内毒素血症、细胞因子在失血性休克发展过程中的作用及治疗对策
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资料包括： 论文(4页3812字)
说明：
关键词： 失血性休克,内毒素,细胞因子,治疗
失血性休克是临床上较常见的危重症之一，主要的治疗手段是补充血容量、应用升压药物等。但是有些患者即使血容量已被补足，升压药用到了极量，休克仍不能得到纠正，最终发展至死亡。因此，顽固性休克的治疗成为临床上的一大难点，彻底弄清休克的发病机制是进行针对性治疗的关键。近年来，人们对于细菌及内毒素移位、细胞因子等在失血性休克由可逆向不可逆发展过程中的作用进行了深入研究，取得了很大进展，为临床休克的治疗提供了某些理论依据，本文对此作一综述。
1 肠源性菌血症、内毒素血症的作用
1.1 失血性休克时的菌血症、内毒素血症 许多研究发现，失血性休克发生后出现了明显的内毒素血症，休克复苏后内毒素血症仍持续存在［1～3］。但对于菌血症、内毒素血症在休克发展中有无意义却出现了争议。有人认为，并发失血性休克后的内毒素血症只是休克过程中的一种生理现象，可能无任何病理意义。但大多数学者认为，失血性休克后的菌血症、内毒素血症是促使休克向不可逆性转化的重要原因之一，与休克的预后有明显关系［4，5］。其中内毒素血症比菌血症具有更重要的意义，因为内毒素血症可以诱发大量炎性因子释放入血，过量的炎性因子参与对机体的病理损害过程，导致休克进一步恶化。
目录：
1 肠源性菌血症、内毒素血症的作用
2 细胞因子的作用
参考文献：
［1］Yao YM, Tian HM, Wang YP, et al. Protective effect of Re-LPS antiserum on experimental multiple system organ failure. Chin Med J, 1992, 105: 833-838.
［2］Jiang JX, Bahrami S, Leichtfried G,et al. Kinetics of endotoxin and tumorsis factor appearance in protal and system circulation after hemorrhagic shock in rats. Ann Surg, 1995, 221(1): 100-106.
［3］Sorol AJ, Rush BF, Lysz TW, et al. The gut as sorese of sepsis after hemorrhgic shock. Am J Surg, 1988, 155: 187-192.
［4］Chang TW. Improvement of survival from hemorrhagic shock by enterectomy in rats: finding to implicate the role of the gut for irreversibillty of hemorrhagic shock. J Trauma, 1997, 42: 223-230.
［5］Rush BF,Sori AJ, Murphy TF, et al. Endotoxemia and bacteremia during hemorrhagic shock. Ann Surg, 1988, 207: 549-544.
［6］Rush BF. Irreversibility in hemorrhagic shock is caused by sepsis. Am Surg, 1989, 55: 204.
［7］Antonsson JB, et al. The role of the gut in shock and multiple system organ failure: clinical review. Eur J Surg, 1991, 157: 3.
［8］Stoutenbeek CP, Van Saene HKF, Miranda DR, et al. The effect of Selective decontamination of the digestive tract on colonization and infection rate in multiple trauma patients. Inten Care Med, 1984, 10: 185.
［9］Kasravi FB, Adawi D, Molin G, et al. Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by Dgalactosamine. J Hepatol, 1997, 26: L417-424.
［10］Bahrami S, Yao YM, Leichtfried G, et al. Monoclonal antibody to endotoxin attenuates hemorrhage-induced lung injury and mortality in rats. Crit Care Med, 1997, 25: 1030-1036.
［11］Weiss J, Olsson I. Cellular and subcellular localization of the bactericidal/permeability increasing protein of neutrophils. Blood, 1987, 69: 652-659.
［12］Marra MN, Wilde CG, Griffith JE, et al. Bactericidal/permeability-increasing protein has endotoxin-neutralizing activity. J Immunol, 1990, 144: 662-668.
［13］Yao YM, Bahrami S, Leichtfried G, et al. Pathogensis of hemorrhage-induced bacteria/endotoxin translocation in rats: Effects of recombinant bactericidal-increasing protein(rBPI21). Ann Surg, 1995, 221: 398-405.
