牛磺胆酸钠致急性胰腺炎时大鼠胰腺微血流的变化

作者观察了４２只大鼠用不同浓度牛磺胆酸钠诱导的急性出血坏死性胰腺炎时平均动脉压、胰腺微区血流量、血清淀粉酶和脂肪酶和脂肪酶及胰腺病理形态的变化。发现在大鼠胰腺炎早期、平均动脉压尚无明显改变时，胰腺微区血流量降低；且随着诱导剂浓度的增加，血清淀粉酶和脂肪酰进一步高，胰腺病理损害加重，胰腺微血流进一步恶化。表明胰腺炎早期即可出现明显的胰腺微血流障碍，胰腺微血流障碍的程度与胰腺炎时释放入血的胰酶及胰腺炎     

牛磺胆酸钠致大鼠急性出血坏死性胰腺炎早期胰腺血流的测定

作者以5％的牛磺胆酸钠(Na-Tc)注入大鼠胆胰导管内,引起急性出血坏死性胰腺炎,以注射生理盐水为实验对照组,测定血清脂肪酶和淀粉酶活性,结果注射Na-Tc后3小时此两酶的活性均显著升高,12小时最明显;用~(36)RbCl示踪法测定,显示胰腺血流量和胰组织灌流量于注射Na-Tc后1小时明显升高,并维持较高水平至12小时下降。这些结果提示:Na-Tc致大鼠急性出血坏死性胰腺炎早期胰腺血流量增加,为一般炎症充血反应。     

牛磺胆酸钠致大鼠急性出血坏死性胰腺炎胰腺组织的光镜和电镜观察

作者以5％的牛磺胆酸钠(Na-Tc)注入大鼠胆胰导管内引起急性出血坏死性胰腺炎。光镜和电镜观察结果显示:注入Na-Tc后10分钟到1小时,胰腺小叶出现细胞膜性结构溶解的灶性坏死,血管少许破坏和轻度出血;注入Na-Tc后3到 6小时,胰腺多个小叶成片坏死,血管溶解和重度出血。坏死前的胰腺细胞内出现大量含有酶原颗粒等细胞器的自噬泡。     

肠壁穿刺逆行胰胆管注射牛磺胆酸钠重症急性胰腺炎造模52例分析

目的:探讨肠壁穿刺逆行胰胆管注射牛磺胆酸钠造模过程中的操作注意事项,以提高造模成功率.方法:52例SD大鼠通过肠壁穿刺逆行胰胆管注射牛磺胆酸钠建立重症急性胰腺炎模型.术后24 h取胰腺组织行HE染色,判断模型是否成功.结果:52例中造模成功38例,占73.1％,24 h成活率86.5％.结论:在造模过程中注意麻醉深度、穿刺角度等问题可以有效提高造模成功率,减少死亡率.     

牛磺脱氧胆酸钠镇咳祛痰抗炎作用的研究

目的 研究牛磺脱氧胆酸钠的镇咳、祛痰和抗炎作用。方法 将牛磺脱氧胆酸钠及其对照药物灌胃给药,观察牛磺脱氧胆酸钠对氨水引咳小鼠的镇咳作用,同时观察该药对小鼠气和内注入酚红溶液的排泄,小鼠耳肿胀和大鼠足肿胀方面是作用。结果４００ｍｇ／ｋｇ牛磺脱氧胆酸钠可明显抑制氨水刺激所致小鼠咳嗽,延长小鼠咳嗽潜伏期,增加小鼠气管酚红排泌量,对二甲苯致小鼠耳朵肿胀有的抑制作用;此外,１５０ｍｇ／ｋｇ牛磺脱氧胆酸钠可明     

牛磺胆酸钠滴眼剂的制备及药效学初步研究

以胆酸为原料合成牛磺胆酸钠，制备了牛磺胆酸钠滴眼剂，并对其pH值、渗透压及稳定性等理化性质进行了测定。通过动物实验证实，该滴眼剂无明显刺激性。在此基础上，以家兔为实验动物，采用哆眼石灰碱烧伤模型进行药效学观察，结果表明，牛磺胆酸钠滴眼剂有较显著的疗效。提示：用人工合成的方法制备的牛磺胆酸钠滴眼剂对治疗眼科疾病具有一定的临床意义和开发价值。     

大鼠重症急性胰腺炎模型制备方法的建立与探讨

目的 建立一种操作简单,诱导成功率高且病变典型的重症急性胰腺炎(SAP)大鼠模型.方法 36只健康雄性SD大鼠随机分为模型组(n=18)和对照组(n=18).模型组用微量输液泵经胰胆管逆行注入3.5%牛磺胆酸钠诱导SAP大鼠模型;对照组仅翻动胰腺和十二指肠.观察两组大鼠术后3h、6h、12h腹水及血清淀粉酶、脂肪酶的变化,观察胰腺组织大体形态以及病理改变,并进行评分.结果 模型组胰腺组织结构破坏明显,其大体及病理评分均显著高于对照组(P<0.01),腹水量、血清淀粉酶、脂肪酶也均较对照组显著增加(P<0.01).结论 逆行胰胆管注射牛磺胆酸钠能成功诱导大鼠SAP,具有创伤小、操作简便、可重复性好及诱导成功率高的特点,是一种较为理想的SAP动物模型制备方法.     

