Role of the parasympathetic nervous system in cardioprotection by remote hindlimb ischemic preconditioning

DONATO M; BUCHHOLZ B; RODRÍGUEZ M; PEREZ V; INSERTE J; GARCIA-DORADO D; GELPI RJ

EXPERIMENTAL PHYSIOLOGY.

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2013 vol. 98 p. 425 - 434

0958-0670

EL PRIMER Y SEGUNDO AUTOR CONTRIBUYERON POR IGUAL AL PRESENTE TRABAJO This investigation was designed to determine the participation of the vagus nerve and muscarinic receptors in the remote ischemic preconditioning (rIPC) mechanism. New Zealand rabbits were anesthetized, and the femoral artery was dissected. After 30 min of monitoring, the hearts were isolated and subjected to 30 min of global no-flow ischemia and 180 min of reperfusion (non-rIPC group). The ventricular function was evaluated considering the left ventricular developed pressure and the left ventricular end diastolic pressure. In rIPC group, the rabbits were subjected to a three-cycle hind limb ischemia (5 min) and reperfusion (5 min) and the same protocol used in non-rIPC group was then repeated. In order to evaluate the afferent neural pathway during the rIPC protocol, we performed two different groups: one in which the femoral and sciatic nerves were sectioned and the other in which the spinal cord was sectioned (T9-T10 level). To study the efferent neural pathway during rIPC protocol, the vagus nerve was sectioned and, in a separated group, atropine was administered. The effect of vagal stimulation was also evaluated. An infarct size of 40.8±3.1% was obtained in non-rIPC group whereas in rIPC group, the infarct size decreased to 16.4±3.5% (p<0.01). During preconditioning protocol, the vagus nerve section and the atropine administration each abolished the effect of rIPC on infarct size. Vagal stimulation mimicked the effect of rIPC, decreasing infarct size to 15.2±4.7% (p<0.01). There was a trend for attenuation of the rIPC protection that was not statistically significant with the sections of femoral and sciatic nerves. However, we demonstrated the presence of a neural afferent pathway since the spinal cord section completely abolished the effect of rIPC on infarct size. In conclusion, rIPC activates a neural afferent pathway and the cardioprotective signal reaches the heart through the vagus nerve (efferent pathway) and acetylcholine activates the IPC phenomenon when acting on the muscarinic receptors.±3.1% was obtained in non-rIPC group whereas in rIPC group, the infarct size decreased to 16.4±3.5% (p<0.01). During preconditioning protocol, the vagus nerve section and the atropine administration each abolished the effect of rIPC on infarct size. Vagal stimulation mimicked the effect of rIPC, decreasing infarct size to 15.2±4.7% (p<0.01). There was a trend for attenuation of the rIPC protection that was not statistically significant with the sections of femoral and sciatic nerves. However, we demonstrated the presence of a neural afferent pathway since the spinal cord section completely abolished the effect of rIPC on infarct size. In conclusion, rIPC activates a neural afferent pathway and the cardioprotective signal reaches the heart through the vagus nerve (efferent pathway) and acetylcholine activates the IPC phenomenon when acting on the muscarinic receptors.