论文部分内容阅读
大量临床和实验研究证明,失血性休克引起严重的细胞免疫抑制并增加对脓毒症的易感性,后者可能与巨噬细胞释放前列腺素 E_2(PCE_2)增加有关。休克后 PCE_2的过量产生和释放,被认为是引起免疫抑制的介质。氯喹可抑制离体巨噬细胞分泌 PGE_2。本实验在失血性休克时应用氯喹,研究其对休克后免疫抑制的影响。采用近交系 C_3H/HeN 雄性小鼠,年龄6～8周,体重20～25g,分成假手术组、休克后不治疗组(注射生理盐水)及休克治疗组(注射氯喹)。股动脉放血至平均血压为35mmHg,维持60分钟后复苏。在休克前2小时或复苏后即刻肌肉注射生理盐水或氯喹。复苏后2或24小时处死。测定腹腔巨噬细胞释
A large number of clinical and experimental studies have shown that hemorrhagic shock caused by severe cellular immunosuppression and increased susceptibility to sepsis, the latter may be related to the release of macrophages prostaglandin E_2 (PCE_2). Overproduction and release of PCE2 after shock is considered as a mediator of immunosuppression. Chloroquine inhibits the secretion of PGE_2 by macrophages in vitro. In this experiment, chloroquine was used in hemorrhagic shock to study its effect on immune suppression after shock. Inbred line C_3H / HeN male mice aged 6 to 8 weeks and weighing 20 ~ 25g were divided into sham operation group, shock untreated group (injection of saline) and shock treatment group (injection of chloroquine). Femoral artery blood pressure to an average of 35mmHg, to maintain recovery after 60 minutes. Intramuscular injection of saline or chloroquine 2 hours before shock or immediately after resuscitation. Two or 24 hours after the resuscitation were executed. Peritoneal macrophage release was measured