(713.9) Remote ischemic preconditioning promotes cardioprotection through a central nervous system dependent mechanism

Poster Board Number: E53

Ashline Paul Manoucheca Amilcar (National Institute of Cardiology Ignacio Chávez), Lorena Rosas-Martínez (National Institute of Cardiology Ignacio Chávez), Juan Carlos Torres-Narváez (National Institute of Cardiology Ignacio Chávez), Araceli Sánchez-López (Center for Research and Advanced Studies of the National Polytechnic Institute), Luz Graciela Cervantes-Pérez (National Institute of Cardiology Ignacio Chávez), David Centurión (Center for Research and Advanced Studies of the National Polytechnic Institute), Alicia Sánchez-Mendoza (National Institute of Cardiology Ignacio Chávez)

Remote ischemic preconditioning (rIPC) is the phenomenon of brief periods of ischemia and reperfusion applied to a distant organ promote cardioprotection against a subsequent ischemia/reperfusion injury (I/R). Although a neurohumoral hypothesis has been proposed, the cardioprotective mechanisms of rIPC have not been fully elucidated. We investigated whether rIPC could induce cardioprotection in a pithed Wistar rat model hypothesizing that the absence of central nervous system (CNS) structures would prevent its cardioprotective effect. rIPC protocol consisting of 3 cycles of 4 minutes of ischemia and 4 minutes of reperfusion was applied to the left posterior extremity of male Wistar rats. I/R was induced surgically by left coronary descending artery ligation for 30 minutes followed by 2h of reperfusion. Isolated rat hearts were perfused in a Langendorff system to measure coronary vascular resistance (CVR). Finally, the infarct size was evaluated by Evans blue and triphenyltetrazolium staining. rIPC reduced the infarct size of the ischemic hearts; however, this effect was abolished in pithed rats. rIPC also prevented the rise of CVR of ischemic hearts while there was no difference compared to pithed rats. We concluded that rIPC reduces the infarct size of hearts during I/R preserving the coronary artery tone through a CNS-dependent mechanism.