奥曲肽对犬急性重症胰腺炎Oddi括约肌的影响

目的 观察急性重症胰腺炎Ｏｄｄｉ括约肌（ＳＯ）的压力变化及奥曲肽对之影响,方法 １５只犬分为２组,急性重症胰腺炎非治疗组（５只）,奥曲肽组（１０只）;制备犬急性急症胰腺炎模型,于制备前,后及给药后各时间点分别测定ＳＯ的基础压和时相收缩幅度。结果 急性重症胰腺炎时ＳＯ压力显著升高（Ｐ＝０．０００１）;奥曲肽能显著降低重症胰腺炎时ＳＯ的基础压（Ｐ＝０．０００３）;但对时相收缩幅度无影响（Ｐ＝０．２３０     

奥曲肽对犬Oddi括约肌作用的实验研究

奥曲肽对犬Ｏｄｄｉ括约肌作用的实验研究谢苏庆，许国铭，李兆申生长抑素类似物－奥曲肽（ｏｃｔｒｅｏｔｉｄｅ，商品名：善得定）作为一种有力的胰外分泌抑制剂已被应用于多种原因引起的急性胰腺炎及术后胰瘘的治疗［１，２］。但关于对Ｏｄｄｉ括约肌的作用如何尚存在...     

生长抑素对Oddi括约肌功能的影响

为证实生长抑素对Ｏｄｄｉ括约肌功能的作用，用逆行胰胆管造影下Ｏｄｄｉ括约肌测压研究了生长抑素对２０例患者Ｏｄｄｉ括约肌运动功能的影响。２０例患者中胆总管结石６例，胆总管轻度扩张３例，肝门癌３例，未见明显异常者８例。用低顺应性水灌注系统，三通道测压导管，分别于用药前及静注生长抑素２５０μｇ１分钟后进行Ｏｄｄｉ括约肌测压，以观察Ｏｄｄｉ括约肌的基础压、收缩频率、收缩幅度、收缩间期、传播方式和胆管内压变化。结果显示：用药后Ｏｄｄｉ括约肌基础压降低、收缩频率减慢，其余指标无明显变化。我们认为：生长抑素对Ｏｄｄｉ括约肌有抑制性作用，有利于胆汁和胰液的排出。     

重症急性胰腺炎的非手术治疗

近年来,急性胰腺炎（ＡＰ）发病日益增多,其中不少是重症急性胰腺炎（ＳＡＰ）。诱发ＳＡＰ是多种因素联合作用所致,包括胰管阻塞或胆汁返流（胆石嵌顿及一过性微小结石嵌顿）、肥胖及高脂血症、高脂高蛋白食物对胆囊收缩素（ＣＣＫ）的过度刺激、酒精（有引起Ｏｄｄｉ括约肌痉挛等多种作用）、缺血及低灌注等［１］。近１０年来,随着认识水平及诊疗技术的提高,ＳＡＰ的病死率已降到１２％左右。本文就ＳＡＰ的非手术治疗作一概述。１基本治疗 基本或称传统的内科治疗包括禁食、胃肠减压、静脉补液、全身支持疗法、解痉止痛、抗感染、…     

急性坏死性胰腺炎肠粘膜屏障功能障碍及生长激素的作用

目的 探讨急性坏死性胰腺炎（ＡＮＰ）肠粘膜屏障形态和功能的变化及生长激素（ＧＨ）的作用。方法 采用胰胆管内逆行注射５％牛磺胆酸钠溶液诱导大鼠ＡＮＰ。实验分３组：假手术组、ＡＮＰ＋生理盐水（ＮＳ）组、及ＡＮＰ＋ＧＨ组。术后２４h取末端回肠,观察病理形态变化;应用＾１２５Ⅰ－白蛋白测定肠壁通透性;ＲＴ－ＰＣＲ检测胰岛素样生长因子（ＩＧＦ－１）mＲＮＡ表达。结果 ＡＮＰ大鼠肠粘膜间质充血水肿,炎症细胞浸     

