兔出血性休克并腹内压升高后中性粒细胞免疫机能抑制

南方医科大学学报 ›› 2004, Vol. 24 ›› Issue (03): 325-328.

兔出血性休克并腹内压升高后中性粒细胞免疫机能抑制

吕琦¹, 庄颜峰¹, 王万明¹, 陈学明¹, 徐皓¹, 坂本吉正², 高原佐代子², 西田昌道², 小林国男²

1. 南京军区福州总医院骨科, 福建, 福州, 350000;
2. 帝京大学医学院救急救命中心, 日本东京, 173-0003

出版日期:2004-03-20 发布日期:2004-03-20
基金资助:
收稿日期:2003-9-29。
作者简介:吕琦(1968- ),男,1998年毕业于第一军医大学,硕士,主治医师,电话:0591-3771042,E-mail:androluqi@hotmai1.com

Suppression of neutrophil immune function in rabbit models of hemorrhagic shock complicated by intra-abdominal hypertension

LU Qi¹, ZHUANG Yan-feng¹, WANG Wan-ming¹, CHENG Xue-ming¹, XU Hao¹, Yoshimasa Sakamoto², Sayoko Takahara², Masamichi Nishida², Kunio Kobayashi²

1. 南京军区福州总医院骨科, 福建, 福州, 350000;
2. 帝京大学医学院救急救命中心, 日本东京, 173-0003

Online:2004-03-20 Published:2004-03-20

摘要/Abstract

摘要： 目的探讨腹内压升高对外周血中性粒细胞炎性反应能力的影响。方法将24只家兔随机均分为A(出血性休克并发腹内压升高)、B(出血性休克)、C(腹内压升高)、D(对照)4组。分别于创伤前、创伤后及创伤后4 h,采用流式细胞仪检查中性粒细胞内细胞因子的产生、化学发光法检查中性粒细胞的吞噬能力、免疫细胞化学检测NF-κB的表达。结果创伤后4 h,A组较创伤前及其余各组中性粒细胞内细胞因子产生减少、吞噬能力下降,NF-κB表达抑制(P<0.05);B和C组除在创伤早期有所变化外,创伤后4 h恢复到创伤前水平;D组各时间点无显著变化。结论出血性休克后腹内压升高对机体形成序贯性二次打击,导致中性粒细胞对内毒素的刺激反应性下降,免疫机能抑制。这可能有助于解释腹部间区综合征中发生败血症的病理生理学机制。

Abstract: Objective To investigate the effects of hemorrhagic shock and intra-abdominal hypertension (IAH) on inflammatory responses of peripheral circulating neutrophils such as intracellular cytokine production, phagocytic capacity and expression of nuclear factor (NF)-κB. Methods Twenty-four rabbits were divided equally into 4 groups including a hemorrhagic shock (HS) group complicated by abdominal compartment syndrome (ACS) (Group A), a HS group (Group B), a ACS group (Group C) and a normal control group (Group D). Intracellular interleukin (IL)-8 production in the peripheral neutrophils were measured in the rabbits by flow cytometry, phagocytic function of the neutrophils evaluated by a chemiluminescence method and the NF-κB expression detected by immunocytochemistry before, immediately and 4 h after the traumatization. Results Four hours after the trauma, decreased intracellular IL-8 production and impaired phagocytic function of the peripheral neutrophils were observed in Group A along with suppressed NF-κB expression. But in Group B and Group C, the intracellular IL-8 production, phagocytic function and expression of NF-κB returned to the normal levels 4 hours after the trauma following the early-stage changes. In Group D, no significant changes occurred during the observation. Conclusions Responsiveness and function of the neutrophils to the stimuli by endotoxin are suppressed by the sequential second-hit of IAH after hemorrhagic shock, which may contribute to the occurrence of sepsis in ACS.

中图分类号:

R364.1

吕琦¹, 庄颜峰¹, 王万明¹, 陈学明¹, 徐皓¹, 坂本吉正², 高原佐代子², 西田昌道², 小林国男². 兔出血性休克并腹内压升高后中性粒细胞免疫机能抑制[J]. 南方医科大学学报, 2004, 24(03): 325-328.

