可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:
[1]Sodi-Pallares D,Testelli MR,Fishleder BL,et al.Effects of an intravenous infusion of a potassium-glucose-insulin solution on the electrocardiographic signs of myocardial infarction:a preliminary clinical report[J].Am J Cardiol,1962,2(9):166-181.
[2]Mehta SR,Yusuf S,Díaz R,et al.Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction:the CREATE-ECLA randomized controlled trial[J].JAMA,2005,293(4):437-446.
[3]MacKenzie A.Endothelium-derived vasoactive agents,AT1 receptors and inflammation[J].Pharmacol Ther,2011,131(2):187-203.
[4]Kakihana Y,Ito T,Nakahara M,et al.Sepsis-induced myocardial dysfunction:pathophysiology and management[J].J Intensive Care,2016,4:22.
[5]Rudiger A,Singer M.Mechanisms of sepsis-induced cardiac dysfunction[J].Crit Care Med,2007,35(6):1599-1608.
[6]Sato R,Nasu M. A review of sepsis-induced cardiomyopathy[J].J Intensive Care,2015,3:48.
[7]Bruni FD,Komwatana P,Soulsby ME,et al.Endotoxin and myocardial failure:role of the myofibril and venous return[J].Am J Physiol,1978,235(2):H150-H156.
[8] Cunnion RE,Schaer GL,Parker MM,et al.The coronary circulation in human septic shock[J].Circulation(Baltimore),1986,73(4):637-644.
[9]Fallach R,Shainberg A,Avlas O,et al.Cardiomyocyte Toll-like receptor 4 is in volved in heart dysfunction following septic shock or myocardial ischemia[J].Mol Cell Cardiol,2010,48 (6):1236-1244.
[10]Dhanantwari P,Nadaraj S,Kenessey A,et al.Macrophage migration inhibitory factor induces cardiomyocyte apoptosis[J].Biochem Biophys Res Commun,2008,371(2):298-303.
[11]Sips PY,Irie T,Zou L,et al.Reduction of cardiomyocyte S-nitrosylation by S-nitrosoglutathione reductase protects against sepsis-induced myocardial depression[J].Am J Physiol Heart Circ Physiol,2013,304(8):H1134-H1146.
[12]Tavernier B,Garrigue D,Boulle C,et al.Myofilament calcium sensitivity is decreased in skinned cardiac fibres of endotoxin-treated rabbits[J].Cardiovasc Res,1998,38(2):472-479.
[13]刘亚凤,李文强.补体系统的激活对脓毒症心肌病的不利影响[J].中国急救医学,2011,31(7):658-661.
[14]Bartz RR,Suliman HB,Piantadosi CA.Redox mechanisms of cardiomyocyte mitochondrial protection[J].Front Physiol,2015,6:291.
[15]陈昌勤,张召才,严 静.脓毒症和心肌线粒体损伤(综述)[J].中国危重病急救医学,2007,19(10):630-632.
[16]Bronsveld W,van Lambalgen AA,van Velzen D,et al.Myocardial metabolic and morphometric changes during canine endotoxin shock before and after glucose-insulin-potassium[J].Cardiovasc Res,1985,19:455-464.
[17]Tuynman HA,Thijs LG,Straub JP,et al.Effects of glucose-insulin-potassium(GIK)on the position of the oxyhemoglobin dissociation curve,2.3-diphosphoglycerate, and oxygen consumption in canine endotoxin shock[J].J Surg Res,1983,34(3):246-253.
[18]Hinshaw LB,Archer LT,Benjamin B,et al.Effects of glucose or insulin on myocardial performance in endotoxin shock[J].Proc Soc Exp Biol Med,1976,152(4):529-534.
[19]Das UN.Insulin:an endogenous cardioprotector[J].Curr Opin Crit Care,2003,9(5):375-383.
[20]Bronsveld W,van Lambalgen AA,van Velzen D,et al.Myocardial metabolic and morphometric changes during canine endotoxin shock before and after glucose-insulin-potassium[J].Cardiovasc Res,1985,19(8):455-464.
[21]Tuynman HA,Thijs LG,Straub JP,et al.Effects of glucose-insulin-potassium(GIK)on the position of the oxyhemoglobin dissociation curve,2.3-diphosphoglycerate, and oxygen consumption in canine endotoxin shock[J].J Surg Res,1983,34(3):246-253.
[22]Gao F,Gao E,Yue TL,et al.Nitric oxide mediates the antiapoptotic effect of insulin in myocardial ischemia-reperfusion: the roles of PI3-kinase,Akt,and endothelial nitric oxide synthase phosphorylation[J].Circulation,2002,105(12):1497-1502.
[23]Jeschke MG,Einspanier R,Klein D,et al.Insulin attenuates the systemic inflammatory response to thermal trauma[J].Mol Med, 2002, 8(8):443-450.
[24]Rossig L,Haendeler J,Hermann C,et al.Nitric oxide down-regulates MKP-3 mRNA levels:involvement in endothelial cell protection from apoptosis[J].J Biol Chem,2000,275(33):25502-25507.
[25]Kaynar AM,Bakalov V,Laverde SM,et al.Cost of surviving sepsis:a novel model of recovery from sepsis in Drosophila melanogaster[J].Intensive Care Med Exp, 2016, 4(1):4.
[26]Selker HP, Beshansky JR, Sheehan PR, et al. Out-of-hospital administration of intravenous glucose-insulin-potassium in patients with suspected acute coronary syndromes:the IMMEDIATE randomized controlled trial[J].JAMA,2012,307(18):1925-1933.
[27]Das UN.Pyruvate is an endogenous anti-inflammatory and anti-oxidant molecule[J].Med Sci Monit,2006,12(5):RA79-RA84.
[28]Díaz A,Humeres C,González V,et al.Insulin/NFκB protects against ischemia-induced necrotic cardiomyocyte death[J].Biochem Biophys Res Commun,2015,467(2):451-457.
[29]Jin PY,Zhang HS,Guo XY,et al.Glucose-insulin-potassium therapy in patients with acute coronary syndrome:a meta-analysis of randomized controlled trials[J].BMC Cardiovasc Disord,2014,14:169.
[30]Puskarich MA,Runyon MS,Trzeciak S,et al.Effect of Glucose-Insulin-Potassium Infusion on Mortality in Critical Care Settings:A Systematic Review and Meta-Analysis[J].Clin Pharmacol,2009,49(7):758-767.
[31]Ali-Hassan-Sayegh S,Mirhosseini SJ,Zeriouh M,et al.Safety and efficacy of glucose-insulin-potassium treatment in coronary artery bypass graft surgery and percutaneous coronary intervention[J].Interact Cardiovasc Thorac Surg,2015,21(5):667676.
[32]Mehta SR,Yusuf S,Diaz R,et al.CREATE-ECLA Trial Group Investigators:Effect of glucose-insulin-potassium infusion on mortality in patients with acute ST-segment elevation myocardial infarction:the CREATE-ECLA randomized controlled trial[J].JAMA,2005,293(4):437-446.
[33]Meldrum DR, Donnahoo KK. Role of TNF in mediating renal insufficiency following cardiac surgery: evidence of a postbypass cardiorenal syndrome[J].Surg Res,1999,85(2):185-199.