Oddi括约肌运动功能障碍的诊断和治疗

Ｏｄｄｉ括约肌运动功能障碍（ＳｐｈｉｎｃｔｅｒｏｆＯｄｄｉＤｙｓｆｕｎｃｔｉｏｎ,ＳＯＤ）指该括约肌运动异常致患者胆汁、胰液排出受阻,使胆管、胰管内压升高,临床上表现为胆汁瘀积、胰原性腹痛或急性胰腺炎［１］。ＳＯＤ的发病率报道不一,Ｂａｒ－Ｍｅｉｒ等［２］报道胆囊切除术后有１％发生ＳＯＤ,其中有症状者发病率可达１４％。Ｔｏｏｕｌｉ等［３］用测压方法研究发现特发性复发性胰腺炎患者发病率为３９％。ＳＯＤ的诊断ＳＯＤ需与胆道或胰腺器质性病变、非胆道或胰腺原因功能性或器质性消化不良以及肠道易激综合征相鉴…     

胃—食管返流的临床研究

作者采用国产ＳＧＹ－３型多功能消化道检测仪对８０例具有胃－食管返流（ＧＥＲ）症状患者进行了食管测压研究。患者分别为两组：Ａ组３３例、内镜及活检食管粘膜正常；Ｂ组４７例，内及活检均证实有食管炎。正常对照组６０例。食管炎患者给予吗丁啉口服。结果显示，（１）Ａ、Ｂ两组患者食管下括约肌压力（ＬＥＳＰ）、胃－食管屏障压、食管下括约肌（ＬＥＳ）松驰率明显降低，ＬＥＳ松弛时间明显延长，ＬＥＳ长度（ＬＥＳＬ）短于     

Oddi括约肌测压及内镜下十二批肠乳头切开术对Oddi括约肌运动…

目的：对６０例胆囊切除术后复发腹病患者进行Ｏｄｄｉ括约肌测压研究，并探讨内镜下十二指肠乳头切开术（ＥＰＴ）对Ｏｄｄｉ括约肌基础压升高患者疗效。方法：用低顺应性灌注系统，三通道测压导管，观察Ｏｄｄｉ括约肌基础压，Ｏｄｄｉ括约肌基础收缩幅度、频率和传播方式。对Ｏｄｄｉ括约肌基础压〉６．３２ｋＰａ（３５ｍｍＨｇ）者，随机分为两组，一组予以ＥＰＴ治疗，另一组作为对照，并随访其疗效。结果：Ｏｄｄｉ括约肌测压     

活动期、愈合期及瘢痕期球溃疡患者胃酸及胃窦粘膜胃肠激素的变化

作者比较了活动期（ＡＤＵ）、愈合期（ＨＤＵ）及瘢痕期（ＳＤＵ）球溃疡（ＤＵ）患者和非溃疡对照（ＮＵ），患者的基础胃酸分泌量（ＢＡＯ）、高峰胃酸分泌量（ＰＡＯ）及胃窦粘膜内胃泌素（Ｇａｓ）、生长抑素（ＳＳ）、血管活性肠肽（ＶＩＰ）、Ｐ物质（ＳＰ）的含量。发现各期球溃疡患者ＰＡＯ均明显高于ＮＵ组；ＡＤＵ组胃窦粘膜Ｇａｓ及ＳＰ含量比ＮＵ组明显增加；ＳＤＵ组胃窦粘膜内ＳＳ较ＮＵ组明显增加。本文结果说明壁细胞泌酸能力增加是ＤＵ发病的重要病理生理基础，基础胃酸高分泌状态是ＤＵ患者溃疡活动的重要条件。ＡＤＵ患者ＢＡＯ增加与胃窦粘膜内Ｇａｓ增加有关。ＳＤＵ患者胃窦粘膜内ＳＳ有稳定基础胃酸分泌的作用。     

奥曲肽对急性坏死性胰腺炎炎症介质的调节作用

目的 观察奥曲肽对急性坏死胰腺炎（ＡＮＰ）大鼠肿瘤坏死因子ａ（ＴＮＦａ）、一氧化氮（ＮＯ）和内毒素等炎症介质的影响,并探讨其对ＡＮＰ大鼠的治疗作用。方法 ＳＤ大鼠９３只,随机分为３组：ＡＮＰ生理盐水处理组（ＡＮＰ＋ＮＳ组）、ＡＮＰ奥曲肽治疗组（ＡＮＰ＋奥曲肽组）和假手术组（ＳＯ组）。观察各组大鼠的平均存活时间和存活率、血清淀粉酶活性、腹水量、胰腺系数及病理形态变化;测定血浆内毒素、血清ＴＮＦａ及血     

