胸段硬膜外阻滞预防急性胰腺炎重型化的实验研究

发布时间：2018-06-14 17:17

本文选题：硬膜外阻滞 + 急性胰腺炎　；参考：《福建医科大学》2013年硕士论文

【摘要】：目的本研究通过建立大鼠急性胰腺炎重型化模型并用硬膜外阻滞对模型水肿阶段进行干预，观察大鼠肿瘤坏死因子-α（tumor necrosis factor alpha，TNF-α）、白介素-6（interleukin-6，IL-6）、血清淀粉酶（AMY）的变化及腺泡细胞凋亡情况，探讨胸段硬膜外阻滞对急性胰腺炎进行干预后的影响。方法清洁级SD雄性大鼠随机分为四组：正常对照组（C组，n=8）、急性胰腺炎组(AP组，n=16)、硬膜外生理盐水治疗组(NS组，n=16)、硬膜外罗哌卡因治疗组(TEA组，n=16)。其中AP组、NS组、TEA组又随机分为12、24h两个时点（12h，n=8；24h，n=8），腹腔内注射8%L-精氨酸溶液（3×150mg/100g大鼠体重bm），每次注射间隔1小时建立大鼠急性胰腺炎模型。C组同法腹腔注射等量的生理盐水。建模后12h对三组24h点大鼠做如下处理：TEA组硬膜外每两个小时输注一次0.1%罗哌卡因（0.01ml／100g bm），NS组同法输注生理盐水（0.01ml／100g bm），AP组不做处理。每组大鼠均于造模前(T0)、造模后12小时(T1)、造模后24小时(T2)采集血液标本，并于T1时处死12时相点大鼠、T2时处死其余大鼠并观察腹腔情况。采用全自动生化分析仪检测血清淀粉酶（AMY）水平； ELISA法检测血清TNF-α和IL-6含量；胰腺组织HE染色后光学显微镜观察并行病理学评分；TUNEL法检测24h时相点大鼠胰腺组织中腺泡细胞的凋亡情况。结果⑴血清生化指标：①与C组相比，各处理组血清AMY、TNF-α和IL-6水平显著升高（P0.01）②与AP组和NS组比较，T2时TEA组血清TNF-α、 IL-6水平显著降低（P0.05），T1时无显著差异（P＞0.05）；③T2与T1时比较， TEA组血清AMY、TNF-α和IL-6水平无显著差异（P＞0.05），AP组和NS组显著升高（P0.05）；T1与T0时比较，三组都明显升高（P0.01）；C组在各时间点无明显变化（P＞0.05）。⑵病理学观察：①T1时AP组、NS组、TEA组胰腺组织主要表现为间质水肿，腺泡肿胀，炎症细胞浸润。T2时AP组、NS组可见大片出血坏死和腺泡小叶结构破坏，周围有大量炎症细胞浸润；TEA组细胞坏死明显减轻，炎症细胞少②与C组比较，各处理组病理评分显著升高（P0.01）；与AP组、NS组比较，T2时TEA组病理评分显著降低（P0.05）。胰腺组织病理评分与TNF-α和IL-6浓度呈正相关（r=0.89，r=0.77，P0.01）⑶腺泡细胞凋亡：C组很少或未观察到，AP组、NS组观察到少量的凋亡细胞, TEA组有大量的凋亡细胞结论①腹腔内注射8%L-精氨酸溶液（3×150mg/100g），每次注射间隔1小时能构建大鼠急性胰腺炎重型化模型。②炎性因子及腺泡细胞凋亡在AP的病程中发挥重要作用。③硬膜外阻滞能够预防AP的重型化，其可能机制有：能阻断伤害性刺激的传入，降低应激反应，抑制炎性介质的释放，从而诱导腺泡细胞凋亡，改善胰腺的转归。
[Abstract]:Objective to observe the changes of TNF- 伪, interleukin-6 (IL-6) and serum amylase (amylase) and acinar cell apoptosis in necrosis factor alpha-TNF- 伪, interleukin-6 (IL-6) and serum amylase (amylase) in rats with severe acute pancreatitis (AP) and intervention with epidural block on the edema stage of the model in this study, and to observe the changes of TNF- 伪, interleukin-6, amylase in serum and apoptosis of acinar cells in rats. To investigate the effect of thoracic epidural block on acute pancreatitis. Methods male SD rats of clean grade were randomly divided into four groups: control group (n = 8), acute pancreatitis group (n = 16), NS group (n = 16), epidural ropivacaine group (n = 16), tea group (n = 16). Among them, the AP group and the NS group were randomly divided into two groups: 12h, 12h, 12h, 12h, 8h, 24h, and 8L arginine solution was injected intraperitoneally into the body weight of 3 脳 150mg/100g rats. The model of acute pancreatitis in group C was established by intraperitoneal injection of the same amount of normal saline at the interval of 1 hour each time. 12 h after modeling, three groups of rats at 24 h were treated as follows: 0.1% ropivacaine 0.01ml / 100g bmMN was infused once every two hours in the control group. The NS group received 0.01ml / 100g saline and 0.01ml / 100g BP respectively. Blood samples were collected at 12 hours after modeling and 24 hours after modeling. The other rats were killed at 12:00 at T 2 and observed the abdominal cavity. The levels of serum amylase (AMY), the levels of TNF- 伪 and IL-6 in serum were detected by Elisa, and the pathological scores were observed by optical microscope after HE staining. Apoptosis of acinar cells in pancreatic tissue of rats at 24 h was detected by Tunel method. Results (1) compared with group C, the serum levels of AMYTNF- 伪 and IL-6 in each treatment group were significantly higher than those in AP group and NS group. There was no significant difference in serum TNF- 伪 and IL-6 levels in tea group when compared with AP group and NS group (P > 0.05). 3There was no significant difference between T 2 and T 1 in the serum levels of AMYN TNF- 伪 and IL-6 in tea group (P > 0.05). The levels of TNF- 伪 and IL-6 in T _ 2 group were significantly higher than those in T _ 1 group (P > 0.05), and the levels of P _ (0.01) in all three groups were significantly higher than those in T _ (0) group. There was no significant change at each time point in group C (P > 0.05). The pathological observation showed that the pancreatic tissue of AP group was mainly characterized by interstitial edema and acinar swelling at 1: 1 T1, and the pancreatic tissue of group C was mainly characterized by interstitial edema and acinar swelling. Large hemorrhage necrosis and acinar lobule structure destruction were observed in AP group and NS group when inflammatory cells were infiltrated at T 2. The necrosis in tea group was obviously alleviated by a large number of inflammatory cells infiltrating in the surrounding group, and there were 2 fewer inflammatory cells in group A than in group C. The pathological score of each treatment group was significantly higher than that of AP group, and the pathological score of tea group was significantly lower than that of AP group. Pancreatic histopathological score was positively correlated with TNF- 伪 and IL-6 concentrations. There were few or no apoptotic cells in acinar cells in group C: C, and a large number of apoptotic cells were observed in tea group. Intracavitary injection of L- arginine solution 3 脳 150 mg / 100 g / 100 g / L injection at an interval of 1 hour per injection could construct a rat model of acute pancreatitis with severe pancreatitis. 2 inflammatory factors and apoptosis of acinar cells played an important role in the course of AP. 3. 3 epidural block could prevent the severity of AP. The possible mechanisms include blocking the afferent of nociceptive stimulation, decreasing the stress response, inhibiting the release of inflammatory mediators, thus inducing the apoptosis of acinar cells and improving the prognosis of the pancreas.
【学位授予单位】：福建医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R657.51

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