IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
The arm and hindlimb ischemia trigger different communication pathways in remote ischemic preconditioning
Autor/es:
BIN EP; ZAOBORNYJ T; DONATO M; PAEZ D; GELPI RJ
Lugar:
Mar del Plata
Reunión:
Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2019
Institución organizadora:
Sociedad Argentina de Investigación Clínica
Resumen:
Background: Remote ischemic preconditioning (rIPC) is a cardioprotective phenomenon by which transient non-lethal ischemia and reperfusion of one organ or tissue confers resistance to a later episode of lethal ischemia reperfusion injury in a remote organ or tissue.Objective: The aim was to determine the most appropriate anatomical site to stimulate rIPC and achieve protection. A second objective was to evaluate some of the possible pathways (neural and humoral) involved in the rIPC mechanism.Methods: Isolated rat hearts (n=6 per group) were subjected to 30 min of global ischemia followed by 60 min of reperfusion (I/R), in a Langendorff system. In additional groups, a rIPC protocol of 3 cycles of I/R were performed on both in leg and the arm. We studied the involvement of a vagal neural pathway by performing a bilateral cervical vagotomy (BCV) prior to the rIPC protocol. The humoral pathway was evaluated by administering DPCPX (adenosine A1 receptor blocker) before rIPC. The opening of mitochondrial permeability transition pore (MPTP) was assessed in fresh isolated left ventricle mitochondria by the occurrence of cyclosporin A sensitive mitochondrial membrane potential disruption followed by swelling as determined by the changes in optical density of the mitochondrial suspension.Results: The ischemia/reperfusion protocol induced an infarct size of 47.1±0.8 %. The hindlimb and arm rIPC reduced infarct size to 35.6±1.2 (p