Effects of Hypoxia and Drugs on the Cardiovascular Dynamics of the Atlantic HagfishMyxine Glutinosa

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Abstract
Cardiac output, ventral and dorsal aortic blood pressure and heart rate were recorded simultaneously in unanaesthetized hagfish, Myxine glutinosa L. Mean cardiac output was S.Tmlmin-1kg-1 and mean heart rate 22.3beatsmin-1. The absence of beat-to-beat oscillations in heart rate was consistent with the lack of an extrinsic cardiac innervation in hagfish. Mean blood pressures were 1.04 kPa (ventral aorta) and 0.77kPa (dorsal aorta). Injection of adrenaline into the caudal vein significantly increased cardiac output, stroke volume, heart rate and blood pressures of both aortas. Peak cardiac output was close to 25 ml min-1 kg-1. Injection of the β-adrenoreceptor antagonist sotalol decreased resting heart rate significantly. We conclude that endogenous catecholamines from chromaffin cells of the heart are instrumental in the regulation of cardiac function in Myxine. Injection of acetylcholine had little direct effect on the recorded cardiac variables, but caused marked branchial vasoconstriction. Heart rate increased as the pressor response subsided. The cholinergic antagonist atropine had no effect on any of the resting parameters. Injection of adenosine had no direct cardiac effects but reduced the systemic vascular resistance. Severe hypoxia (PwO2=1.5-2.2kPa for 15–35 min) had very little effect on the cardiovascular variables recorded. The remarkable ability of the hagfish heart to maintain normal cardiac output during severe hypoxia is discussed with respect to the anaerobic pumping capacity of the heart. Pump-perfused, in situ gill preparations were used to examine branchial vasoactivity. Acetylcholine and adrenaline produced dose-dependent vasoconstriction, whereas isoprenaline, noradrenaline and adenosine dilated the branchial vasculature.