［14］姚咏明，田惠民，王亚军，等.大鼠出血性休克后肠源性内毒素血症及TNF、IL-1变化的动态观察.中国病理生理杂志，1993，9(5)：585-589.
［15］Yao YM, Tian HM, Sheng ZY, et al. Inhibitory effects of low-dose polymyxin B on hemorrhage-induced endotoxin/bacterial translocation and cytokine formation. J Trauma, 1995, 38: 924-930.
［16］蒋建新，田昆仑，陈惠孙，等.家兔创伤性休克后血浆内毒素、TNF和IL-6的动态变化.中华麻醉学杂志，1997，17(3)：171-173.
［17］Couturier C, Jahns G, Haeffner-Cavaillon N, et al. Membrane molecules which trigger the production of interleukin-1 and tumor necrosis factor-alpha by lipopolysaccharide-stimulated human monocytes. Eur J Immunol, 1992, 22: 1461-1466.
［18］Heumann D, Gallay P, Barras C, et al. Control of lipopolysaccharide (LPS) binding and LPS-induced tumor necrosis factor secretion in human peripheral blood monocytes. J Immunol, 1992, 148: 3505-3512.
［19］姚咏明，陈劲松，于燕，等.延迟应用TNF-α单抗治疗重度失血性休克的实验.中华麻醉学杂志，1998，18(8)：486-489.
［20］Pruitt JH, Copeland EMI, Moldawer LL. Interleukin-1 and interleulkin-1 antagonism in sepsis, systemic inflammation response syndrome, and septic shock. Shock, 1995, 3: 235-251.
［21］Starnes HF Jr, Pearce MK, Tewari A, et al. Anti-IL-6 monoclonal antibodies protect against lethal escherichia coli infection and lethal tumor necrosis facfor-α challenge in mice. J Immunol, 1990, 145: 4185-4191.
［22］Harada A, Sekido N, Akahoshi T, et al. Essential involvement of interleukin-8(IL-8) in acute inflammation. J Leukoc Biol 1994; 56: 559-564.
资料包括： 论文(4页3812字)
说明：
关键词： 失血性休克,内毒素,细胞因子,治疗
失血性休克是临床上较常见的危重症之一，主要的治疗手段是补充血容量、应用升压药物等。但是有些患者即使血容量已被补足，升压药用到了极量，休克仍不能得到纠正，最终发展至死亡。因此，顽固性休克的治疗成为临床上的一大难点，彻底弄清休克的发病机制是进行针对性治疗的关键。近年来，人们对于细菌及内毒素移位、细胞因子等在失血性休克由可逆向不可逆发展过程中的作用进行了深入研究，取得了很大进展，为临床休克的治疗提供了某些理论依据，本文对此作一综述。
1 肠源性菌血症、内毒素血症的作用
1.1 失血性休克时的菌血症、内毒素血症 许多研究发现，失血性休克发生后出现了明显的内毒素血症，休克复苏后内毒素血症仍持续存在［1～3］。但对于菌血症、内毒素血症在休克发展中有无意义却出现了争议。有人认为，并发失血性休克后的内毒素血症只是休克过程中的一种生理现象，可能无任何病理意义。但大多数学者认为，失血性休克后的菌血症、内毒素血症是促使休克向不可逆性转化的重要原因之一，与休克的预后有明显关系［4，5］。其中内毒素血症比菌血症具有更重要的意义，因为内毒素血症可以诱发大量炎性因子释放入血，过量的炎性因子参与对机体的病理损害过程，导致休克进一步恶化。
目录：
1 肠源性菌血症、内毒素血症的作用
2 细胞因子的作用
参考文献：
［1］Yao YM, Tian HM, Wang YP, et al. Protective effect of Re-LPS antiserum on experimental multiple system organ failure. Chin Med J, 1992, 105: 833-838.
［2］Jiang JX, Bahrami S, Leichtfried G,et al. Kinetics of endotoxin and tumorsis factor appearance in protal and system circulation after hemorrhagic shock in rats. Ann Surg, 1995, 221(1): 100-106.