Effect of emodin on small intestinal peristalsis of mice and relevant mechanism

AIM: To investigate the effect of emodin on small intestinal peristalsis of mice and to explore its relevant mechanisms. METHODS: The effect of emodin on small intestinal peristalsis of mice was observed by charcoal powder propelling test of small intestine. The contents of motilin and somatostatin in small intestine of mice were determinated by radioimmunoassay. The electrical potential difference (PD) related to Na+ and glucose transport was measured across the wall of reverted intestinal sacs. Na+-K+-ATPase activity of small intestinal mucosa was measured by spectroscopic analysis. RESULTS: Different dosages of emodin can improve small intestinal peristalsis of mice. Emodin increased the content of motilin, while reduced the content of somatostatin in small intestine of mice significantly. Emodin 0.2, 0.4, 0.8, and 1.6 g/L decreased PD when there was glucose. However, emodin had little effect when glucose was free. The Na+-K+-ATPase activity of small intestinal mucosa of mice in emodin groups was inhibited obviously. CONCLUSION: Emodin can enhance the function of small intestinal peristalsis of mice by mechanisms of promoting secretion of motilin, lowering the content of somatostatin and inhibiting Na+-K+-ATPase activity of small intestinal mucosa.     

Emodin alleviates intestinal mucosal injury in rats with severe acute pancreatitis via the caspase-1 inhibition

BACKGROUND:Emodin,a traditional Chinese medicine,has a therapeutic effect on severe acute pancreatitis(SAP),whereas the underlying mechanism is still unclear.Studies showed that the intestinal mucosa impairment,and subsequent release of endotoxin and proinflammatory cytokines such as IL-1β,which further leads to the dysfunction of multiple organs,is the potentially lethal mechanism of SAP.Caspase-1,an IL-1β-converting enzyme,plays an important role in this cytokine cascade process.Investigation of the effect of emodin on regulating the caspase-1 expression and the release proinflammatory cytokines will help to reveal mechanism of emodin in treating SAP.METHODS:Eighty Sprague-Dawley rats were randomly divided into four groups(n=20 each group):SAP,sham-operated(SO),emodin-treated(EM) and caspase-1 inhibitor-treated(ICE-I) groups.SAP was induced by retrograde infusion of 3.5% sodium taurocholate into the pancreatic duct.Emodin and caspase-1 inhibitor were given 30 minutes before and 12 hours after SAP induction.Serum levels of IL-1β,IL-18 and endotoxin,histopathological alteration of pancreas tissues,intestinal mucosa,and the intestinal caspase-1 m RNA and protein expressions were assessed 24 hours after SAP induction.RESULTS:Rats in the SAP group had higher serum levels of IL-1β and IL-18(P0.05),pancreatic and gut pathological scores(P0.05),and caspase-1 m RNA and protein expressions(P0.05) compared with the SO group.Compared with the SAP group,rats in the EM and ICE-I groups had lower IL-1β and IL-18 levels(P0.05),lower pancreatic and gut pathological scores(P0.05),and decreased expression of intestine caspase-1 m RNA(P0.05).Ultrastructural analysis by transmission electron microscopy found that rats in the SAP group had vaguer epithelial junctions,more disappeared intercellular joints,and more damaged intracellular organelles compared with those in the SO group or the EM and ICE-I groups.CONCLUSIONS:Emodin alleviated pancreatic and intestinal mucosa injury in experimental SAP.Its mechanism may partly be mediated by the inhibition of caspase-1 and its downstream inflammatory cytokines,including IL-1β and IL-18.Our animal data may be applicable in clinical practice.     

大黄素通过p53途径抑制血管平滑肌细胞增殖的实验研究

目的探讨p53途径在大黄素抑制血管平滑肌细胞增殖作用中的地位。方法通过细胞计数、老化相关β-半乳糖苷酶染色、Annexin V标记等方法观察大黄素抑制血管平滑肌细胞增殖的特点。^3H-胸苷掺入法测定DNA合成、流式细胞仪了解细胞周期变化、Western blot检测p53蛋白表达变化、基因芯片观察mRNA表达水平。结果（1）1．6～3．1μg／ml大黄素延缓细胞生长,6．3～12．5μg／ml大黄素促进细胞老化,25．0μg／ml大黄素则可显著诱导细胞凋亡。（2）大黄素干预24h后,出现非计划性DNA合成现象,这是DNA损伤的敏感性标志。p53基因和蛋白表达水平呈大黄素浓度依赖性上调。除了细胞增殖基因表达下调,其他基因表达均上调,如细胞老化基因、细胞凋亡基因、DNA损伤修复基因。（3）大黄素能够迅速渗透进入细胞,在细胞内的分布具有明显的选择性,绝大多数以颗粒形态分布于细胞胞浆中,细胞核中也有少量分布。结论大黄素通过损伤DNA激活p53途径。随着大黄素浓度升高,p53途径激活程度也随之增强并产生多种细胞增殖抑制效应,即生长停滞、细胞老化和细胞凋亡。     

