Effects of coronary artery occlusion and reperfusion on the idioventricular rate in anesthetized dogs
Related Experiment Video
Updated: Jun 30, 2026
Primary Outcome Assessment in a Pig Model of Acute Myocardial Infarction
Published on: October 14, 2016
1Department of Investigative Medicine, Mount Sinai Medical Center, Cleveland, Ohio 44106.
Objectives:
We evaluated the effects of alpha 1- and beta-adrenergic receptor blockade on the changes in idioventricular rate induced by occlusion and reperfusion of the left anterior descending coronary artery in anesthetized dogs.
Background:
Because sinus rate usually exceeds idioventricular rate, the experimental induction of complete atrioventricular (AV) block may improve the definition of the effects of coronary occlusion and reperfusion on idioventricular pacemaker mechanisms.
Methods:
We injected formaldehyde into the AV node to induce complete AV block in 35 chloralose-anesthetized dogs. Animals were assigned to untreated (n = 22), prazosin-treated (n = 6) and propranolol-treated (n = 7) groups. We paced the hearts at 120 beats/min during a 20- to 60-min period of complete coronary occlusion, but we did not pace the heart during reperfusion.
Results:
In the untreated group, the idioventricular rate did not change significantly during coronary artery occlusions of 20 or 40 min, but it did increase significantly during the last 20 min of a 60-min occlusion. Prazosin and propranolol each attenuated but did not abolish this rate increase. The idioventricular rate increased markedly but transiently soon after reperfusion in all untreated animals. This tachycardia was virtually abolished by either prazosin or propranolol.
Conclusions:
The increase in idioventricular rate that develops during the last 20 min of a 60-min coronary occlusion is modulated but probably not mediated by adrenergic mechanisms. The pronounced ventricular tachycardia after reperfusion is virtually abolished by either alpha 1- or beta-adrenergic antagonists. Hence, this tachycardia requires the simultaneous activation of alpha 1- and beta-adrenergic mechanisms in dogs.
