The protective effects of hypoxia-induced hypometabolism in the Nautilus

Specimens of Nautilus pompilius were trapped at depths of 225 300 m off the sunken barrier reef southeast of Port Moresby, Papua New Guinea. Animals t ransported to the Motupore island laboratory were acclimated to normal habi tat temperatures of 18 degrees C and then cannulated for arterial and venou s blood sampling. When animals were forced to undergo a period of progressi ve hypoxia eventually to encounter ambient partial pressure of oxygen (PO2) levels Of similar to 10 mmHg land corresponding arterial PO2's of similar to 5 mmHg), they responded by lowering their aerobic metabolic rates to 5-1 0% of those seen in resting normoxic animals. Coincident with this profound metabolic suppression was an overall decrease in activity, with brief peri ods of jet propulsion punctuating long periods of rest, Below ambient PO2 l evels of 30-40 mmHg, ventilatory movements became highly periodic and at th e lowest PO2 levels encountered, ventilation occasionally ceased altogether . Cardiac output estimated by the Fick equation decreased during progressiv e hypoxia by as much as 75 80%, and in the deepest hypometabolic states hea rt rates slowed to one to two cycles of very low amplitude per minute. By t he end of 500 min exposure to ambient PO2 levels of 10 mmHg or less, the an aerobic end products octopine and succinate had increased significantly in adductor muscle and heart, respectively. Increased concentrations of octopi ne in adductor muscle apparently contributed to a small intracellular acido sis and to the development of a combined respiratory and metabolic acidosis in the extracellular compartment, On the other hand, increases in succinat e in heart muscle occurred in the absence of any change in cardiac pHi. Tak en together, we estimate that these anaerobic end products would make up le ss than 2% of the energy deficit arising from the decrease in aerobic metab olism. Thus, metabolic suppression is combined with a massive downregulatio n of systemic O-2 delivery to match metabolic supply to demand.