大黄素对肝纤维化大鼠肝功能的影响

目的 研究大黄素对肝纤维化大鼠肝功能的影响。方法 采用40％四氯化碳(CCl_4)给大鼠皮下注射制备肝纤维化模型并以小、中和大剂量大黄素(20、40和80mg/kg体重)治疗,通过常规方法测定大鼠血清谷丙转氨酶(ALT)、碱性磷酸酶(AKP)、总蛋白(TP)、白蛋白(ALB)和球蛋白(G)。结果 与正常组比较,大黄素组大鼠血清ALT、AKP显著降低(P<0.05～0.01);TP、ALB显著升高(P<0.05～0.01);G降低,白蛋白/球蛋白(A/G)比值升高,但无统计学差异。结论 大黄素对肝纤维化大鼠肝功能有一定的保护作用。     

Signal pathways involved in emodin-induced contraction of smooth muscle cells from rat colon

AIM: To investigate the effects induced by emodin on single smooth muscle cells from rat colon in vitro, and to determine the signal pathways involved.METHODS: Cells were isolated from the muscle layers of Wistar rat colon by enzymatic digestion. Cell length was measured by computerized image micrometry. Intracellular Ca^2+ ([Ca^2+]i) signals were studied using the fluorescent Ca^2+ indicator fluo-3 and confocal microscopy. PKCα distribution at rest state or after stimulation was measured with immunofluorescence confocal microscopy.RESULTS: (1) Emodin dose-dependently caused colonic smooth muscle cells contraction, (2) emodin induced an increase in intracellular Ca^2+ concentration; (3) the contractile responses induced by emodin were respectively inhibited by preincubation of the cells with ML-7 (an inhibitor of MLCK) and calphostin C (an inhibitor of PKC), (4) Incubation of cells with emodin caused translocation of PKCα from cytosolic area to the membrane.CONCLUSION: Emodin has a direct contractile effect on colonic smooth muscle cell. This signal cascade induced by emodin is initiated by increased [Ca^2+]i and PKCα translocation,which in turn lead to the activation of MLCK and the suppression of MLCP. Both of them contribute to the emodininduced contraction.     

Emodin alleviates lung ischemia–reperfusion injury by suppressing gasdermin D-mediated pyroptosis in rats

Background

Pyroptosis refers to programmed cell death associated with inflammation. Emodin has been reported to alleviate lung injuries caused by various pathological processes and attenuate ischemia–reperfusion (I/R) injuries in diverse tissues.

Methods

Lewis rats were assigned into the sham, the I/R, and the I/R + emodin groups. Emodin and phosphate-buffered saline were intraperitoneally injected into rats of the emodin group and I/R group for 30 min, respectively. These rats were then subjected to left thoracotomy followed by 90-min clamping of the left hilum and 120-min reperfusion. Sham-operated rats underwent 210-min ventilation. Lung functions, histological changes, lung edema, and cytokine levels were assessed. Protein levels were measured by western blotting. Immunofluorescence staining was conducted to evaluate pyroptosis.

Results

Emodin alleviated the I/R-induced lung dysfunction, lung damages, and inflammation. Protective effects of emodin against I/R-mediated endothelial pyroptosis was observed in vivo and in vitro. Mechanistically, emodin inactivated the TLR4/MyD88/NF-κB/NLRP3 pathway.

Conclusion

Emodin attenuates lung ischemia–reperfusion injury by inhibiting GSDMD-mediated pyroptosis in rats.     

Effect of somatostatin on the sphincter of Oddi in patients with acute non-biliary pancreatitis

