[5]Huston JM, Ochani M, Rosas-Ballina M, Liao H, Ochani K, Pavlov VA, et al. Splenectomy in-activates the cholinergic antiinflammatory pathway during lethal endotoxemia and polymicrobial sepsis[J].J Exp Med, 2006, 203 (7):1623-1628.
[6]Tracey KJ. Physiology and immunology of the cholinergic anti-inflammatory pathway[J].J Clin Invest, 2007, 117(2):289-296.
[7]Huston JM, Gallowitsch-Puerta M, Ochani M, Ochani K, Yuan R, Rosas-Ballina M, et al. Transcutaneous vagus nerve stimulation reduces serum high mobility group box 1 levels and improves survival in murine sepsis[J].Crit Care Med, 2007, 35(12):2762-2768.
[8]Wang H, Liao H, Ochani M, Justiniani M, Lin X, Yang L, et al. Cholinergic agonists inhibit H-MGB1 release and improve survival in experimental sepsis[J].Nat Med, 2004, 10(11): 1216-1221.
[9]Bergmann M, Sautner T.Immunomodulatory effects of vasoactive catecholamines[J]. Wien Klin Wochenschr, 2002,114(17-18):752-761.
[10]Wang H, Yu M, Ochani M, Amella CA, Tanovic M, Susarla S, et al. Nicotinic acetylcholine receptor alpha 7 subunit is an essential regulator of inflammation[J].Nature, 2003, 421(6921): 384-388.
[11]Law WR, Valli VE, Conlon BA. Therapeutic potential for transient inhibition of adenosine deaminase in systemic inflammatory response syndrome[J].Crit Care Med, 2003, 31(5):1475-1481.
[12]Oberbeck R. Catecholamines: physiological immunomodulators during health and illness[J].Curr Med Chem, 2006, 13(17):1979-1989.
[13]Oberbeck R, Schmitz D, Wilsenack K, Schüler M, Pehle B, Schedlowski M, et al. Adrenergic modulation of survival and cellular immune functions during polymicrobial sepsis[J].Neuroimmunomodulation, 2004, 11(4):214-223.
[14]Freestone PP, Williams PH, Haigh RD, Maggs AF, Neal CP, Lyte M.Growth stimulation of intestinal commensal Escherichia coli by catecholamines: a possible contributory factor in trauma-induced sepsis[J].Shock, 2002, 18(5):465-470.
[15]Flierl MA, Rittirsch D, Chen AJ, Nadeau BA, Day DE, Sarma JV, et al. The complement anaphylatoxin C5a induces apoptosis in adrenomedullary cells during experimental sepsis[J].PLoS One, 2008, 3(7):e2560.
[18]Gosain A, Gamelli RL. Role of the gastrointestinal tract in burn sepsis[J].J Burn Care Rehabil, 2005, 26(1):85-91.
[19]Magnotti LJ, Deitch EA. Burns, bacterial translocation, gut barrier function, and failure[J].J Burn Care Rehabil, 2005, 26(5): 383-391.
[20]Larauche M, Bradesi S, Million M, McLean P, Taché Y, Mayer EA, et al. Corticotropin-releasing factor type 1 receptors mediate the visceral hyperalgesia induced by repeated psychological stress in rats[J].Am J Physiol Gastrointest Liver Physiol, 2008, 294(4): G1033-1040.
[21]Zhou M, Das P, Simms HH, Wang P.Gut-derived norepinephrine plays an important role in up-regulating IL-1beta and IL-10[J].Biochim Biophys Acta, 2005, 1740(3):446-452.
[22]Yang S, Zhou M, Chaudry IH, Wang P. Norepinephrine-induced hepatocellular dysfunction in early sepsis is mediated by activation of alpha 2-adrenoceptors[J].Am J Physiol Gastrointest Liver Physiol, 2001, 281(4):G1014-1021.
[23]Yang S, Koo DJ, Zhou M, Chaudry IH, Wang P. Gut-derived norepinephrine plays a critical role in producing hepatocellular dysfunction during early sepsis[J].Am J Physiol Gastrointest Liver Physiol, 2000, 279(6):G1274-1281.
[24]Zhou M, Yang S, Koo DJ, Ornan DA, Chaudry IH, Wang P.The role of Kupffer cell alpha(2)-adrenoceptors in norepinephrine-induced TNF-alpha production[J].Biochim Biophys Acta, 2001, 1537(1):49-57.