继发感染致急性坏死性胰腺炎病变加重的机制探讨

Mechanisms of secondary infection resulting in worsening of acute necrotizing pancreatitis

目的探讨继发感染致急性坏死性胰腺炎病变加重的机制。方法24只SD大鼠平均随机分成3组:对照组、坏死性胰腺炎(ANP)组、感染性坏死性胰腺炎(INP)组。8 h后抽血测定血清淀粉酶、α-肿瘤坏死因子、白介素-1,并取胰腺组织行光镜、电镜检查和细菌培养。结果(1)胰腺组织细菌培养阳性率:对照组为0(0/8);ANP组为12.5%(1/8);INP组为100%(8/8)。(2)光镜检查结果:对照组未见出血、坏死改变;ANP组可见出血,偶可见点灶状坏死,中等量炎细胞浸润;INP组出血常见,多见片状的坏死,大量炎细胞浸润。(3)电镜检查结果:对照组未见异常改变;ANP组可见分泌颗粒增多,粗面内质网轻度扩张;INP组可见分泌颗粒明显增多,粗面内质网扩张明显。(4)对照组、无菌性胰腺坏死(SNP)组、INP组的血清淀粉酶、α-TNF、IL-1检测结果分别为[(1903.8±224.6)U/L,(19.03±5.09)pg/ml,(7.73±0.92)pg/l],[(9371.4±1451.8)U/L,(48.55±14.92)pg/ml,(20.36±4.90)pg/1],[(16980.0±2745.3)U/L,(131.40±39.17)pg/m1,(32.03±5.57)pg/1],其中INP组和SNP组与对照组相比有显著升高(P<0.01),INP组比SNP组有明显升高(P<0.01)。结论(1)继发感染可导致无菌性胰腺坏死病变明显加重;(2)以促炎细胞因子过度分泌为特征的全身炎症反应可能是继发细菌感染致无菌性胰腺坏死病变加重的主要机制之一。

Objective To study the mechanisms of secondary infection resulting in worsening of acute necrotizing pancreatitis （ANP）. Methods Twenty-four Sprague Dawley rats were randomized into the control group, ANP group and infected necrotizing pancreatitis group （INP group）. Eight hours after the models were established in different groups, the levels of amylase, α-tumor necrosis factor （α-TNF） and interleukin-1 （IL-1） in serum were determined. After the animals were sacrificed, the pancreatic tissue was examined with optical microscopy, electron microscopy and germ culture. Results （1） The positive rate of germ culture in the control group, ANP group and INP group was 0 （0/8）, 12.5% （1/8）, 100% （8/8）, respectively. （2） Optical microscopy showed that there was no hemorrhage and necrosis in the control group： there were Cellular edema, hemorrhage and loci necrosis, moderate quantity of inflammatory cell infiltration in ANP group and cellular edema, frequent hemorrhage, massive and thorough necrosis and a great quantity of inflammatory cell infiltration in ANP group. （3）Electronic microscopy revealed that the pathological change was not visible in the control group： there were increase of the quantity of exocrine granules and slight dilatation of rough endoplasmic reticulum in ANP group and marked increase of the quantity of exocrine granules and remarkable dilatation of rough endoplasmic reticulum in INP group. （4） The serum levels of amylase, α-TNF and IL-1 in the control group, the sterile necrotizing pancreatitis group（SNP group）, INP group were [（1903.8±224.6） U/L,（19.03±5.09） pg/ml, （7. 73±0.92） pg/l],[（9371.4±1451.8） U/L, （48. 555±14.92） pg/ml, （20.36±4.90） pg/l], [（16980.0±2745.3） U/L, （131. 405±39. 17） pg/ ml, （32. 035±5.57） pg/l], respectively. The serum level of the 3 parameters were significantly higher in SNP group and INP group than in the control group （P〈0.01） and they were markedly higher in SNP group higher than in ANP group （P〈0.01）. Conclusion （1） Secondary infection might result in outstanding worsening of sterile pancreatic necrosis. （2） Excessive systemic inflammatory reaction might be one of main mechanisms of secondary infection resulting in worsening of ANP.