SIRS发展在胰腺坏死、继发感染致胰腺炎病变加重中的作用

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.

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

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 for SAP treatment.