Key result
Acute normovolemic hemodilution increased cardiac output in all dogs, driven by heart rate increases in dogs with low baseline rates and stroke volume increases in those with high baseline rates.
Why the study?
What is the mechanism of hemodynamic response during acute normovolemic hemodilution in anesthetized dogs?
What is the mechanism of hemodynamic response during acute normovolemic hemodilution in anesthetized dogs?
In anesthetized dogs, the increase in cardiac output during acute normovolemic hemodilution is driven by vagally-mediated tachycardia in those with low baseline heart rates, and by increased stroke volume in those with high baseline heart rates.
Does not support human practice changes; leaves open translation of baseline rate-dependent mechanisms from canine models.
Acute normovolemic hemodilution was induced by progressive replacement of blood by dextran (molecular weight 150,000) in anesthetized artificially ventilated dogs. Experiments were performed on dogs with intact autonomic innervation, dogs with beta-adrenergic blockade, dogs with cholinergic blockade, dogs with bilateral vagotomy, and dogs with combined bilateral vagotomy plus beta-adrenergic blockade. Hemodilution induced an increase in cardiac-output in all the groups. However, in dogs with low control heart rate (dogs with intact autonomic innervation, and dogs with beta-adrenergic blockade), cardiac-output increase was almost wholly due to an increase in heart rate. Whereas, in dogs with high control heart rate (dogs with cholinergic blockade, dogs with bilateral vagotomy, and dogs with combined bilateral vagotomy plus beta-adrenergic blockade), the increase in cardiac-output was almost wholly due to an increase in the stroke-volume. The increase in heart rate in dogs with intact autonomic innervation was not significantly different from the heart rate increase in dogs with beta-adrenergic blockade. In dogs with low control heart rate (beta-receptor blockade), hemodilution induced tachycardia, which was not significantly different from the response induced in intact dogs. This shows that the cardioacceleration was primarily mediated through the efferent vagus nerves, and the efferent sympathetic nerves did not make significant contribution in the reflex.
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Fahim et al. (1992) studied Anesthetized artificially ventilated dogs. Acute normovolemic hemodilution was evaluated on Cardiac output, heart rate, and stroke volume. Acute normovolemic hemodilution increased cardiac output in all dogs, driven by heart rate increases in dogs with low baseline rates and stroke volume increases in those with high baseline rates.
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