Acute effects of Helicobacter pylori extracts on gastric mucosal blood flow in the mouse

AIM： To investigate the mechanisms underlying the reduction in gastric blood flow induced by a luminal water extract of Hellcobacter pylori （HPE）. METHODS： The stomachs of isoflurane-anesthetized mice were exteriorized, and the mucosal surface exposed. Blood flow was measured with the laserDoppler technique, and systemic arterial blood pressure monitored. C57BL/6 mice were exposed to water extract produced from Hpylori strain 88-23. To investigate the role of a nerveor iNOS-mediated pathway, we used intraluminal lidocaine and iNOS-/- mice. Blood flow response to the endogenous nitric oxide synthase inhibitor asymmetric dimethyl arginine （ADMA） was also assessed. RESULTS： In wild-type mice, HPE decreased mucosal blood flow by approximately 30%. This reduction was abolished in iNOS-deficient mice, and by pre-treatment with lidocaine. Luminally applied ADMA resulted in reduction in blood flow similar to that observed in wildtype mice exposed to HPE. CONCLUSION： A H py/ori water extract reduces gastric mucosal blood flow acutely through iNOS- and nerve-mediated pathways.

Changes of Gastric Mucosal Blood Flow in the Healing Process of Peptic Ulcers

Changes of gastro-duodenal mucosal blood flow (GDMBF) in the healingprocess of 82 patients with gastric ulcer,130 with duodenal ulcer and 9 with active ul-cer induced by gastric polypectomy were studied by endoscopic laser Doppler flowme-try.In 108 normal subjects,the mucosal blood flow at the angle and antrum of the les-ser curvature and on the anterior wall of the duodenal bulb was the smallest (P【0.01).In patients with gastric ulcer,gastric mucosal blood flow (GMBF)significantly decrea-Sed at the active stage and increased at the healing stage (P【0.01 ).GDMBF significan-tly increased (P【0.01) at the active stage and returned to normal at the healing stage ofduodenal ulcer.GDMBF was unchanged in the healing process of the active ulcer inducedby gastric polypectomy.The mucosal blood flow at ulcer centre and margins significan-tly decreased at the active stage and markedly increased at the healing stage as compa-red with that of surrounding mucosa.We conclude that GMBF plays an importantrole in the developing and healing process of peptic ulcers.

Gastric Mucosal Blood Flow and Acid Secretion in Rats

The relationship between gastric mucosal blood flow (GMBF) and gastric acid secretionwere studied in rats by using secretory stimulant (pentagastrin)and inhibitor(cimetidine). GMBFwas measured by Laser Doppler flowmetry (LDF) and gastric mucosal pH determined by microglasspH electrode. GMBF increased and gastric mucosal pH decreased significantly after intravenous injec-tion of 6μg/kg of pentagastrin; nevertheless GMBF decreased and gastric mucosal pH increasedmarkedly after intravenous administration of 100mg/kg of cimetidine. This indicates that pentagastrincan increase GMBF and gastric acid secretion, and cimetidine can decrease GMBF and gastric acidsecretion in rats, proving the close relationship between GMBF and gastric acid secretion in rats.

EFFECT OF ELECTROACUPUNCTURE OF "ZUSANLI" ON VIP CONTENTS OF THE PERIPHERAL BLOOD, GASTRIC MUCOSAL AND BRAIN TISSUES IN GASTRIC MUCOSAL INJURY RATS

Objective: To observe the therapeutic effect of electroacupuncture (EA) of "Zusanli"(ST 36) on vasoactive intestinal peptide (VIP) levels in the peripheral blood, gastric mucosal and brain tissues in experimental gastric injury rats. Methods: Gastric mucosal injury model was established by using cold restraining stress method. 40 Wistar rats were randomly and evenly divided into normal control group, model group, EA group and non acupoint group. VIP contents of plasma and gastric mucosal and medulla oblongata tissues were assayed using radioimmunoassay and gastric mucosal blood flow (GMBF) was measured by employing hydrogen clearing method. Results: In cold restraining stress rats, spot and strip like bleeding necrosis foci in the gastric mucous primarily in the gastric antrum could be seen clearly, GMBF and VIP contents in plasma, gastric mucous and brain tissues declined significantly (P<0.05, 0.01), while the gastric mucosal lesion index (LI) raised significantly (P<0.05) in comparison with those of normal control group. Following EA of "Zusanli" (ST 36), GMBF decreased pronouncedly, VIP contents of the plasma, bulba and gastric mucosal tissues increased strikingly in comparison with model group (P<0.01). Conclusion: EA of "Zusanli" (ST 36) possesses a protection effect on gastric mucous under stress condition and VIP is involved in the effect of EA.

