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目的探讨脾脏在急性胰腺炎(AP)病情发展过程中的作用。方法SD大鼠分为5组每组24只,分别为对照组、脾切组、AP组、脾切+AP组、脾切+AP+tuflsin组。胰胆管逆行注射4%牛磺胆酸钠建立AP模型,tuftsin组自制模20 min后从股静脉注入tuftsin 75μg/kg。按随机原则在制模后0、3、6、12 h分批处死,留取胰腺(体部)组织HE染色光镜观察胰腺病理改变程度进行病理学评分。结果制模后0、3、6、12 h各组胰腺病理学评分均比对照组和单纯脾切组明显升高;AP组和脾切+AP+tuftsin组制模后随时间的延长胰腺病理改变程度逐渐加重;脾切+AP组在制模后6 h内胰腺病变程度逐渐加重,在制模后12 h与6 h比较胰腺病理学评分无显著性差异;与AP组比较,脾切+AP组在制模后3、6 h对胰腺病理改变无影响,在制模后12 h明显减轻胰腺病理改变;脾切+AP+tuftsin组在制模后36、h对胰腺病理改变程度无明显影响,在制模后12 h胰腺病理改变明显加重,与AP组比较差异有显著性;脾切+AP+tuftsin组与脾切+AP组相比在制模后3 h无差异,在制模后61、2 h胰腺病变程度明显加重。结论脾脏在急性胰腺炎病情发展过程中有一定的影响,表现为脾切除可减轻或阻止急性胰腺炎病情发展,外源性tuftsin可加重急性胰腺炎胰腺病理改变。
Objective To investigate the role of spleen in the development of acute pancreatitis (AP). Methods SD rats were divided into 5 groups of 24 rats in each group, which were control group, splenectomy group, AP group, splenectomy + AP group, spleen-cut + AP + tuflsin group respectively. The AP model was established by retrograde injection of 4% sodium taurocholate into the pancreaticobiliary duct. Tuftsin 75μg / kg was injected from the femoral vein after 20 min in the tuftsin group. According to the principle of randomness, the rats were sacrificed at 0, 3, 6 and 12 h after model establishment. The pathological changes of the pancreas were observed by HE staining and histopathological examination. Results The pathological scores of pancreas at 0, 3, 6 and 12 h after model establishment in each group were significantly higher than those in control group and simple splenectomy group. The pancreatic pathology The severity of pancreatic lesions increased gradually within 6 h after splenectomy + AP group. There was no significant difference in pancreatic pathology scores between 12 h and 6 h after modeling. Compared with AP group, AP group had no effect on pathological changes of pancreas at 3h and 6h after model establishment, and pathological changes of pancreas were alleviated 12h after model establishment. There was no significant change in the pathological changes of pancreas at 36h after spleenttage + AP + tuftsin group The pathological changes of pancreas were significantly increased at 12 h after modeling, which was significantly different from that in AP group. There was no difference at 3 h after spleen incision + AP + tuftsin group compared with spleen incision + AP group, After 61,2 h pancreatic lesions significantly increased. Conclusion The spleen has certain influence on the development of acute pancreatitis. Spleen resection can reduce or prevent the development of acute pancreatitis. Exogenous tuftsin can aggravate the pathological changes of pancreas in acute pancreatitis.