Abstract
BackgroundIschemic Postconditioning (IPC) reduces ischemia/reperfusion (I/R) injury under normal conditions. HMG-CoA reductase inhibitors (statins), which inhibit the synthesis of mevalonate, can interfere with the cardioprotective effect of IPC. However, the beneficial role of IPC in hyperlipidemic patients, post-acute administration of statins remains unknown. This study was to determine if acute administration of atorvastatin affect the infarct size-limiting effect of IPC in hyperlipidemic rats.ResultsCompared to control group, infarct size decreased more significantly in atorvastatin+IPC and atorvastatin+IPC+wortmannin groups than IPC or atorvastatin+IPC+PD98059 groups. Phosphorylation of PI3K/Akt was attenuated in atorvastatin + IPC+ wortmannin group, phosphorylation of P42 MAPK/ERK was increased in atorvastatin+IPC and atorvastatin+IPC+wortmannin groups.Materials and MethodsNinety four-weeks old male SD rats fed with cholesterol enriched diet for six weeks were randomized into nine groups (n = 10/group) - sham group, control group, IPC group, atorvastatin group, wortmannin group, PD98059 group, atorvastatin+IPC group, atorvastatin+IPC+wortmannin group and atorvastatin+IPC+PD98059 group. Atorvastatin was administered orally 12 hours before myocardial reperfusion.ConclusionsPost-translational activation of P42 MAPK/ERK, rather than PI3K/Akt, participates in the net protective effect of IPC and atorvastatin in hyperlipidemia.
Highlights
Ischemic heart disease is the leading cause of death in the industrialized world
Phosphorylation of PI3K/Akt was attenuated in atorvastatin + Ischemic Postconditioning (IPC)+ wortmannin group, phosphorylation of P42 mitogen-activated protein kinase (MAPK)/ERK was increased in atorvastatin+IPC and atorvastatin+IPC+wortmannin groups
I/R ratio between myocardial infarction sizes (IS) and area at risk (AAR) was not significantly different between the control (I/R group in which the rats were fed with cholesterol enriched diet) and IPC groups
Summary
Ischemic heart disease is the leading cause of death in the industrialized world. Myocardium reperfusion can lead to myocardial infarction, cardiac arrhythmias, and contractile dysfunction [1]. Numerous studies have confirmed the myocardial protective effect of IPC since its first demonstration more than a decade ago [2]. The majority of these studies were performed in animal models, in which ischemia/reperfusion was imposed in the absence of comorbidities [1]. It has been shown that the infarct size-limiting effect of IPC is attenuated in hyperlipidemic rabbits [3, 4] and cholesterolfed rats [5]. This study was to determine if acute administration of atorvastatin affect the infarct size-limiting effect of IPC in hyperlipidemic rats
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