in Hyperlipidemic Animals through the Activation of K+ATP Channels. J Clinic Experiment Cardiol S5:001. doi:10.4172/2155-9880.S5-001

Copyright: © 2011 Riera ARP, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Reverse-mode activation of the Na+-Ca2+ exchanger (NCX) at the time of reperfusion following ischemia contributes to Ca2+ overload and cardiomyocyte injury, KB-R7943, as a selective reverse-mode NCX inhibitor, reduces lethal reperfusion injury under normal conditions, but its effectiveness under certain pathological states is in dispute. In the present study, we sought to determine the effect of KB-R7943 in hyperlipidemic animals and assess if the K+ATP are involved in the protective mechanisms. Anesthetized rats were randomized into five groups, as follows, and were subjected to 25min global ischemia (GI) followed by 120 min reperfusion (R). Normally fe