目的:比较窒息与电刺激两种方法诱发心搏骤停大鼠模型脑损伤的严重程度。方法:将42只健康成年雄性SD大鼠按随机数字表法分为假手术组（n n＝6）、窒息组（n n＝18）和电刺激组（n n＝18）。各组大鼠均给予气管插管机械通气并经股动静脉置管监测血压和补液。窒息组夹闭气管导管致大鼠心搏骤停，电刺激组经食道电刺激诱发大鼠心搏骤停，均于4 min后开始心肺复苏（CPR）；假手术组大鼠仅麻醉后气管插管及经股动静脉置管，不诱发心搏骤停。观察模型大鼠72 h存活情况，并绘制Kaplan-Meier生存曲线。分别于复苏后24 h和72 h测定大鼠神经功能缺损评分（NDS）；取下腔静脉血，采用酶联免疫吸附试验（ELISA）测定血清脑损伤相关指标神经元特异性烯醇化酶（NSE）和钙结合蛋白S100B的水平；取脑组织，苏木素-伊红（HE）染色后光镜下观察大脑海马CA1区病理学改变。n 结果:窒息组和电刺激组均成功诱发出心搏骤停，CPR后自主循环恢复（ROSC）率分别为94.4%（17/18）和88.9%（16/18）。Kaplan-Meier生存曲线分析显示，窒息组大鼠72 h累积存活率与电刺激组比较差异无统计学意义（Log-Rank检验：n χ2＝0.040，n P＝0.841）。复苏后24 h窒息组和电刺激组大鼠NDS均显著高于假手术组（分：37.50±4.26、32.17±4.02比8.33±2.33，均n P<0.01）；复苏后72 h两个模型组NDS评分有下降趋势，以电刺激组下降更为显著，与窒息组比较差异有统计学意义（分：14.00±2.89比26.33±4.84，n P<0.05）。ELISA结果显示，复苏后24 h窒息组和电刺激组大鼠血清NSE水平均较假手术组明显升高（μg/L：1.02±0.07、1.02±0.02比0.87±0.02，均n P<0.05）。复苏后72 h窒息组血清NSE水平仍明显高于假手术组，差异有统计学意义（μg/L：1.03±0.05比0.87±0.02，n P0.05）。各组大鼠复苏后各时间点S100B水平比较差异均无统计学意义。光镜下显示，与假手术组相比，复苏后24 h两个模型组大鼠海马CA1区均无明显神经元损伤；72 h时两组有部分神经元损伤，以窒息组较电刺激组更严重。n 结论:窒息法和电刺激法诱发心搏骤停并成功复苏后的大鼠均有一定程度的脑损伤，以窒息法诱发的心搏骤停后脑损伤较电刺激法更严重。“,”Objective:To compare the severity of brain injury between asphyxia and electrical stimulation induced cardiac arrest in rats.Methods:Forty-two healthy male Sprague-Dawley (SD) rats were randomized into sham group (n n = 6), asphyxia group (n n = 18) and electrical stimulation group (n n = 18). Rats in each group were given invasive mechanical ventilation and femoral blood vessels catheterization for monitoring blood pressure and fluid infusion. In the asphyxia group, the tracheal tube was clamped to induce cardiac arrest, and in the electrical stimulation group, the esophageal electrical stimulation was used to induce cardiac arrest, and cardiopulmonary resuscitation (CPR) was performed 4 minutes after cardiac arrest. In the sham group, only tracheal intubation and femoral artery intubation were performed after anesthesia, but cardiac arrest was not induced. Animals were allowed to survive until 72 hours after resuscitation, and survival analysis was performed using Kaplan-Meier curves. At 24 hours and 72 hours after resuscitation, the neurological deficit score (NDS) was measured. The vena cava blood was collected, and the brain injury associated serum biomarkers, neuron-specific enolase (NSE) and S100B, were detected by enzyme-linked immunosorbent assay (ELISA). The brain tissues were then harvested to perform hematoxylin-eosin (HE) staining for observing pathological changes in the hippocampal CA1 area with light microscopy.n Results:Cardiac arrest was successfully induced in both the asphyxia group and the electrical stimulation group, 94.4% (17/18) and 88.9% (16/18) animals were resuscitated successfully in the two groups respectively. Kaplan-Meier curves analysis showed that 72-hour cumulative survival rate was similar in the asphyxia group and the electrical stimulation group (Log-Rank test: n χ2 = 0.040, n P = 0.841). Both asphyxia group and electrical stimulation group had higher NDS score than sham group at 24 hours after resuscitation (37.50±4.26, 32.17±4.02 vs. 8.33±2.33, both n P < 0.01). NDS score showed a downwards trend at 72 hours after resuscitation in both model groups, and the decline was more significant in the electrical stimulation group, which was significantly different as compared with asphyxia group (14.00±2.89 vs. 26.33±4.84, n P < 0.05). ELISA results showed that the levels of serum NSE at 24 hours after resuscitation in the asphyxia and electrical stimulation groups were significantly higher than those in the sham group (μg/L: 1.02±0.07, 1.02±0.02 vs. 0.87±0.02, both n P < 0.05). NSE kept increasing at 72 hours after resuscitation in the asphyxia group, which showed significant difference as compared with sham group (μg/L: 1.03±0.05 vs. 0.87±0.02, n P 0.05). There was no significant difference in S100B level at different time points after resuscitation among three groups. It was displayed under light microscope that there was no significant neuronal damage in the hippocampal CA1 area in the two model groups at 24 hours after resuscitation as compared with the sham group. At 72 hours, there were certain damages in the hippocampal CA1 area in both model groups, which were more obvious in the asphyxia group.n Conclusions:Both cardiac arrest models induced by asphyxia and electrical stimulation show a certain degree of brain injuries after resuscitation. Brain injuries are more severe in asphyxia-induced cardiac arrest compared with trans-esophageal electrical stimulation method.