SIRS发展在胰腺坏死、继发感染致胰腺炎病变加重中的作用  

The role of SIRS in pancreatitis lesions caused by in pancreatic necrosis and secondary infection

作　　者：余夙慧[1] 康牧星[1] 孙洪伟[1] 陈必成[1] 周蒙滔[1] 张启瑜[1] 

机构地区：[1]温州医科大学附属第一医院肝胆外科,浙江温州325000

出　　处：《肝胆胰外科杂志》2014年第1期43-47,共5页Journal of Hepatopancreatobiliary Surgery

摘　　要：目的探讨全身炎症反应综合征(SIRS)在胰腺坏死、继发感染致胰腺炎病变加重中的作用。方法健康雄性SD大鼠46只,随机分为四组:SO组仅翻动胰腺,I、II、III组经胰管逆行注射1%、3%、5%牛磺胆酸钠+104/mL大肠杆菌混合液。8 h后处死大鼠,检测胰腺组织细菌培养、脂肪酶、磷脂酶A2、C反应蛋白、TNF-α、IL-1β、IL-6水平,进行胰腺组织病理学检查及Schmidt评分。结果①SO、I、II、III组胰腺组织细菌培养阳性率分别为0(0/10)、0(0/12)、25%(3/12)、90%(9/10),其中III组与SO、I、II组比较有统计学差异(P<0.01)。②SO、I、II、III组血清脂肪酶、C反应蛋白、TNF-α、IL-1β、IL-6、Schmidt评分逐渐升高,各组间差别有统计学意义(P<0.05)。③I、II、III组血清磷脂酶A2水平较SO组有显著性升高(P<0.01),III、II组比I组亦有显著性升高(P<0.01)。④病理学检查结果:SO组未见明显病变;I组可见胰腺水肿,炎性细胞浸润;II组腺泡水肿,炎性细胞浸润,血管内充血,散在坏死灶与出血点;III组可见凝固性坏死灶,大量炎性细胞浸润,微血管破裂,片状出血,甚至可见微脓肿。结论①胰腺坏死程度越重,其继发感染的概率越大;②SIRS可能是胰腺坏死、继发感染致胰腺炎病变加重的共同机制,抑制SIRS有助于SAP的治疗。Objective To investigate the role of SIRS in pancreatitis lesions caused by pancreatic necrosis and secondary infection. Methods Forty-six healthy male Sprague-Dawley （SD） rats were randomly divided into 4 groups： group sham operation （SO）, which only flip the pancreas; group I, II and III, which were induced by retrograde injection of a mixture of 1%, 3 %, 5 % sodium taurocholate and escherichia coli （104/mL） separately through pancreatic duct. After 8 h the rats were killed, and then bacterial culture of pancreas tissue, serum lipase, phospholipase A2, C-reactive protein, TNF-α, IL-1β and IL-6 levels were detected, and Schmidt score of pancreatic histopathology were performed. Results O The bacterial rate of cultured pancreas tissue was 0 （0/10）, 0 （0/ 12）, 25% （3/12） and 90% （9/10） respectively, and there was significant difference between group 11I and the others （P〈0.01）. ② Serum lipase, C-reactive protein, TNF-α IL-1β, IL-6 and Schmidt score gradually increased in group SO, I, II and III, the difference among groups was statistically significant （P〈0.05）. ③The serum phospho-lipase A2 level of I, II and III was much higher than that of SO group （P〈0.01）; the level of which in group III and II was also significantly increased in comparison with group I （P〈0.01）. ④Pathological results： There is no significant lesions in group SO; group I showed pancreatic edema and inflammatory cells infiltration; Acinar edema, inflammatory cell infiltration, vascular congestion, scattered necrosis and bleeding were found in group II; Group III exhibited coagulation of necrosis, inflammatory cell infiltration, capillary rupture, hemorrhage, and even visible micro-abscesses. Conclusion ① These results demonstrate that the more severe the pancreatic necrosis, the greater the chance of secondary infection;②SIRS may be the common mechanism for pancreatitis lesions caused by pancreatic necrosis and secondary infection of pancreas. Alleviate SIRS would be helpful

关 键 词：胰腺炎 全身炎症反应综合征 胰腺坏死 继发感染 大鼠 

分 类 号：R657.51[医药卫生—外科学]