LU Qi¹, ZHUANG Yan-feng¹, WANG Wan-ming¹, CHENG Xue-ming¹, XU Hao¹, Yoshimasa Sakamoto², Sayoko Takahara², Masamichi Nishida², Kunio Kobayashi². Suppression of neutrophil immune function in rabbit models of hemorrhagic shock complicated by intra-abdominal hypertension[J]. Journal of Southern Medical University, 2004, 24(03): 325-328.

参考文献

[1] Nakatani T, Sakamoto Y, Kaneko I, et al. Effects of intra-abdominal hypertension on hepatic energy metabolism in a rabbit model [J]. JTrauma, 1998, 44(3): 446-53.
[2] Diebel LN, Dulchavsky SA, Brown WJ. Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome [J]. J Trauma, 1997, 43(5): 852-4.
[3] Doty JM, Oda J, Ivatury RI, et al. The effects of hemodynamic shock and increased intra-abdominal pressure on bacterial translocation[J]. J Trauma, 2002, 52(1): 13-7.
[4]
[5] Zallen G, Moore EE, Johnson JL, et al. Postinjury suppression of human neutrophil cytokine production results from the stabilization of inhibitory κB[J]. Shock, 1999, 11 (2):77-8 1.
[6] Ono Y, Kunii O, Kobayashi K, et al. Evaluation ofopsonophagocyt ic dysfunctions in severely burned patients by luminol-dependent chemiluminescence[J]. Microbiol Immunol, 1993, 37(7): 563-71.
[7] Jung T, Schauer U, Heusser C, et al. Detection of intracellular cy tokines by flow cytometry[J]. J Immunol Method, 1993, 159(2): 197-207.
[8] Foulds S, Galustian C, Mansfield AO, et al. Transcription factor NF κB expression and postsurgical organ dysfunction [J]. Ann Surg, 2001,233(1): 70-8.
[9] Nourbakhsh M, Kalble S, Dorrie A, et al. The NF-kappa b repress ing factor is involved in basal repression and interleukin (IL)-l-in duced activation of IL-8 transcription by binding to a conservedNF-kappa b-flanking sequence element [J]. J Boil Chem, 2001, 276 (6): 4501-8.
[10] Adrie C, Pinsky MR. The inflammatory balance in human sepsis[J]. Intensive Care Med, 2000, 26(4): 363-75.
[11] Adib-conquy M, Adrie C, Moine P, et al. NFκB expression in mono nuclear cells of patients with sepsis resembles that observed in lipopolysaccharide tolerance [J]. Am J Crit Care Med, 2000, 162(5): 1877-83.
[12] Ertel W Kremer J, Kenney J, et al. Down-regulation of proinflam matory cytokine release in whole blood from septic patients [J]. Blood, 1995, 85(5): 1341 - 7.
[13] Oda J, Ivatury RI, Blocher CR, et al. Amplified cytokine response and lung injury by sequential hemorrhagic shock and abdominal compartment syndrome in a laboratory model of ischemia-reperfu sion[J]. J Trauma, 2002, 52(2): 625-32.
[14] Pritts T, Hungness E, Wang Q, et al. Mucosal and enterocyte IL-6 production during sepsis and endotoxemia-role of transcription factors and regulation by the stress response [J]. Am J Surg, 2002, 183(4): 372-83.
[15] 郑健生,方向东,郑庆亦,等吸入性损伤患者血浆IL-8水平的变化[J].第一军医大学学报,2000,20(6):551-2Zheng JS, Fang YD, Zheng QY, et al. Changes of plasma IL-8 levels in patients with inhalation injury [J]. J Firs Mil Med Univ/Di Yi JunYi Da Xue Xue Bao, 2000, 20(6): 551-2.
[16] McDonald PP, Bald A, Cassatella MA. Activation of the NF-kappa B pathway by inflammatory stimuli in the human neutrophils [J]. Blood, 1997, 89(9): 3421-33.