In anesthetized dogs, isoproterenol, calcium, acetylstrophanthidin, and sympathetic stimulation markedly increased atrial contractile force, whereas vagal stimulation produced marked decreases.
How do pharmacological agents and autonomic stimulation affect atrial contractile force in an intact canine heart model?
This preclinical study demonstrates that atrial contractile force is augmented by sympathetic stimulation and positive inotropes, and depressed by vagal stimulation.
Atrial contractile force was recorded in anesthetized open-chested dogs using a specially designed adjustable strain-gauge arch, linear over a wide range of forces. The shape of both resting and active atrial length-tension curves as well as the maximum force developed was similar to those described for the ventricle, after corrections for differences in muscle mass. Increasing heart rate by right atrial stimulation had no significant effect on atrial force. Isoproterenol, calcium, and acetylstrophanthidin each produced marked increases in the force of contraction. Sympathetic stimulation, produced by direct stellate stimulation or reflexly induced by carotid hypotension, increased atrial force, whereas direct vagal stimulation or vagal stimulation produced reflexly by balloon inflation in the thoracic aorta produced marked decreases in atrial force. Both atria were depressed more by direct stimulation of the right vagus nerve than of the left, and right atrial force was affected more than was left atrial force when either vagus nerve was stimulated.
Williams et al. (Wed,) conducted a other in anesthetized open-chested dogs. Isoproterenol, calcium, acetylstrophanthidin, sympathetic and vagal stimulation was evaluated on Atrial contractile force. In anesthetized dogs, isoproterenol, calcium, acetylstrophanthidin, and sympathetic stimulation markedly increased atrial contractile force, whereas vagal stimulation produced marked decreases.