Changes in the loading conditions induced by vagal stimulation modify the myocardial infarct size through sympathetic-parasympathetic interactions.

BUCHHOLZ B; DONATO M; REY DEUTSCH A; GOYENECHE MA; GARMENDIA C; HOCHT C; DEL MAURO J; RODRIGUEZ M; GELPI RJ

Melbourne

Congreso; World Congress of Cardiology Scientific Sessions 2014; 2014

World Heart Federation

ABSTRACT In a previous research we described that vagal stimulation increases the infarct size by co-activation of the sympathetic nervous system. The aim of this study was to determine if hemodynamic changes secondary to the vagal stimulation are able to activate sympathetic compensatory neural reflexes, responsible for increasing the infarct size. A second goal was to determine if intermittent vagal stimulation avoids sympathetic activation and reduces infarct size. We used rabbits subject to the following protocols: a) Regional 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 with a 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). Vagal stimulation increases the infarct size in the groups VNS (70.7±4.3%) and VNS/RS (68.6±4.1%) compared with the group I/R (52.0±3.7%) (p