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目的观察伴有胃肠动力障碍的重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠结肠肠神经系统(enteric nervous system,ENS)肌间神经丛一氧化氮合成酶(nitric oxide synthase,NOS)神经元的变化,以探讨SAP胃肠动力障碍的神经机制。方法20只SD大鼠随机均分为假手术组和SAP组,逆行胰胆管穿刺逆行注射5%牛磺胆酸钠制作SAP模型。检测腹部X线、小肠推进比,胰腺病理评分。制作肌间神经丛全层标本,应用双重免疫荧光染色法观察NOS神经元的形态及占总神经元的百分比。结果与假手术组相比,SAP组大鼠肠管明显扩张,SAP组小肠推进比显著降低(P<0.01),胰腺病理评分明显增高(P<0.01),NOS神经元胞体大而染色深,结间束NOS神经纤维粗大,NOS神经元比例为(40.74±5.15)%明显高于假手术组(P<0.01)。结论结肠肌间丛NOS神经元表达增多可能是大鼠SAP胃肠动力障碍神经机制之一。
Objective To observe the changes of nitric oxide synthase (NOS) nerve in the myenteric plexus of patients with severe acute pancreatitis (SAP) accompanied by gastrointestinal motility disorder in the colon of the enteric nervous system (ENS) Meta-changes to explore the neural mechanism of SAP gastrointestinal motility disorders. Methods Twenty SD rats were randomly divided into sham operation group and SAP group. SAP model was made by retrograde cholangiopancreatography retrograde injection of 5% sodium taurocholate. Abdominal X-ray examination, intestinal propulsion ratio, pancreatic pathology score. Making full-thickness specimens of myenteric plexus, double immunofluorescence staining was used to observe the morphology of the NOS neurons and the percentage of the total neurons. Results Compared with the sham-operation group, the intestine of SAP group was obviously dilated. The intestinal propulsion ratio of SAP group was significantly decreased (P <0.01), the pathological score of pancreatic tissue was significantly increased (P <0.01) The bundle of NOS nerve fibers were thick and the proportion of NOS neurons was (40.74 ± 5.15)% in the sham-operation group (P <0.01). Conclusion The increased expression of NOS in colonic myenteric plexus may be one of the neural mechanisms of gastrointestinal motility disorder in rats.