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目的:观察缓激肽后处理对心肺复苏（CPR）大鼠的神经保护作用，并探讨其可能机制。方法:将48只成年雄性SD大鼠按随机数字表法分为假手术组（Sham组）、心搏骤停组（CA组）、缓激肽后处理组（BK组）、腺苷酸活化蛋白激酶（AMPK）抑制剂Compound C+缓激肽后处理组（CP+BK组），每组最终取8只大鼠进行后续实验。采用窒息法诱导大鼠心搏骤停模型；Sham组仅给予动静脉置管、气管插管及机械通气等有创操作，未用窒息法诱导心搏骤停。心搏骤停前30 min，CP+BK组大鼠腹腔注射Compound C（250 μg/kg），其余各组大鼠经腹腔注射相同剂量的二甲亚砜（DMSO），自主循环恢复（ROSC）后48 h BK组和CP+BK组经腹腔注射缓激肽150 μg/kg，其余各组经腹腔注射相同剂量的生理盐水。ROSC后72 h用神经功能缺损评分（NDS）量表评价各组大鼠神经功能；采用免疫组化法检测自噬相关蛋白微管相关蛋白1轻链3（LC3）、p62的表达；透射电镜下观察各组自噬小体形成情况；采用原位末端缺刻标记试验（TUNEL）检测各组海马CA1区神经元凋亡情况。结果:与Sham组比较，CA组NDS评分明显降低（分：60.75±5.80比80.00±0.00，n P<0.01），LC3、p62蛋白表达量明显增多〔LC3（n A值）：1.04±0.64比0.40±0.14，p62（n A值）：2.75±0.57比0.36±0.12，均n P<0.05〕，自噬小体明显增多，细胞凋亡率明显升高〔（39.00±8.00）%比（3.87±1.90）%，n P<0.05〕。与CA组比较，BK组NDS升高（分：67.75±6.32比60.75±5.80，n P<0.05），LC3蛋白表达量明显升高（n A值：1.60±0.34比1.04±0.64，n P<0.05），自噬小体数量增多，p62蛋白表达量及细胞凋亡率明显降低〔p62（n A值）：1.51±0.32比2.75±0.57，细胞凋亡率：（23.03±1.91）%比（39.00±8.00）%，均n P<0.05〕。与BK组比较，CP+BK组NDS降低（分：59.00± 8.19比67.75±6.32，n P<0.05），自噬小体数量减少，自噬相关蛋白LC3表达量明显降低（n A值：0.62±0.41比1.60± 0.34，n P<0.05），p62表达量和细胞凋亡率均明显升高〔p62（n A值）：3.50±0.47比1.51±0.32，细胞凋亡率：（44.53±10.15）%比（23.03±1.91）%，均n P<0.05〕。n 结论:缓激肽后处理可以通过激活自噬、减少神经元凋亡，从而发挥神经保护作用。“,”Objective:To explore the protective effects of bradykinin postconditioning on cardiopulmonary resuscitation (CPR) rats, and to assess the underlying mechanisms.Methods:Forty-eight adult male Sprague-Dawley (SD) rats were randomly divided into four groups according to random number table: Sham operation group, cardiac arrest (CA) group, bradykinin treatment (BK) group, and AMP-activated protein kinase (AMPK) inhibitor Compound C+ bradykinin treatment (CP+BK) group, finally, 8 rats in each group were taken for follow-up experiment. CA was induced by asphyxia. Rats in the Sham group received arteriovenous catheterization, endotracheal intubation, and mechanical ventilation, without CA. Compound C (250 μg/kg) was intraperitoneally injected in CP+BK group 30 minutes before CA, and the same volume of dimethyl sulfoxide (DMSO) was given in the remaining groups. Bradykinin (150 μg/kg) was intraperitoneally injected in BK group and CP+BK group 48 hours after restoration of spontaneous circulation (ROSC), and same volume of saline was given in the remaining groups. The neural function of rats in each group was evaluated with neurological deficit score (NDS) 72 hours after ROSC. Microtubule-associated protein light chain 3 (LC3) and p62 expressions were detected by immunohistochemistry, autophagosomes were observed by transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method (TUNEL) assay was used to assess apoptosis.Results:Compared with the Sham group, the NDS was decreased (60.75±5.80 vs. 80.00±0.00, n P < 0.01), the expression levels of LC3 and p62 elevated [LC3 ( n A value): 1.04±0.64 vs. 0.40±0.14, p62 (n A value): 2.75±0.57 vs. 0.36±0.12, both n P < 0.05], the number of autophagosomes and apoptotic cells increased in the CA group [(39.00±8.00)% vs. (3.87±1.90)%, n P < 0.05]. Compared with the CA group, the NDS (67.75±6.32 vs. 60.75±5.80, n P < 0.05), the expression of LC3 ( n A value: 1.60±0.34 vs. 1.04±0.64, n P < 0.05), and the number of autophagosomes increased in the BK group, while the expression of p62 and the rate of apoptotic cells reduced [p62 ( n A value): 1.51±0.32 vs. 2.75±0.57, apoptotic cells rate: (23.03±1.91)% vs. (39.00±8.00)%, both n P < 0.05]. Compared with the BK group, the NDS (59.00±8.19 vs. 67.75±6.32, n P < 0.05), the expression of LC3 ( n A value: 0.62±0.41 vs. 1.60±0.34, n P < 0.05) and the number of autophagosomes declined in the CP+BK group, while the expression of p62 and the rate of apoptotic cells elevated [p62 ( n A value): 3.50±0.47 vs. 1.51±0.32, apoptotic cells rate: (44.53±10.15)% vs. (23.03±1.91)%, both n P < 0.05].n Conclusion:Bradykinin postconditioning played a neuroprotective role in CPR rats by activating autophagy and reducing apoptosis.