Vagal stabilization of the ischemic canine ventricle.
To determine whether vagal activity during myocardial ischemia functions to stabilize the heart, the left anterior descending coronary artery in dogs was occluded for periods of 3 1/2 minutes with and without concurrent vagal stimulation. Bipolar electrograms were measured from the surface of the canine left ventricle within and outside the regions of intended ischemia. Ischemia in the absence of vagal stimulation depressed both the electrogram amplitude and the upstroke velocity of the electrogram signal. Vagal stimulation significantly decreased the absolute magnitude of the ischemia-induced decrease of the electrogram signal, which indicates that it tended to stabilize the insulted heart. This stabilizing influence however, was seen only in the presence of adrenergic blockade with practolol. The vagal response was only partially blocked by atropine, whereas it was abolished by lidocaine. These results suggest that a vagally mediated stabilization of the ischemic canine ventricle can occur and is unmasked only in the absence of sympathetic neural activity.
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004558:Electric Stimulation; D004562:Electrocardiography; D005260:Female; D006892:Hydroxydopamines / Q000494:pharmacology; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D011217:Practolol / Q000494:pharmacology; D013997:Time Factors; D014630:Vagus Nerve / Q000187:drug effects / Q000502:physiology*
D006892:Hydroxydopamines; D001285:Atropine; D008012:Lidocaine; D011217:Practolol