Why the study?
Do ischemic preconditioning and mito-KATP channel openers attenuate chronic left ventricular remodeling in rats subjected to ischemia-reperfusion?
Do ischemic preconditioning and mito-KATP channel openers attenuate chronic left ventricular remodeling in rats subjected to ischemia-reperfusion?
Ischemic preconditioning and mito-KATP channel openers attenuate chronic left ventricular remodeling and reduce infarct size in a rat model of ischemia-reperfusion.
Mito-KATP activation attenuates post-I/R remodeling in rats; hypothesis-generating and leaves open human translation.
The influence of ischemic preconditioning (IP) and mitochondrial ATP-sensitive potassium (mito-KATP) channel openers on chronic left ventricular (LV) remodeling remains unknown, so the effect of IP and mito-KATP channel openers on the LV pressure-volume curve was assessed in rats subjected to 30 min ischemia followed by a 3-week reperfusion. Infarct size was histologically determined at 3 weeks after reperfusion. The LV pressure-volume curve was significantly shifted left by IP, diazoxide and nicorandil compared with the controls. These effects were blocked by the selective mito-KATP channel blocker 5-hydroxydecanoate. The LV remodeling and the infarct size at 3 weeks after reperfusion correlated well, indicating that the reduction of LV remodeling in the ischemic-reperfused model was strongly influenced by attenuation of the ischemic injury. LV remodeling in the chronic phase is attenuated by IP and mito-KATP channel openers with concomitant reduction of infarct size.
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Dairaku et al. (2002) studied this question.
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