Hypertrophied Myocardium Is Refractory to Sevoflurane-Induced Protection With Alteration of Reperfusion Injury Salvage Kinase/Glycogen Synthase Kinase 3β Signals

• DOI: 10.1097/shk.0b013e3182a0674b
• Publication Date: 2013-07-11T12:26:57Z
• Authors: Lei-Lei Ma; Fei-Jiang Zhang; Fei-Juan Kong; Ling-Bo Qian; Hong Ma; Jian-An Wang; Min Yan
• Keywords: Cardioprotection; Tensin; GSK3B

Recent studies have demonstrated that volatile anesthetic postconditioning confers myocardial protection against ischemia-reperfusion injury through activation of the reperfusion salvage kinase (RISK) pathway. As RISK has been shown to be impaired by ventricular hypertrophy, we investigate whether anesthetic-induced cardiac was maintained in rat hearts with hypertrophy. Transverse aortic constriction operation performed on male Sprague-Dawley rats induce left (LV) then sham-operated or hypertrophied were subjected 40 min global ischemia and 2 h reperfusion. The isolated received 3% sevoflurane for 10 six cycles 10-s ischemia/10-s after hemodynamics, infarct size, PTEN (phosphatase tensin homolog deleted chromosome ten), phosphorylated Akt, extracellular regulated protein (ERK) 1/2, glycogen synthase 3β (GSK3β) determined. We found expression PTEN, ERK1/2, GSK3β did not significantly differ between transverse constriction-control groups. Both ischemic improved LV reduced increased phosphorylation their downstream target hearts. In contrast, neither nor hemodynamic, myocardium. All results above indicate hypertrophy abrogated sevoflurane-induced cardioprotection alteration RISK/GSK3β signals.