2[1]Kirkeboen KA, Strand OA. The role of nitric oxide in sepsis an overview[J]. Acta Anaesthesiol Scand, 1999, 43(3): 275-88.
3[2]Szabo C, Thiemermann C. Invited opinion: role of nitric oxide in hemorrhagic, traumatic, and anaphylactic shock and thermal injury [J]. Shock, 1994, 2(2): 145-55.
4[3]Yao YM, Bahrami S, Leichtfried G, et al. Significance of NO in hemorrhage-induced hemodynamic alterations, organ injury, and mortality in rats[J]. Am J Physiol, 1996, 270(5 Pt 2): 1616-23.
5[4]Goris RJ. Pathophysiology of shock in trauma[J]. Eur J Surg, 2000,166(1): 100-11.
6[5]Schlag G, Redl H. Shock, sepsis and organ failure-nitric oxide[M].Germany: Springer-Verlag Berlin Heidelberg, 1995.84-96.
7[6]Smail N, Catanla R A, Wang P, et al. Gut and liver: the organs responsible for increased nitric oxide production after trauma-hemor-rhage and resuscitation[J]. Arch Surg, 1998, 133(4): 399-405.
8[7]Gebhard F, Nussler AK, Rosch M, et al. Early posttraumatic increase in production of nitric oxide in humans[J]. Shock, 1998, 10(4):237-42.
9[8]Hansen PR. Inflammatory alterations in the myocardial microcirculation[J ]. J Mol Cell Cardiol, 1998, 30(12): 2555-9.
10[9]Delonca J, Balteaux V, Giraud T, et al. EDRF/NO and endothelial functions[J]. Arch Mal Coeur Vaiss, 1993, 86(11): 1617-24.
