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目的观察生长抑素联合清胰汤对急性重症胰腺炎模型大鼠血ET、NO、ET/NO和TXA_2、PGI_2、TXA_2/PGI_2的变化,探讨生长抑素、清胰汤对大鼠急性重症胰腺炎的作用机制,为临床应用提供依据。方法 SD大鼠90只,体重(271.59±11.13)g,雄性,常规适应性喂养1周,实验前12h禁食,自由饮水。随机分成5组:假手术组(NC);急性重症胰腺炎(SAP)组;清胰汤治疗组(QY);生长抑素治疗组(SZ);联合治疗组(LH);每组18只。并将各组随机分成6h、12h、24h3个亚组,每个亚组6只。SAP模型组经胰胆管逆行注入5%牛磺胆酸钠(0.1ml/100g),假手术组胰胆管不穿刺、注药,仅翻动胰腺;生长抑素治疗组、清胰汤治疗组、联合治疗组的大鼠分别于造模成功即刻、5h、11h给予生长抑素(1μg/100g)背部皮下注射、清胰汤(1ml/100g)灌胃及两药联合治疗。动态观察记录各组及亚组(6h、12h、24h)Amy(淀粉酶测定速率法)、NO(硝酸还原酶法)、ET(放射免疫测定法)、TXA_2(放射免疫测定法)、PGI2(放射免疫测定法)含量。结果与假手术组比较,急性重症胰腺炎组各时间点血清AMY、NO、ET、TXB2值明显升高;ET/NO、TXB2/6-Keto-PGF1a比值明显升高;差异有统计学意义(P﹤0.01);与SAP组比较,生长抑素治疗组、清胰汤治疗组血清AMY、NO、ET、TXB2、6-Keto-PGF1a值降低,AMY、ET、TXB_2与SAP组比较差异有统计学意义(P﹤0.01);ET/NO、TXB_2/6-Keto-PGF1a比值降低;与清胰汤治疗组、生长抑素治疗组比较,联合治疗组血清AMY、ET、TXB2降低;差异有统计学意义(P﹤0.05);ET/NO、TXB_2/6-Keto-PGF1a比值降低趋于平衡(P﹤0.05)。结论 SAP时,NO、ET、TXB_2、6-Keto-PGF1a参与病变的发生发展过程,说明NO、ET、TXB_2、6-Keto-PGF1a是微循环变化的重要介质。
Objective To observe the effects of somatostatin combined with Qingyi decoction on the changes of ET, NO, ET / NO and TXA_2, PGI_2 and TXA_2 / PGI_2 in rats with acute severe pancreatitis, and to explore the effects of somatostatin and Qingyi decoction on acute severe pancreas in rats The mechanism of inflammation, provide the basis for clinical application. Methods Ninety Sprague-Dawley rats weighing 272.59 ± 11.13 g were male, fed for 1 week with normal adaptability, and fasted for 12 hours before the experiment to freely drink water. The rats in each group were randomly divided into 5 groups: sham operation group (NC), acute severe pancreatitis (SAP) group, Qingyitang treatment group (QY), somatostatin treatment group (SZ) . Each group was randomly divided into 6h, 12h, 24h3 subgroups, 6 in each subgroup. In the SAP model group, 5% sodium taurocholate (0.1ml / 100g) was infused through the pancreaticobiliary duct retrogradely. The pancreatic duct of the sham operation group was not punctured and injected with drug only to turn the pancreas. The somatostatin treatment group and Qingyi decoction group were combined The rats in the treatment group were given subcutaneous injection of somatostatin (1μg / 100g), qianyi decoction (1ml / 100g) intragastrically and the combination of two drugs at 5h and 11h respectively. The Amy (amylase assay rate), NO (nitrate reductase), ET (radioimmunoassay), TXA_2 (radioimmunoassay), PGI2 Radioimmunoassay) content. Results Compared with the sham operation group, the serum levels of AMY, NO, ET and TXB2 were significantly increased at each time point in acute severe pancreatitis group, and the ratios of ET / NO, TXB2 / 6-Keto-PGF1a were significantly increased P <0.01). Compared with SAP group, serum AMY, NO, ET, TXB2 and 6-Keto-PGF1a in the somatostatin treatment group and Qingyi decoction treatment group were lower than those in the SAP group (P <0.01). The ratio of ET / NO, TXB2 / 6-Keto-PGF1a decreased. Compared with the Qingyitang treatment group and somatostatin treatment group, the serum levels of AMY, ET and TXB2 in the combination therapy group decreased (P <0.05). The ratio of ET / NO, TXB2 / 6-Keto-PGF1a tended to balance (P <0.05). Conclusions NO, ET, TXB_2, 6-Keto-PGF1a are involved in the pathogenesis of SAP, indicating that NO, ET, TXB_2, 6-Keto-PGF1a are important mediators of microcirculation.