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对细胞素和补体激活在内毒素诱导的粘膜损伤和细菌易位发生机理中的作用进行了研究,并定量研究了内毒素诱导的肠粘膜渗透性变化的大小。采用内毒素低反应的C_3 H/HeJ小鼠和补体缺陷的(C_3和C_5)DBA/2小鼠,测定其内毒素诱导细菌易位的能力。非近交的ICR小鼠作为对照。采用非近交小鼠,在内毒素接种前6小时经腹腔给多克隆抗TNF抗体,检验该抗体阻止内毒素诱导的细菌易位的能力。抗体的用量足以防止内毒素诱导的小鼠死亡。内毒素
The role of cytokines and complement activation in endotoxin-induced mucosal injury and the mechanism of bacterial translocation was studied and the extent of endotoxin-induced changes in intestinal mucosal permeability was quantified. Endotoxin-induced C_3H / HeJ mice and complement-deficient (C_3 and C_5) DBA / 2 mice were used to determine the endotoxin-induced bacterial translocation. Non-inbred ICR mice served as controls. Non-inbred mice were used to intraperitoneally polyclonal anti-TNF antibody 6 hours prior to endotoxin inoculation to examine the antibody’s ability to prevent endotoxin-induced bacterial translocation. Antibodies are used in an amount sufficient to prevent endotoxin-induced mouse death. Endotoxin