生长抑素治疗急性胰腺炎对患者胰腺血流及胰腺功能的影响

目的探讨生长抑素对急性胰腺炎患者胰腺血流及胰腺功能的保护作用。方法选取2012年12月至2014年2月于本院进行诊治的76例急性胰腺炎患者为研究对象,所有患者根据随机数字表法分为对照组和观察组各38例,对照组采用常规治疗,观察组则在常规治疗的基础上增加生长抑素治疗,检测并比较两组患者治疗前和治疗后1 d、3 d及7 d的胰腺血流及胰腺内外分泌系统相关指标。结果治疗前两组患者间各项观察指标比较差异均无统计学意义(P>0.05)。治疗后1 d、3 d及7 d观察组患者的血清正铜蓝蛋白(CP)及胰岛素(INS)水平均高于对照组(P<0.05),胰高血糖素(GLU)、脂肪酶(LIP)、淀粉酶(AMY)和胰蛋白酶原-2(TPS-2)水平则低于对照组(P<0.05);观察组的血流量(BF)及血容量(BV)均高于对照组(P<0.05),毛细血管表面通透性(PS)则低于对照组(P<0.05)。结论生长抑素对急性胰腺炎患者胰腺血流及胰腺功能的保护作用均较为明显,对患者胰腺综合状态的改善作用较为突出。     

Verapamil对胰腺炎大鼠胰腺血流的影响

目的:研究胰腺炎大鼠胰腺血流下降的机理及 Verapamil(Ver)的治疗作用。方法:大鼠胰管内注入5%牛磺胆酸钠,制成急性坏死性胰腺炎(ANP)模型。结果:胰头部血流立即下降;胰腺组织中性粒细胞髓过氧化酶(MPO)、磷脂酶 A_2(PLA_2)活性及胰腺毛细血管通透性明显升高。血浆血栓素 A_2(TXA_2)与前列环素(PGl_2)比例增加。预先使用 Ver 可延缓胰头部血流下降;降低 MPO、PLA_2及毛细血管通透性;对 TXA_2PGl_2均有显著抑制作用。结论:ANP 初期存在缺血再灌注过程。胰头部血流下降是血管活性物质平衡失调致血管运动功能紊乱;中性粒细胞(PMN)活化释放氧自由基致内皮细胞损伤的结果。钙离子(Ca~(2+))异常内流可能在上述过程中发挥了关键作用。     

重症急性胰腺炎大鼠模型制作方法的改进

目的:探讨4%牛磺胆酸钠逆行胆胰管注射诱导重症急性胰腺炎(SAP)大鼠模型的相关技术的改良。方法:将36只健康SD大鼠随机分为模型组(n=18)和假手术组(n=18),应用细针经胆胰管近十二指肠开口端逆行刺入注射4%牛磺胆酸钠,诱导重症急性胰腺炎动物模型;2组均在模型诱导后3、6、12h后检测腹水量及血淀粉酶,观察胰腺组织形态变化,光镜下进行胰腺病变程度评分。结果:模型组在模型诱导后3、6、12h腹水量、血淀粉酶、胰腺组织学评分均较假手术组明显升高(P<0.05)。结论:该方法可成功诱导重症急性胰腺炎,具有创伤小、操作简便及模型诱导成功率高的特点,是较为理想的SAP动物模型。     

大鼠重症急性胰腺炎胰腺蛋白组学的初步研究

目的观察牛磺胆酸钠诱导的重症急性胰腺炎（SAP）大鼠的胰腺组织在不同时间点蛋白组学的变化。方法 36只SD大鼠分为假手术组、SAP组,分别于24 h、48 h、72 h 3个时间点处死大鼠,每时间点6只。动物经胆胰管逆行注射5%牛磺胆酸钠诱发SAP,对照组以生理盐水代替5%牛黄胆酸钠行假手术。通过双向电泳分离、硝酸银染色和图谱分析模型组与对照组蛋白点的差异。结果牛磺胆酸钠诱导出SAP典型组织病理学改变,伴随有胰外肺、肾、胃肠器官的损伤。通过图像分析软件分析胰腺组织蛋白组学变化：24 h时SAP组与假手术组有46个差异点,其中9个点蛋白上调,37个点下调;48 h时SAP组与假手术组有97个差异点,其中43个点蛋白上调,54个点下调;72 h时间点SAP组与假手术组有80个差异点,其中10个点蛋白上调,70个点下调。结论牛磺胆酸钠诱导的大鼠SAP模型胰腺组织在不同时间点蛋白组学的变化存在差异。     