［3］Sorol AJ, Rush BF, Lysz TW, et al. The gut as sorese of sepsis after hemorrhgic shock. Am J Surg, 1988, 155: 187-192.
［4］Chang TW. Improvement of survival from hemorrhagic shock by enterectomy in rats: finding to implicate the role of the gut for irreversibillty of hemorrhagic shock. J Trauma, 1997, 42: 223-230.
［5］Rush BF,Sori AJ, Murphy TF, et al. Endotoxemia and bacteremia during hemorrhagic shock. Ann Surg, 1988, 207: 549-544.
［6］Rush BF. Irreversibility in hemorrhagic shock is caused by sepsis. Am Surg, 1989, 55: 204.
［7］Antonsson JB, et al. The role of the gut in shock and multiple system organ failure: clinical review. Eur J Surg, 1991, 157: 3.
［8］Stoutenbeek CP, Van Saene HKF, Miranda DR, et al. The effect of Selective decontamination of the digestive tract on colonization and infection rate in multiple trauma patients. Inten Care Med, 1984, 10: 185.
［9］Kasravi FB, Adawi D, Molin G, et al. Effect of oral supplementation of lactobacilli on bacterial translocation in acute liver injury induced by Dgalactosamine. J Hepatol, 1997, 26: L417-424.
［10］Bahrami S, Yao YM, Leichtfried G, et al. Monoclonal antibody to endotoxin attenuates hemorrhage-induced lung injury and mortality in rats. Crit Care Med, 1997, 25: 1030-1036.
［11］Weiss J, Olsson I. Cellular and subcellular localization of the bactericidal/permeability increasing protein of neutrophils. Blood, 1987, 69: 652-659.
［12］Marra MN, Wilde CG, Griffith JE, et al. Bactericidal/permeability-increasing protein has endotoxin-neutralizing activity. J Immunol, 1990, 144: 662-668.
［13］Yao YM, Bahrami S, Leichtfried G, et al. Pathogensis of hemorrhage-induced bacteria/endotoxin translocation in rats: Effects of recombinant bactericidal-increasing protein(rBPI21). Ann Surg, 1995, 221: 398-405.
［14］姚咏明，田惠民，王亚军，等.大鼠出血性休克后肠源性内毒素血症及TNF、IL-1变化的动态观察.中国病理生理杂志，1993，9(5)：585-589.
［15］Yao YM, Tian HM, Sheng ZY, et al. Inhibitory effects of low-dose polymyxin B on hemorrhage-induced endotoxin/bacterial translocation and cytokine formation. J Trauma, 1995, 38: 924-930.
［16］蒋建新，田昆仑，陈惠孙，等.家兔创伤性休克后血浆内毒素、TNF和IL-6的动态变化.中华麻醉学杂志，1997，17(3)：171-173.
［17］Couturier C, Jahns G, Haeffner-Cavaillon N, et al. Membrane molecules which trigger the production of interleukin-1 and tumor necrosis factor-alpha by lipopolysaccharide-stimulated human monocytes. Eur J Immunol, 1992, 22: 1461-1466.
［18］Heumann D, Gallay P, Barras C, et al. Control of lipopolysaccharide (LPS) binding and LPS-induced tumor necrosis factor secretion in human peripheral blood monocytes. J Immunol, 1992, 148: 3505-3512.
［19］姚咏明，陈劲松，于燕，等.延迟应用TNF-α单抗治疗重度失血性休克的实验.中华麻醉学杂志，1998，18(8)：486-489.
［20］Pruitt JH, Copeland EMI, Moldawer LL. Interleukin-1 and interleulkin-1 antagonism in sepsis, systemic inflammation response syndrome, and septic shock. Shock, 1995, 3: 235-251.
［21］Starnes HF Jr, Pearce MK, Tewari A, et al. Anti-IL-6 monoclonal antibodies protect against lethal escherichia coli infection and lethal tumor necrosis facfor-α challenge in mice. J Immunol, 1990, 145: 4185-4191.
［22］Harada A, Sekido N, Akahoshi T, et al. Essential involvement of interleukin-8(IL-8) in acute inflammation. J Leukoc Biol 1994; 56: 559-564.