BACKGROUND: Somatostatin has been used to prevent pancreatitis after endoscopic retrograde cholangiopancreatography but its effect on acute non-biliary pancreatitis is still unclear. AIM: The purpose of this study was to evaluate the function of the sphincter of Oddi (SO) and the effect of somatostatin on patients with non-biliary pancreatitis. METHODS: Twenty patients (18 males, two females) with acute pancreatitis (alcoholic 18, idiopathic two) received SO manometry within one week after admission. After baseline measurement, a bolus dose of somatostatin (Stilamin, Serono) 250 microg was infused slowly, and SO manometry was repeated after five minutes. Continuous infusion of somatostatin 250 microg/h was given for 12 hours after SO manometry. Serum amylase, lipase, glucose, and C reactive protein (CRP) levels were examined before and after somatostatin infusion. RESULTS: SO manometry was unsuccessful in six patients due to contracted sphincter. In the remaining 14 patients, high SO basal pressure (SOBP >40 mm Hg) was found in seven patients. After somatostatin infusion, mean SOBP decreased from 48.8 (29) to 31.9 (22) mm Hg (p<0.01). One patient had a paradoxical reaction to somatostatin (SOBP increased from 30 to 50 mm Hg) while the other 13 patients had a fall in SOBP after somatostatin. One patient developed abdominal pain with a serum amylase level of 2516 IU/l after SO manometry. No other side effects or changes in amylase, lipase, glucose, or CRP levels were observed in the other 19 patients after SO manometry and somatostatin infusion. DISCUSSION: Sphincter of Oddi dysfunction is common in patients with acute non-biliary pancreatitis and in most cases somatostatin can relax the sphincter.     

芍药甙与生长抑素及其类似物对犬重症急性胰腺炎Oddi括约肌影响的比较研究

传统医学应用白芍作为松弛平滑肌的药物之一,芍药甙为白芍的主要有效成分,对重症急性胰腺炎(SAP)时的Oddi括约肌功能障碍可能具有潜在治疗作用.目的:比较芍药甙与生长抑素及其类似物对实验性SAP犬Oddi括约肌的影响.方法:将20条犬随机分为SAP非治疗组、芍药甙治疗组、奥曲肽治疗组和生长抑素治疗组,以注射5%牛磺酸钠和自身胆汁混合液制备SAP模型.分别于造模前后以及给药后5、10、30、60、120和180 min测定Oddi括约肌基础压和时相收缩幅度(PCA).结果:造模后,SAP非治疗组的Oddi括约肌基础压显著升高(P=0.000 1).芍药甙、奥曲肽和生长抑素均能显著降低SAP时的Oddi括约肌基础压(P＜0.05);生长抑素还能显著降低SAP时的Oddi括约肌PCA(P=0.000 3),芍药甙和奥曲肽则无明显作用(P＞0.05).比较给药后Oddi括约肌基础压降低的差值,结果显示生长抑素在给药初期(给药后5 min和10 min)表现出较为明显的降压作用(P＜0.05),以后各时间点三者的作用无统计学差异(P＞0.05).结论:Oddi括约肌压力异常是SAP发展以及影响其严重程度的重要因素,芍药甙通过降低Oddi括约肌基础压而对SAP具有潜在治疗作用,且该作用在一定程度上与生长抑素及其类似物相当.     

血管活性肠肽对急性坏死性胰腺炎大鼠肠黏膜屏障功能的影响

目的 探讨血管活性肠肽(VIP)对ANP大鼠肠黏膜损伤的影响.方法 54只SD大鼠随机分成假手术组(SO)、ANP组和VIP组,每组分制模后1 h、6 h、12 h 3个时间点,各6只.采用4%牛磺胆酸钠胰胆管逆行注射制备ANP模型,VIP组在制模后5 min腹腔内注射VIP 5 nmol.ELISA法检测血浆及肠组织匀浆VIP水平;MB-80微生物快速动态检测系统检测血浆内毒素水平;RT-PCR法检测肠黏膜组织TNF-α、IL-6、IL-10 mRNA表达;肠黏膜行病理学检查.结果 ANP组肠黏膜结构损害明显,VIP组病变减轻.ANP组血浆及肠黏膜VIP水平在制模后6 h分别为(49.582 ±3.735)pg/ml和(87.731 ±4.601)pg/g pro,均显著低于SO组(P＜0.05),制模后12 h分别为(65.192±5.785)pg/ml和(110.978 ±6.420)pg/g pro,高于SO组;ANP组制模后6 h血浆内毒素水平、肠黏膜TNF-α、IL-6、IL-10mRNA表达量分别为(29.570±5.127)pg/ml、0.861±0.081、1.150±0.187和0.786±0.102,均显著高于SO组(P＜0.05).VIP组制模后6 h血浆内毒素水平、肠黏膜TNF-α、IL-6 mRNA表达分别为(20.486 ±2.811)pg/ml、0.707 ±0.095和0.889 ±0.136,均较ANP组下降(P＜0.05);IL-10 mRNA表达为0.992 ±0.126,较ANP组增高(P＜0.05).结论 VIP对ANP大鼠肠黏膜损伤具有明显的保护作用.