Establishment of an Infected Necrotizing Pancreatitis Model by Retrograde Pancreatic Duct Injection of Sodium Taurocholate and E. coli in Rats

A stable and reliable infected necrotizing pancreatitis （INP） model in rats was established in order to study the pathophysiological mechanism and pathological development role of INP and explore the new therapeutic methods for the diseases. Forty-six SD rats were randomly divided into 5 groups. The animals in group A received the injection of 5% sodium taurocholate into the pancreatic duct and those in group B underwent that of E. coli into the pancreatic duct. The rats in groups C, D and E were subjected to the injection of 5% sodium taurocholate in combination with different concentrations of E. coli （10^3, 10^4, 10^5/mE, respectively） into the pancreatic duct. The dose of injection was 0.1 mL/100 g and the velocity of injection was 0.2 mL/min in all the 5 groups. Eight h after the injection, the survival rate of animals was recorded and the surviving rats were killed to determine the serum content of amylase and perform pathological examination and germ cultivation of the pancreatic tissue. The results showed that acute necrotizing pancreatitis model was induced by injection of 5% sodium taurocholate into the pancreatic duct. The positive rate of germ cultivation in group A was 12.5%. The acute necrotizing pancreatitis model was not induced by injection of E. coli into the pancreatic duct and the positive rate of germ cultivation in group B was 0. The INP model was established in groups C to E. The positive rate of germ cultivation was 60%, 100% and 100% and 8-h survival-rate 100%, 100% and 70% in groups C, D and E, respectively. It was concluded that a stable and reliable model of INP was established by injection of 5% sodium taurocholate in combination with 10^4/mL E. coli into the pancreatic duct with a dose of 0.1 mL/100 g and a velocity of 0.2 mL/min. The pathogenesis of INP might be that the hemorrhage and necrosis of pancreatic tissue induced by sodium taurocholate results in weakness of pancreatic tissue in fighting against the germs. Meanwhile, the necrotic pancreatic tissue provides a good p     

Effects and Mechanisms of Emodin and Sandostatin on Pancreatic Ischemia in Acute Haemorrhagic Necrotizing Pancreatitis

About15%～25%ofthecaseswithacutepancreatitisshoweditselfasacutehaemorrhagicnecrotizingpancreatitis(AHNP),apromptlylife--threateningcriticaldisorder,whichhasbeenviewedtobeinitiatedmainlyfromseverepancreaticischemiaattheearlystage(').Rhubarb(RadixetRhizomaRhei),adrugintraditionalChinesemedicine,andsandostatin(SMS201--995,octreotide),asomatostatinanalogue,arebotheffectiveintreatingAHNP,butsofarnoresearchhasbeenreportedabouttheireffectsonpancreaticischemiaandrelatedf.cto..(2'3).Weusedemodin,…     

Effects and Mechanism of Emodin and Sandostatin on Pancreatic Ischemia in Acute Haemorrhagic Necrotizing Pancreatitis

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胰腺缺血在胰腺炎由水肿向坏死转变中的研究

目的：本实验旨在研究急性水肿性胰腺炎（ＡＥＰ）向坏死性胰腺炎（ＡＮＰ）转变中胰微循环障碍的作用机理。方法：将９６只大鼠随机分三组：Ⅰ组,假手术组;Ⅱ组,采用胰管结扎及静脉推注蛙皮素（１００μｇ／ｋｇ）、促胰液素（１０μｇ／ｋｇ）诱发ＡＥＰ;Ⅲ组,在ＡＥＰ模型同时静注１０％高分子右旋糖酐（分子量１１００００）５００ｍｇ／ｋｇ诱发ＡＮＰ。应用荧光探针Ｆｕｒａ２研究钙超负荷情况。结果：发现ＡＮＰ模型后１、３、６、９小时腺泡细胞胞浆游离钙离子浓度持续增高（Ｐ＜００５）,而胰腺细胞质膜Ｃａ２＋－ＡＴＰａｓｅ活性持续降低（Ｐ＜００５）。结论：细胞钙超负荷可能介导胰腺缺血性损害促使ＡＥＰ向ＡＮＰ转变。     

