Preischemic efferent vagal stimulation increased the size of myocardial infarction in rabbits.

BUCHHOLZ B; DONATO M; IVALDE FC; HÖCHT CH; BUITRAGO E; PEREZ V; RODRÍGUEZ M; GELPI RJ

INTERNATIONAL JOURNAL OF CARDIOLOGY

ELSEVIER IRELAND LTD

Lugar: Amsterdam; Año: 2012 vol. 155 p. 490 - 491

0167-5273

Background: Exogenously administered acetylcholine activates ischemic preconditioning, whereas prolonged vagal nerve stimulation (VNS) reduces mortality secondary to heart failure. With respect to the effects of VNS applied before ischemia, there are no conclusive data on myocardial infarction. The aim of this work was to evaluate the effects of preischemic VNS on myocardial infarction in rabbits. Methods: Coronary artery was ligated for 45 min followed by 4 h of reperfusion (Group 1, control; n=14). Group 2 (n=9) received the same protocol as Group 1, except that, before ischemia, it received right efferent VNS for 10 min followed by 5 min of recovery. Group 3 (n=5) received the same protocol as Group 2, but atropine was administered during VNS. Group 4 (n=6) received the same protocol as Group 2, but atenolol was administered. Group 5 (n=4) received atenolol during ischemia and reperfusion, but VNS was not performed. Group 6 (n=5) received the same protocol as group 2 but reserpine was administered 24 h before VNS. Group 7 (n=4) received reserpine, but VNS was not performed. Results: VNS increased the infarct size from 45.2±2.4 in group 1 to 62.9±3.1% in group 2 (p <0.05), whereas atropine reversed this effect (44.8±3.9%; p <0.05 vs. Group 2). Atenolol administration in the presence of VNS decreased infarct size to 48.5±2.8% (p <0.05 vs. Group 2). Reserpine abolished the effect of VNS on infarct size (44.0±2.6%). Conclusion: Preischemic efferent vagal stimulation significantly increased infarct size by a muscarinic cholinergic mechanism, and a possible co-activation of sympathetic nervous system.