1Sanders KM Ward SM. Nitric oxide as a mediator of nonadrenergic, non-cholinergic, neurotransmtssion [J ]. Am J Physiol, 1992, 262: 379-383.
2HochRC. RodriguezR. ManningT, et al. Effects of accidental trauma on cytokine and endotoxin production [J]. Crit Care Med. 1993, 197: 1556-1562.
3Grumbled M, Virri I, Tolonen I, et al. A controlled immunohistochemical study of inflammatory cells in disc herniation tssue [J]. Spine, 1994, 19 (24): 2745-2751.
4KangID, Georgescu HI, LoriMI, et al. Herniated lumber interoertebral discs spontaneously produce matrix metalloproteinase, nitric oxide [J]. interleukill-6 and pnstaglandin E2[J]. Spine, 1996, 21 (3): 271-277.
5Tels S, Pichard CF, Teffrey A S. high levels of inflanunatory phospholipase A2. activity in lumber disc herniations [J ].Spine, 1990, 15: 674-678.
6Vadas SE, Oryzabsju W Influence of plasma proteins on actioity of proinflammatory enzyme phospholipase [J ]. Inflammation, 1986, 10: 183-193.
7Nygaard OP, Mcllgren SI. Osrerud B. The inflammatory properties of contained and noncontained lumber disc hernation [J]. Spine, 1997, 21 (1): 22-26.
8Saal JS. The role of inflammation in lumber pain [J]. Spine,1995, 20: 1821-1826.
9McCarron RF, Marc W, Hudgins PG. The Infoammatory Effect of Nucleus Pulposus: A Possible Element in the Pathogenesis of Low-back Pain [J]. Spine, 1987, 12: 760-764.
10Kirkaldy-Willis WH. The reaction of Structural pathology to the nerver root [J]. Spine, 1984, 9.. 49-52.
