Myocardial ischaemia reperfusion injury: the challenge of translating ischaemic and anaesthetic protection from animal models to humans Z. Xia, H. Li,

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Myocardial ischaemia reperfusion injury: the challenge of translating ischaemic and anaesthetic protection from animal models to humans Z. Xia, H. Li, M.G. Irwin British Journal of Anaesthesia Volume 117, Pages ii44-ii62 (January 2016) DOI: 10.1093/bja/aew267 Copyright © 2016 The Author(s) Terms and Conditions

Fig 1 Schematic of proposed mechanism of myocardial ischaemia reperfusion injury. Myocardial ischaemia reperfusion increases mitochondrial permeability transition pore (mPTP) opening which elevates reactive oxygen species (ROS) generation, decreases nitric oxide (NO) bioavailability, and disrupts intracellular distribution of Ca2+, Na+ and pH, resulting in cardiomyocyte death and subsequent irreversible myocardial injury. British Journal of Anaesthesia 2016 117, ii44-ii62DOI: (10.1093/bja/aew267) Copyright © 2016 The Author(s) Terms and Conditions

Fig 2 Schematic of proposed mechanism of ischaemic preconditioning cardioprotection. Ischaemic preconditioning exerts its cardioprotection through the reperfusion injury salvage kinase (RISK) pathway that involves the activation of PI3K/Akt and MEK1/2 and, subsequently, activates PKA, eNOS, P70S6K and GSK-3β, leading to a decrease in mitochondrial permeability transition pore (mPTP) opening and increase in the mitochondrial KATP (Mito KATP) channel opening which attenuates myocardial ischaemia reperfusion injury. British Journal of Anaesthesia 2016 117, ii44-ii62DOI: (10.1093/bja/aew267) Copyright © 2016 The Author(s) Terms and Conditions

Fig 3 Schematic of proposed mechanism of myocardial ischaemic postconditioning cardioprotection. Ischaemic postconditioning confers cardioprotection through the survivor activating factor enhancement (SAFE) and reperfusion injury salvage kinase (RISK) pathways. These involve the activation of Jak/STAT3 and PI3K/Akt, which subsequently decreases mitochondrial permeability transition pore (mPTP) opening and increases mitochondrial KATP (Mito KATP) channel opening, which attenuates myocardial ischaemia reperfusion injury. British Journal of Anaesthesia 2016 117, ii44-ii62DOI: (10.1093/bja/aew267) Copyright © 2016 The Author(s) Terms and Conditions

Fig 4 Schematic of proposed mechanism of myocardial anaesthetic conditioning cardioprotection. Anaesthetic conditioning protects the heart and other organs against ischaemia reperfusion injury through the survivor activating factor enhancement (SAFE) and reperfusion injury salvage kinase (RISK) pathways, which, subsequently, through mitochondrial-dependent and non-mitochondrial-dependent (nuclear or other) signalling pathways, decrease mitochondrial permeability transition pore (mPTP) opening and increase mitochondrial KATP (Mito KATP) channel opening which attenuates ischaemia reperfusion injury. British Journal of Anaesthesia 2016 117, ii44-ii62DOI: (10.1093/bja/aew267) Copyright © 2016 The Author(s) Terms and Conditions