CHANGES IN THE LOADING CONDITIONS INDUCED BY VAGAL STIMULATION MODIFY THE MYOCARDIAL INFARCT SIZE THROUGH SYMPATHETIC-PARASYMPATHETIC INTERACTIONS

BRUNO BUCHHOLZ; MARTÍN DONATO; REY DEUTCH AANA CLARA; GOYENECHE MARÍA AILÍN; HÖCHT CHRISTIAN; DEL MAURO JULIETA; GRECO CARLA; GULLACE FEDERICO; RODRÍGUEZ MANUEL; GELPI RICARDO J

Melbourne

Congreso; World Congress of Cardiology Scientific Sessions 2014; 2014

World Heart Federation

INTRODUCTION: The autonomic imbalance is deleterious for the myocardium. One of the strategies used in recent times to modify this imbalance is electrical vagus nerve stimulation. However, the mechanisms by which vagal stimulation produces its protective effects are not yet entirely known. In a previous research we described that right vagus nerve electrical stimulation, perfomed under certain conditions, increases the infarct size by causing the co-activation of the sympathetic nervous system (SNS). OBJECTIVE: a first aim was to determine if hemodynamic modifications that accompany vagal stimulation are responsible for the co-activation of the SNS, and as a consequence, of the increase in the infarct size. If the co-activation of the SNS is responsible for the deleterious effect of vagal stimulation, then performing a protocol of electrical stimulation without effects over this branch of the autonomic system could be beneficial. Thus, a second goal was to study if vagal stimulation, applied intermittently, avoids this co-activation and produces protective effects on the infarct size. METHODS: We used rabbits subjected to the following protocols: a) myocardial ischemia of 30 minutes and 3 hours of reperfusion (I/R; n=10); b) continuous pre-ischemic electrical stimulation of the right vagus nerve during 10 minutes (VNS; n=7); c) the protocol of the group VNS was repeated but with the right vagus nerve sectioned at a cervical level (VNS/RS; n=11); d) right vagal efferent stimulation prior bilateral vagotomy  (VNS/BS; n=7); e) the protocol of the group VNS/RS was repeated but at constant heart rate (VNS/RS+PAC; n=6); f) intermittent right vagal stimulation was applied (10? ON/50? OFF) prior 30 min of ischemia (VNS Int;n=13). In all protocols plasmatic catecholamines were measured. RESULTS: Vagal stimulation increases infarct size in groups VNS (70.7±4.3%) and VNS/RS (68.6±4.1%) compared with group I/R (52.0±3.7%) (p<0.05). Bilateral vagotomy (VNS/BS) and paced (VNS/RS+PAC) abolished the deleterious effect, reaching an infarct size of 43.3±5.1% and 43.5±2.1%, respectively. Intermittent stimulation reduced the infarct size to 29.8±3.0% (p<0.05). Electrical stimulation of the vagus nerve induced bradycardia and increases the loading conditions and wall stretching as well as plasmatic catecholamines. CONCLUSIONS: The effects of vagal stimulation on the infarct size strongly depend on the sympathetic-parasympathetic interaction. Continuous vagal stimulation co-activates the SNS and increases the infarct size by changes in the cardiac chamber volumes. On the contrary, vagal stimulation performed intermittently antagonizes the sympathetic system and reduces the infarct size.