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Ventilatory and circulatory adjustments in the European eel (Anguilla anguilla L.) exposed to short term hypoxia.

Respiratory and circulatory (measured and calculated) variables were obtained at the same time in resting eels, during normoxia and after 1 h exposure to environmental hypoxia (water PO2 of 40 torr). In normoxia, values of respiratory and circulatory variables appeared less than those reported for most other fish. These differences could be partly explained by a lower level of standard metabolism and a greater uptake of O2 through the skin. Hypoxia caused a marked decrease in heart rate (40%), cardiac output (37%), ventral and dorsal arterial blood pressures (22% and 32%), associated with a constriction of prebranchial veno-venous shunt, and an increase in branchial vascular resistance (30%). Atropine treatment during hypoxia reduced, but did not abolish, bradycardia, and branchial vascular resistance remained unchanged. The lack of increase in cardiac stroke volume as well as the slowing of the heart in atropine-treated eel, could be regarded as metabolic effects of sustained hypoxia. The increase in branchial resistance and constriction of prebranchial veno-venous shunt could be regarded as a direct myogenic effect of hypoxia. Hypoxic exposure resulted in an increase in ventilatory water flow Vg (more than twofold), a decrease in gill O2 uptake (50%) and oxygen partial pressure in arterial (PaO2 80%) and mixed venous blood (PvO2 78%), and in increase in the transfer factor for O2 of the gills, TO2, (+66%). The ventilatory convection requirement increased (fivefold) while extraction (EwO2%) and effectiveness (Eff%) of gill oxygen transfer were maintained in spite of hyperventilation. Hypoxic hyperventilation reduced partial pressure of CO2 (PaCO2 from 3.4 to 0.7 torr) and markedly raised pH (pHa from 7.98 to 8.33) in arterial blood, thus causing a typical respiratory alkalosis, which resulted in increased O2 affinity and capacity of eel haemoglobin.