摘要
目的探讨脾脏在电刺激迷走神经抗大鼠感染性休克中的作用及其机制。方法将64只成年SD大鼠按随机数字表法分为假手术组、模型组、迷切组、迷刺组、脾切组、脾切迷刺组、腹腔干切断组和膈下支切断组8组，每组8只。采用盲肠结扎穿孔术（CLP）制备大鼠感染性休克模型。大鼠行左侧颈迷走神经干分离或切断，CLP前3d行脾脏切除．迷走神经腹腔干支和膈下支于CLP后即刻切断。连续监测大鼠平均动脉压（MAP）；CLP后4h行动脉血气分析，用酶联免疫吸附法（ELISA）检测血浆和脾组织中肿瘤坏死因子-α（TNFα）、白细胞介素-1（IL—1）的含量，用半定量逆转录-聚合酶链反应（RT—PCR）检测脾组织TNF-α、IL-1的mRNA表达。结果与假手术组相比，模型组MAP持续下降，出现乳酸蓄积和代谢性酸中毒，血浆和脾组织中TNF-α、IL-1的含量及脾组织TNF-α、IL-1的mRNA表达均明显增高[血TNF-α（ng／L）113．24±5．69比24．69±2．56，血IL-1（ng／L）226．33±9．12比34．58±3．45；脾TNF-α（ng／g）286．12±6．66比41．33±2．35，脾TNF-αmRNA1．12±0．08比0．22±0．02，脾IL-1（ng／g）447．34±12．36比42．95±2．33，脾IL-1mRNA0．93±0．06比0．28±0．02，均P〈0．01]。与模型组比较，迷刺组MAP下降趋势减缓，动脉血乳酸和剩余碱（BE）负值明显减小，血浆和脾组织TNF-α、IL-1含量及脾组织TNF-α、IL-1的mRNA表达[血TNF-α（ng／L）41．00±3．22，血IL-1（ng／L）63．29±2．56；脾TNF-α（ng／g）74．22±3．12，脾TNF-αmRNA0．32±0．03，脾IL-1（ng／g）81．54±5．48，脾IL-1mRNA0．35±0．03；均显著降低（P〈0．05或P〈0．01）；而脾脏切除后，电刺激颈迷走神经则无迷刺组类似的效应。腹腔干切断组血浆和脾组织中TNF-α、IL-1的含量及脾组织TNF-α、IL-1的mRNA表达（血TNF-α（ng／L）118．38±8．52，血IL-1（ng／L）252．23±9．55；脾
Objective To investigate the role of spleen in vagus nerve stimulation for treatment against septic shock in rats and its underlying mechanism. Methods Sixty-four male Sprague-Dawley （SD） rats were randomly divided into eight groups （n= 8 in each group）： sham group, model group, vagotomy group, vagus nerve stimulation group, splenectomy group, splenectomy and vagus nerve stimulation group, common celiac branch vagotomy group, and selective subdiaphragmatic ventral vagotomy group. The septic shock model was reproduced by cecal ligation and puncture （CLP）. All the animals were subjected to left cervical vagus nerve isolation or vagotomy, splenectomy was done 3 days before CLP, common celiac branch vagotomy and selective subdiaphragmatic ventral vagotomy were performed after CLP. Mean arterial pressure （MAP） was continuously monitored. Blood was collected 4 hours after CLP for arterial blood gas analysis. The concentrations of tumor necrosis factor-α （TNF-α） and interleukin-1 （IL-1） in plasma and spleen were measured by enzyme-linked immunosorbent assay （ELISA）. The spleen mRNA expressions of TNF-α and IL-1 were determined by quantitative reverse transcription-polymerase chain reaction （RT-PCR）. Results Compared with sham group, MAP continuously declined, and lactic acid accumulation and metabolic acidosis appeared in model group, and the contents of TNF-α and IL-1 in plasma and spleen, and mRNA expression of TNF-α and IL 1 in spleen were significantly increased in model group [plasma TNF-α （ng/L） 113.24±5.69 vs. 24.69±2.56, plasma IL-1 （ng/L） 226.33±9.12 vs. 34.58± 3.45, spleen TNF-α （ng/g） 286.12±6.66 vs. 41.33±2.35, spleen TNF-αmRNA 1.12＋0.08vs. 0.22± 0.02, spleen IL-1 （ng/g） 447.34±12.36 vs. 42.95±2.33, spleen IL-1 mRNA 0.93±0.06 vs. 0.28± 0.02, all P〈0.01]. Compared with model group, lowering of MAP was retarded, lactic acid value and the negative value of base excess （BE） were significantly decreased, the contents of TNF-α and IL-1 i
出处
《中国危重病急救医学》
CAS
CSCD
北大核心
2011年第5期263-266,共4页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目（30972852）
