1. During normoxia, heart rate was governed by a vagal tone which increased at higher acclimation temperatures. This tonic influence was exerted predominantly via the branchial cardiac nerves. The increase in heart rate following atropinization or cardiac vagotomy was associated with a reduction in stroke flow in the ventral aorta in accordance with Starling’s Law of the heart.

  2. During slowly induced hypoxia there was a reflex bradycardia, the onset and extent of which varied with acclimation temperature, and which was mediated predominantly via the pair of branchial cardiac vagi. The branchial cardiac vagi were also wholely responsible for the transient marked bradycardia at the onset of rapidly induced hypoxia.

  3. Direct measurement of blood flow to the anterior two pairs of branchial arteries demonstrated that they received approximately 37 % of total cardiac output in normoxia and that this proportion was unchanged during hypoxia.

  4. The bradycardia during hypoxia in control animals was partially offset by a rise in cardiac stroke volume so that cardiac output decreased slightly. Injection of the adrenergic βreceptor blocker, Propranolol, abolished the increase in stroke flow during hypoxia, but did not effect the bradycardia, and the total blood flow was therefore reduced.

  5. The values of during hypoxia from fish acclimated to 17 °C were significantly reduced from the control values following atropinization and either branchial cardiac vagotomy or total cardiac vagotomy.

  6. The apparent power output of the heart was reduced during hypoxia at high acclimation temperatures due to the marked bradycardia.

© 1977 by Company of Biologists
1977
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