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

BUCHHOLZ B; DONATO M; PEREZ V; REY DEUTCH AC; HÖCHT C; DEL MAURO JS; RODRÍGUEZ M; GELPI RJ

PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY

SPRINGER

Lugar: Berlin; Año: 2015 vol. 467 p. 1509 - 1522

0031-6768

In a previous research, we described that vagal stimulation increases the infarct size by sympathetic co-activation. 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 by muscarinic activation of the Akt - GSK-3β pathway. Rabbits were subjected to 30 minutes of regional myocardial ischemia and 3 hours of reperfusion without vagal stimulation, or the following protocols of right vagus nerve stimulation during 10 minutes before ischemia: a) continuous vagal stimulation; b) intermittent vagal stimulation (cycles of 10segON/50segOFF). Continuous vagal stimulation increases infarct size (70.7±4.3%), even after right vagal section (68.6±4.1%) compared with control group (52.0±3.7%, p