1De kock I, Van Daele C. Sepsis and septic shock: pathophysioiogical and cardiovascular background as basis for therapy [ J ]. Acta Clin Belg, 2010, 65 (5): 323-329.
2Schuetz P, Christ-Crain M. Circulating precursor levels of endothelin-1 and adrenomedullin, two endotheliurn-derived, counteracting substances,in sepsis [J]. Endothelium, 2007, 14 (6): 345-351.
3Zanotti Cavazzoni SL, Guglielmi M, et al. Ventricular dilation is associated with improved cardiovascular performance and survival in sepsis [J]. Chest, 2010, 138 (4): 848-855.
4Stefan Frantz, Vincent KA, Feron O, et al. Innate Immunity and Angiogenesis [J]. Circ Res, 2005; 96 (1); 15-26.
5Sennoun N, Meziani F, Dessebe O. Activated protein C improves lipopolysaccharide-induced cardiovascular dysfunction by decreasing tissular inflammation and oxidative stress [ J ]. Crit Care Med, 2009 , 37 (1): 246-255.
6You W, Min X, Zhang X, Qian B. Cardiac-specific expression of heat shock protein 27 attenuated endotoxin-induced cardiac dysfunction and mortality in mice through a PI3K/Akt-dependent mechanism [J]. Shock, 2009, 32 (1): 108-117.
7Can J. Physiol. Nitric oxide and calcium signaling regulate myocardial tumor necrosis factor-α expression and cardiac function in sepsis [J]. Pharmacol, 2010, 88 (2): 92-104.
8Rudiger A, Singer M. et al Mechanisms of sepsis-induced cardiac dysfunction [J]. Crit Care Med, 2007, 35 (6): 1599-1608.
9Piel DA, Deutschman CS, Levy RJ. et al. Exogenous eytochrome C restores myocardial cytochrome oxidase activity into the late phase of sepsis [J]. Shock, 2008, 29 (5) : 612-616.
10Remick DG, Newcomb DE, Bolgos GL, et al . Comparison of the mortality and inflammatory response of two models of sepsis: lipopolysaccharide vs. cecal ligation and puncture [ J ]. Shock, 2000, 13 (2): 110-116.
