摘要目的:探讨辛酸钠对猪创伤性心搏骤停复苏后肾肠缺血再灌注损伤（IRI）的影响。方法:国产巴马小型猪22头，体重（37.6±2.5）kg，按照随机数字表法分为正常组（7只）、IRI组（7只）和IRI治疗组（8只）。猪肾肠IRI模型的建立：使用血泵，经股动脉放血，速度2 ml·kg -1·min -1，直至心搏骤停，无干预观察6 min，6 min后经股静脉回输全血，速度5 ml·kg -1·min -1，回输50%失血量进行复苏。正常组只进行监测操作，不建立肾肠IRI模型；IRI组建立肾肠IRI模型；IRI治疗组建立肾肠IRI模型，于自主循环恢复（ROSC）后5 min时静脉泵入辛酸钠30 mg/kg, 持续1 h。(1）比较三组动物复苏成功率、复苏后4，24 h存活率、达到心搏骤停标准时的失血量、达到ROSC标准时的复苏时间。（2）比较三组动物复苏前及复苏后1，2，4，24 h血清肌酐（SCr）、尿素氮（BUN）、肠型脂肪酸结合蛋白（iFABP）及二胺氧化酶（DAO）水平。（3）复苏后24 h时处死动物，快速获取肾肠组织。采用TUNEL法检测细胞凋亡指数；普鲁士蓝法检测肾肠组织铁沉积面积率；Western blot检测谷胱甘肽过氧化物酶4（GPX4）、长链脂酰辅酶A合成酶4（ACSL4）蛋白表达水平。 结果:三组动物均100%存活，IRI组、IRI治疗组失血量、复苏时间比较，差异无统计学意义（ P均>0.05）。正常组复苏前及复苏后1，2，4，24 h SCr、BUN、iFABP及DAO水平差异无统计学意义（ P均>0.05）；IRI组、IRI治疗组复苏后1，2，4，24 h SCr、BUN、iFABP及DAO水平逐渐升高，与同组复苏前比较，差异有统计学意义（ P均<0.01）；正常组、IRI组、IRI治疗组复苏前SCr、BUN、iFABP及DAO水平差异无统计学意义（ P均>0.05）；IRI组、IRI治疗组复苏后1，2，4，24 h SCr、BUN、iFABP及DAO水平较同时间点正常组升高（ P均<0.01）；IRI组复苏后1，2，4，24 h SCr、BUN、iFABP及DAO水平较同时间点IRI治疗组升高更明显（ P均<0.01）。正常组、IRI组、IRI治疗组复苏后24 h肾组织细胞凋亡指数分别为（2.3±0.8）%、（44.0±5.4）%、（13.8±4.3）%，肠组织细胞凋亡指数分别为（2.6±0.9）%、（61.3±10.4）%、（20.8±3.7）%（ P均<0.01），其中IRI组肾肠组织细胞凋亡指数最高；三组肾组织铁沉积面积率分别为（0.6±0.1）%、（3.9±1.0）%、（1.7±0.3）%，肠组织铁沉积面积率分别为（0.8±0.1）%、（4.9±0.9）%、（2.1±0.5）%（ P均<0.01），其中IRI组肾肠组织铁沉积面积率最高。IRI组、IRI治疗组复苏后24 h肾肠组织GPX4蛋白表达水平较正常组降低（ P均<0.05），其中IRI组表达水平最低；而ACSL4蛋白表达水平较正常组升高（ P均<0.01），其中IRI组表达水平最高。 结论:辛酸钠可减轻猪创伤性心搏骤停复苏后肾肠IRI，其机制可能为辛酸钠可抑制细胞凋亡，同时通过调控GPX4、ACSL4蛋白表达水平来降低细胞铁死亡。

abstractsObjective:To investigate the effect of sodium octanoate on renal-intestinal ischemia- reperfusion injury (IRI) after resuscitation from traumatic cardiac arrest in pigs.Methods:Twenty-two miniature piglets with a body weight of (37.6±2.5)kg were divided into three groups according to the random-number table method: normal group ( n=7), IRI group ( n=7) and IRI-treated group ( n=8). A renal-intestinal IRI model of the pig was established by allowing femoral artery to bleed through blood pump at a rate of 2 ml·kg -1·min -1 until cardiac arrest, followed by whole blood transfusion through the femoral vein at a rate of 5 ml·kg -1·min -1 after observation for 6 minutes, and 50% of total blood loss was reinfused before resuscitation. Both the IRI group and IRI-treated group were with IRI model, while normal group was just monitored without induction of IRI. Besides, IRI-treated group was injected intravenously with sodium octanoate (30 mg/kg) for 1 hour at 5 minutes after restoration of spontaneous circulation (ROSC). (1) The rate of resuscitation success, survival rate at 4, 24 hours after resuscitation, blood loss when reaching cardiac arrest criteria and resuscitation time when reaching the ROSC criteria were compared in the three groups. (2) Levels of serum creatinine (SCr), urea nitrogen (BUN), intestinal fatty acid binding protein (iFABP) and diamine oxidase (DAO) were measured before resuscitation and at 1, 2, 4, 24 hours after resuscitation. (3) The animals were sacrificed at 24 hours post-resuscitation to harvest renal and intestinal tissues rapidly. TUNEL test was applied for the cellular apoptosis index. Prussian blue was used to detect the rate of iron deposition. Western blot analysis was used to measure levels of glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member4 (ACSL4). Results:In three groups, all pigs survived. There was no significant difference in blood loss or resuscitation time between IRI group and IRI-treated group (all P>0.05). There was no significant difference in levels of SCr, BUN, iFABP or DAO before resuscitation and at 1, 2, 4, 24 hours after resuscitation in normal group (all P>0.05). But their levels were gradually increased at 1, 2, 4, 24 hours after resuscitation from that before resuscitation in IRI group and IRI-treated group (all P<0.01). Among three groups, levels of SCr, BUN, iFABP and DAO had no significant difference before resuscitation (all P>0.05), but showed obvious increase in IRI group and the IRI-treated group at 1, 2, 4, 24 hours after resuscitation compared with normal group, especially in IRI group (all P<0.01). In normal group, IRI group and IRI-treated group after 24 hours for resuscitation, the cellular apoptosis index of renal tissues was (2.3±0.8)%, (44.0±5.4)% and (13.8±4.3)%; the cellular apoptosis index of intestinal tissues was (2.6±0.9)%, (61.3±10.4)% and (20.8±3.7)%; the rate of iron deposition of renal tissues was (0.6±0.1)%, (3.9±1.0)% and (1.7±0.3)%; the rate of iron deposition of intestinal tissues was (0.8±0.1)%, (4.9±0.9)% and (2.1±0.5)% (all P<0.01). The cellular apoptosis index and rate of iron deposition of both renal and intestinal tissues were the highest in IRI group. The renal-intestinal expression of GPX4 in IRI group and IRI-treated group was lower than that in normal group at 24 hours after resuscitation (all P<0.05), with the lowest in IRI group. The renal-intestinal expression of ACSL4 in IRI group and IRI-treated group was higher than that in normal group at 24 hours after resuscitation (all P< 0.01), with the highest in IRI group. Conclusion:Sodium octanoate can reduce renal-intestinal IRI after resuscitation from traumatic cardiac arrest in pigs, the mechanism for which is probably due to that sodium octanoate can inhibit cellular apoptosis and reduce ferroptosis by regulating the expression levels of GPX4 and ACSL4.