顺行穿刺注射牛磺胆酸钠制作大鼠重症胰腺炎模型

目的探讨制备大鼠重症胰腺炎模型方法的改进。方法将36只健康sD大鼠随机分为模型组（n=18）和假手术组（n=18）,在胰胆管的近端（肝总管）用细针顺行穿刺胰胆管,注入4％牛磺胆酸钠,诱导重症急性胰腺炎动物模型,创面封闭胶封闭穿刺孔;两组均在模型诱导3、6、12h后检测腹水量及血淀粉酶,观察胰腺组织形态变化,光镜下行胰腺病变程度评分。结果模型组在模型诱导后腹水量（8．52±1．05）ml、血淀粉酶（5247．17±547．07）u／L、胰腺组织学评分（13．60±3．92）较假手术组腹水量（1．21±0．32）ml、血淀粉酶（1289．5±176．67）u／L、胰腺组织学评分（0．83±0．58）在各时间点均明显升高（P〈0．05）。结论此法损伤小,实验器材易于获取,操作简单,不会损伤胰腺和发生胆漏,可重复性好,模型稳定,成功率高,是较理想的重症胰腺炎模型制备方法。     

Effects of verapamil on prostacyclin, thromboxane and pancreatic blood flow of rats with experimental acute pancreatitis]

We studied the effects of the calcium channel blocker, verapamil on experimental acute pancreatitis (AP) in rats. The pancreatic blood flow (PBF) and pancreatic tissue perfusion (PTP) were measured after induction of AP. At the same time, the plasma levels of TXB2 and 6-keto-PGF1 alpha were determined by radioimmunoassay. The survival rate and the mean survival time after induction of AP were determined and the pancreatic histology was examined by light and electron microscopy. The results demonstrated a significant early fall in PBF and PTP, a marked increase in TXB2 levels and a slight increase in 6-keto-PGF1 alpha after induction of AP. Treatment with 0.1 mg/100 g verapamil significantly increased PBF and PTP, and decreased TXB2, resulting in a normalization of TXB2/6-keto-PGF1 alpha ratio. The treated animals also exhibited significant increase in the survival rate and the survival time. They also showed decrease in the severity of pancreatic hemorrhage and necrosis, and in the damage to the cellular ultrastructures. These data suggest that calcium blockade increases PBF and PTP, limits the prostanoid imbalance in the early phase of AP, and may influence the development of experimental acute pancreatitis in rats.     

Apelin-13对急性坏死性胰腺炎大鼠胰腺组织中自噬的影响

目的探讨Apelin-13对大鼠急性坏死性胰腺炎(ANP)时自噬相关蛋白LC3-Ⅱ、Beclin-1的影响。方法取健康清洁SD大鼠54只,随机分为对照组、造模组、给药组,每组18只。每组大鼠分别对应处理后第3、6、12 h检测血清淀粉酶,并取部分胰腺组织做常规病理切片、HE染色观察其病理变化,Western blot检测自噬相关蛋白LC3-Ⅱ、Beclin-1的表达情况。结果造模组各时间点血清淀粉酶、LC3-Ⅱ、Beclin-1表达水平较对照组显著提高,给药组各时间点血清淀粉酶、LC3-Ⅱ、Beclin-1表达较造模组显著降低(P均＜0.05),ANP时自噬相关蛋白表达会随着病理损伤程度加重而增加,且Apelin-13可以显著抑制自噬相关蛋白Beclin-1、LC3-Ⅱ的表达。结论Apelin-13在ANP中通过下调自噬相关蛋白Beclin-1、LC3-Ⅱ的表达发挥对胰腺组织的保护作用。     

甘氨酸治疗大鼠急性坏死性胰腺炎效果观察

目的：探讨甘氨酸对大鼠急性坏死性胰腺炎的治疗作用。方法：雄性Wistar大鼠随机分为假手术组、胰腺炎组和胰腺炎甘氨酸治疗组(1g／kg)。分别测定各组6h、12h和24h血清淀粉酶、肿瘤坏死因子(TNFα)和胰、肺匀浆中谷胱甘肽(GSH)、髓过氧化物酶(MPO)水平,观察胰、肺病理学变化并比较各组动物3d。结果：与胰腺炎组比较．采用甘氨酸治疗后,对各时相的淀粉酶和胰、肺的GSH无明显影响,但可降低24h血清TNFd水平;甘氨酸不改变胰MPO和病变程度,明显降低肺MPO活性并改善急性肺损伤,提高生存率。结论：甘氨酸治疗不改善胰腺炎时胰腺局部病变,但可减轻其并发的肺损伤,可能与其抑制白细胞浸润激活有关。