心跳骤停复苏后大鼠肺部炎症因子的变化
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摘要
目的:建立室颤心脏骤停大鼠模型,探究心肺复苏后大鼠肺部炎症因子的变化。方法:通过右心室交流电致颤法建立未处理8分钟室颤大鼠模型,随机将24只大鼠分为假手术组(Sham组)、复苏后1 h组(ROSC 1h组)、复苏后3 h组(ROSC 3h组)和复苏后6h组(ROSC 6h组)。Sham组不经历心脏骤停和复苏直接取材,另外3组的动物均经历8分钟未处理室颤和6分钟CPR,复苏后分别监测1 h、3 h和6 h后取材。检测4组动物的IL-1α、IL-6和TNF-α。结果:对比于Sham,ROSC 1h的IL-1α、IL-6和TNF-α均显著增高;ROSC 3h组IL-1α、IL-6和TNF-α均显著增高;ROSC 6h的IL-6显著增高。结论:复苏后1h和3h大鼠肺部的炎症因子IL-1α、IL-6和TNF-α均显著增高,复苏后6小时肺部炎症因子IL-1α和TNF-α均回落接近正常水平,而IL-6仍显著增高。
Objective:To establish a rat model of cardiac arrest with ventricular fibrillation and to explore the changes of pulmonary inflammatory factors in rats after cardiopulmonary resuscitation.Methods:A rat model of untreat-ed 8-minute ventricular fibrillation was established by right ventricular alternating current defibrillation. 24 rats were ran-domly divided into sham operation group(Sham group),1 h group after resuscitation(ROSC 1 h group),and 3 h group after resuscitation.(ROSC 3 h group)and 6 h group after resuscitation(ROSC 6 h group). The Sham group did not under-go cardiac arrest and resuscitation directly. The other three groups underwent 8 minutes of untreated ventricular fibrilla-tion and 6 minutes of CPR. After resuscitation,they were monitored for 1 h,3 h and 6 h. IL-1α,IL-6 and TNF-α were detected in 4 groups of animals.Results:Compared with Sham,IL-1α,IL-6 and TNF-α were significantly increased in ROSC 1 h;IL-1α,IL-6 and TNF-α were significantly increased in ROSC 3 h group;IL-6 was significantly increased in ROSC 6 h.Conclusion:The inflammatory cytokines IL-1α,IL-6 and TNF-α in the lungs of rats were significantly in-creased at 1 h and 3 h after resuscitation. The levels of inflammatory cytokines IL-1α and TNF-α decreased to normal lev-els 6 hours after resuscitation. IL-6 is still significantly increased.
Objective:To establish a rat model of cardiac arrest with ventricular fibrillation and to explore the changes of pulmonary inflammatory factors in rats after cardiopulmonary resuscitation.Methods:A rat model of untreat-ed 8-minute ventricular fibrillation was established by right ventricular alternating current defibrillation. 24 rats were ran-domly divided into sham operation group(Sham group),1 h group after resuscitation(ROSC 1 h group),and 3 h group after resuscitation.(ROSC 3 h group)and 6 h group after resuscitation(ROSC 6 h group). The Sham group did not under-go cardiac arrest and resuscitation directly. The other three groups underwent 8 minutes of untreated ventricular fibrilla-tion and 6 minutes of CPR. After resuscitation,they were monitored for 1 h,3 h and 6 h. IL-1α,IL-6 and TNF-α were detected in 4 groups of animals.Results:Compared with Sham,IL-1α,IL-6 and TNF-α were significantly increased in ROSC 1 h;IL-1α,IL-6 and TNF-α were significantly increased in ROSC 3 h group;IL-6 was significantly increased in ROSC 6 h.Conclusion:The inflammatory cytokines IL-1α,IL-6 and TNF-α in the lungs of rats were significantly in-creased at 1 h and 3 h after resuscitation. The levels of inflammatory cytokines IL-1α and TNF-α decreased to normal lev-els 6 hours after resuscitation. IL-6 is still significantly increased.
引文
[1]杨惠玲,潘景轩,吴伟康.高级病理生理学(第二版).科学出版,2006:277-279.
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[2]Cand S,Nanzak S,Morimoto Y,et al.Alteration of soluble-1 and p-selections during cardiac arrest and CPR[J].Intensive Care Med,1999,26(6):588.
[3]Cand S,Nanzak S,MorimotoY,et al.Cardiac arrest increase soluble vascular endothelial adhesion molecules and neatrophile lastate with endothelial of injury[J].Intensive Care Med,2000,26(1):38.
[4]Shy KG,Chang H,Lin CC,et al.Concentration of serum interleukin-8 after successful cardiopulmonary arrest[J].Am Hear J,1997,134:551.
[5]Caty MG,Sehmeling DJ,Friedl HP,et al.A promoter of xanthine oxidase activity in intestinal ischemia reperfusion[J].J Pediatr Surg,1990,25(6):218.
[6]Schwartz,MD,Repine JE.Xanthine oxidase-derived oxygen radicals increase lung cytokine expression in mice subjected to hemorrhagic shock[J].Am J Respire Cell Mol Biol,1995,12(4):434.
[7]LU YT,Hellewell PG,Evans TW,Ischemia reperfusion lung injury:contribution of ischemia,neutrophils,and hydrostatic pressure[J].Am J Physiol,1997,273(17):46.2019 01 18