A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 microgram g-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 microgram g-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water PO2 (PwO2)=1.4 kPa; 10.5 mmHg) for 30 min caused a significant decrease in arterial PO2 (from 11.5+/−1.3 kPa to 1.2+/−0.3 kPa) and arterial O2 content (from 3.9+/−0.3 ml 100 ml-1 to 0.9+/−0.2 ml 100 ml-1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia (PwO2 approximately 0 kPa) or physical disturbance (15 min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60 mmol l-1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20 mmol l-1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10–5-10-4 mol kg-1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue.

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