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] Mutschler DK, Eriksson MB, Wikstrom BG, et al. Microdialysis-evaluated myocardial cyclooxygenase-mediated inflammation and early circulatory depression in porcine endotoxemia[J]. Crit Care Med, 2003, 31(6):1780-1785.[2] Singer M, De Santis V, Vitale D, et al. Multiorgan failure is an adaptive, endocrine-mediated, metabolic response to overwhelming systemic inflammation[J]. Lancet, 2004, 364(9433):S45-S48.[3] Levy RJ, Vijayasarathy C, Raj NR, et al. Competitive and noncompetitive inhibition of myocardial cytochrome C oxidase in sepsis[J]. Shock, 2004, 21(2):110-114.[4] Jia L,Takahashi M, Morimoto H, et al. Changes in cardiac lipid metabolism during sepsis: the role of very low-density lipoprotein receptors[J]. Cardiovasc Res, 2006, 69(2):545 -555. [5] Mink SN, Jacobs H, Bose D, et al. Lysozyme: a mediator of myocardial depression and adrenergic dysfunction in septic shock in dogs[J]. J Mol Cell Cardiol, 2003, 35(3):265-275.[6] Tavener SA, Long EM, Robbins SM, et al. Immune cell Toll-like receptor4 is required for cardiac myocyte impairment during endotoxemia[J]. Circ Res, 2004, 95(7):700-707.[7] Thomas JA, Haudek SB, Koroglu T, et al. IRAK1 deletion disrupts cardiac Toll/IL-1 signaling and protects against contractile dysfunction[J]. Am J Physiol Heart Circ Physiol, 2003, 285(2):H597-H606.[8] Comini L, Boraso A, Bachetti T, et al. Effects od endotoxic shock on neuronal NOS and calcium transients in rat cardiac myocytes[J]. Pharmacol Res, 2005, 51(5):409-417.[9] Hwang TL, Yeh CC. Hemodynamic and hepatic microcirculational changes in endotoxemic rats treated with different NOS inhibitors[J]. Hepatogastroenterology, 2003, 50(49):188-191.[10]Rossi MA, Santos CS. Sepsis-related microvascular myocardial damage with giant cell inflammation and calcification[J]. Virchows Arch, 2003, 443(1):87-92.