the ability of insects to rapidly modulate tracheal conductance.

Phosphorylation potential, adenosine formation, and critical PO2 in stimulated rat cardiomyocytes

This study investigated the relationship between O2 consumption (VO2) and energy status in isolated rat cardiomyocytes using a system in which O2 supply (PO2) was maintained constant. For this purpose, VO2, phosphocreatine, ATP, intracellular pH, and adenosine of quiescent and stimulated cardiomyocytes were measured while the ambient PO2 was clamped between 0.1 and 120 mmHg. In quiescent cardiomyocytes (VO2: 7.9 +/- 1.2 nmol.min-1.mg protein-1), the threshold below which respiration decreased (critical PO2) was 1.4 mmHg. Above this value, energy status remained constant; below 1 mmHg, both free ADP and adenosine increased. Stimulation increased VO2 threefold and shifted the critical PO2 to 10 mmHg. Above this value, free ADP and adenosine remained unchanged; between 10 and 5 mmHg. VO2 was reduced but this did not change free ADP or adenosine. These findings demonstrate that 1) under well-oxygenated conditions (PO2 > 10 mmHg), VO2 is not controlled by ADP; 2) similarly, the adenosine formation is independent of VO2; a PO2 < 5 mmHg is a prerequisite for enhanced adenosine formation; and 3) when O2 supply becomes limiting, ATP consumption is downregulated without measurable changes in energy status (hibernation).

A new function for lactate in the toad Bufo marinus

In the amphibian Bufo marinus, progressive hypoxia below a critical PO2 elicits a transient 50% increase in O2 consumption that coincides with the onset of lactate formation. The present study was designed to test the hypothesis that lactate causes the observed rise in metabolic rate. Arterial bolus infusions of pH-neutral sodium lactate solutions (4 mmol/kg body wt) in toads maintained under hypoxia actually elicit a similar increase in metabolic rate. The application of adrenergic antagonists (bretylium tosylate, phentolamine, propranolol, and reserpine) inhibits this response, suggesting that catecholamines are involved. Moreover, animals injected with lactate move to a cooler environment (behavioral hypothermia), a behavioral response that is beneficial during hypoxia. We hypothesize that, in accordance with Cannon's concept of an emergency response, lactate may function as an alarm signal during hypoxia. However, the signal function of lactate is observed in animals both under hypoxia and under normoxia and should thus be considered in future studies whenever elevated lactate levels are present, e.g., during and after exercise.