中文摘要：

目的探讨促红细胞生成素（EPO）对心搏骤停（CA）大鼠心肺复苏（CPR）后脑组织的保护作用及其机制。方法将120只雄性SD大鼠按随机数字表法分为假手术组、常规按压组、常规按压＋EPO组（EPO组），每组40只；各组再按CA时和自主循环恢复（ROSC）后6、12、24、48h分为5个亚组，每组8只。采用改良Hendrickx经典窒息法制备CA模型，常规胸外按压进行复苏；假手术组仅进行麻醉、气管切开插管及血管穿刺操作，不进行窒息和复苏。EPO组在CA后同时予常规胸外按压＋重组人EPO注射液5kU／kg（制成2mL／kg的溶液）。各组在不同时间点留取血液标本，用酶联免疫吸附试验（ELISA）测定血清S100β蛋白含量；于相应时间点取血后处死大鼠取海马组织，光镜下计算海马组织S100β蛋白阳性细胞数；ROSC后24h观察海马组织病理学改变，并进行病理学评分。结果随ROSC时间延长，常规按压组和EPO组血清S100β蛋白（μg／L）均逐渐升高，24h达高峰（与CA时比较：常规按压组为305．7±29．2比44．4±6．2，EPO组为276．7±28．9比44．7±5.6，均P〈0．05），然后开始下降；EPO组ROSC后各时间点均明显低于常规按压组（6h为83．2±7．5比114．3±15．3，12h为123．9±20．2比184．9±22．2，24h为276．7±28．9比305．7±29．2，48h为256．5±26．6比285．2±23．6，均P〈0．05）。随ROSC时间延长，常规按压组和EPO组大脑皮质S100β蛋白阳性细胞数（个／HP）逐渐增多，24h达高峰（与CA时比较：常规按压组为14．3±2．2比6．7±0．7，EPO组为11．3±1.3比6．8±0．9，均P〈0．05），然后开始下降；EPO组各时间点均明显少低于常规按压组（6h为7．0±0．9比7．9±1．9，12h为8．4±1．1比10．2±2．2，24h为11.3±1．3比14．3±2．2.48h为8．3±0．8比10．8±2．0，均P〈0．05）。光镜下观察显示，常规按压后大鼠大脑皮质组织损伤严重，经EPO?

英文摘要：

Objective To study the protective effect of erythropoietin （EPO） on brain tissue with cardiac arrest-cardiopulmonary resuscitation （CA-CPR） and its mechanism. Methods 120 male Sprague-Dawley （SD） rats were randomly divided into three groups （each n = 40）, namely： sham group, routine chest compression group, and conventional chest compression ＋ EPO group （EPO group）. The rats in each group were subdivided into CA and 6, 12, 24, 48 hours after restoration of spontaneous circulation （ROSC） five subgroups （each n = 8 ）. The model of CA was reproduced according to the Hendrickx classical asphyxia method followed by routine chest compression, and the rats in sham group only underwent anesthesia, tracheostomy intubation and venous-puncture without asphyxia and CPR. The rats in EPO group were given the routine chest compression ＋ EPO 5 kU/kg （2 mL/kg） after CA. Blood sample was collected at different time points of intervention for the determination the content of serum S100 β protein by enzyme linked immunosorbent assay （ELISA）. All the rats were sacrificed at the corresponding time points, and the hippocampus was harvested for the calculation of the number of S100 β protein positive ceils, and to examine the pathological changes and their scores at 24 hours after ROSC by light microscopy. Results With prolongation of ROSC time, the serum levels of S100β protein （μg/L） in the routine chose compression group and the EPO group weresignificantly elevated, peaking at 24 hours （compared with CA： 305.7 ± 29.2 vs. 44.4± 6.2 in routine chest compression group, and 276.7±28.9 vs. 44.7±5.6 in the EPO group, both P 〈 0.05）, followed by a fall. The levels of S100β protein at each time point after ROSC in EPO group were significanthy lower than those of the routine chest compression group （83.2± 7.5 vs. 114.3± 15.3 at 6 hours, 123.9 ± 20.2 vs. 184.9± 22.2 at 12 hours, 276.7± 28.9 vs. 305.7 ± 29.2 at 24 hours, 256.3±26.6 vs. 283.2±23.6 at 48 hours, all P 〈 0.0