Protective effect of electroacupuncture and moxibustion on gastric mucosal damage and its relation with nitric oxide in rats

INTRODUCTION Gastric mucosal injury is one of the common disorders,there are many reports subjicted to its pathogenesis treatment and prevention.We investigated the protective effect

Association of high expression in rat gastric mucosal heat shock protein 70 induced by moxibustion pretreatment with protection against stress injury

AIM:To study the effect of moxibustion on Zusanli or Liangmeng point on gastric mucosa injury in stress-induced ulcer rats and its correlation with the expression of heat shock protein 70 (HSP70). METHODS:Sixty healthy SD rats (30 males,30 females) were divided into control group,injury model group,Zushanli point group,Liangmeng point group. Stress gastric ulcer model was induced by binding cold stress method. Gastric mucosa ulcer injury (UI) index was calculated by Guth method. Gastric mucosa blood flow (GMBF) was recorded with a biological signal analyzer. Protein content and gene expression in gastric mucosal HSP70 were detected by immunohistochemistry (IHC) and reverse transcription polymerase chain reaction (RT-PCR). Thiobarbital method was used to determine malondialdehyde (MDA) content. Gastric mucosal endothelin (ET) and prostaglandin E2 (PGE2) were analyzed by radioimmunoassay. RESULTS:High gastric mucosal UI index,high HSP70 expression,low GMBF and PGF2,elevated MDA and ET were observed in gastric mucosa of rats subjected to cold stress. Moxibustion on Zusanli or Liangmeng point decreased rat gastric mucosal UI index,MDA and ET. Conversely,the expression of HSP70,GMBF,and PGE2 was elevated in gastric mucosa after pretreatment with moxibustion on Zusanli or Liangmeng point. The observed parameters were significantly different between Zusanli and Liangmeng points. CONCLUSION:Pretreatment with moxibustion on Zusanli or Liangmeng point protects gastric mucosa against stress injury. This protection is associated with the higher expression of HSP70 mRNA and protein,leading to release of PGE2 and inhibition of MDA and ET,impairment of gastric mucosal index.

Sex differences and effects of oestrogen in rat gastric mucosal defence

AIM To evaluate sex differences and the effects of oestrogen administration in rat gastric mucosal defence.METHODS Sex differences in gastric mucus thickness and accumulation rate, absolute gastric mucosal blood flow using microspheres, the integrity of the gastric mucosal epithelium in response to a chemical irritant and the effects of oestrogen administration on relative gastric mucosal blood flow in an acute setting was assessed in an in vivo rat experimental model. Subsequently, sex differences in the distribution of oestrogen receptors and calcitonin gene related peptide in the gastric mucosa of animals exposed to oestrogen in the above experiments was evaluated using immunohistochemistry.RESULTS The absolute blood flow in the GI-tract was generally higher in males, but only significantly different in the corpus part of the stomach (1.12 ± 0.12 m L/min·g in males and 0.51 ± 0.03 m L/min·g in females) (P = 0.002). After removal of the loosely adherent mucus layer the thickness of the firmly adherent mucus layer in males and females was 79 ± 1 μm and 80 ± 3 μm respectively. After 60 min the mucus thickness increased to 113 ± 3 μm in males and 121 ± 3 μm in females with no statistically significant difference seen between the sexes. Following oestrogen administration(0.1 followed by 1 μg/kg·min), mean blood flow in the gastric mucosa decreased by 31% [68 ± 13 perfusion units (PFU)] in males which was significantly different compared to baseline(P = 0.02). In females however, mean blood flow remained largely unchanged with a 4% (5 ± 33 PFU) reduction. The permeability of the gastric mucosa increased to a higher level in females than in males (P = 0.01) after taurocholate challenge. However, the calculated mean clearance increase did not significantly differ between the sexes [0.1 ± 0.04 to 1.1 ± 0.1 m L/min·100 g in males and 0.4 ± 0.3 to 2.1 ± 0.3 m L/min·100 g in females(P = 0.065)]. There were no significant differences between 17β-Estradiol treated males (mean ratio of positive staining ± SEM)(0.06 ± 0.07) and females(0.11 ± 0.11) in the staining of ERα (P = 0.24). Also, there were no significant differences between 17β-Estradiol treated males (0.18 ± 0.21) and females (0.06 ± 0.12) in the staining of ERβ (P = 0.11). Finally, there were no significant differences between 17β-Estradiol treated males (0.04 ± 0.05) and females (0.11 ± 0.10) in the staining of CGRP(P = 0.14).CONCLUSION Gastric mucosal blood flow is higher in male than in female rats and is reduced in male rats by oestrogen administration.

胃复春胶囊联合西药治疗脾虚型慢性萎缩性胃炎临床研究

目的:观察胃复春胶囊联合西药治疗脾虚型慢性萎缩性胃炎(CAG)的临床疗效。方法:选取92例脾虚型CAG患者为研究对象,采用随机数字表法分为试验组和对照组各46例。对照组采用常规西药治疗,试验组在对照组基础上加用胃复春胶囊,均治疗12周。比较2组治疗前后中医证候积分、胃镜病理积分,胃液中游离酸、乳酸、总酸度及pH值,胃黏膜血流量情况。结果:治疗前,2组中医证候积分、胃镜病理积分比较,差异无统计学意义(P>0.05);治疗后,试验组中医证候积分、胃镜病理积分均降低(P<0.05),且试验组低于对照组(P<0.05)。治疗前,2组胃液中游离酸、乳酸、总酸比较,差异无统计学意义(P>0.05)。治疗后,2组游离酸、总酸含量均升高(P<0.05),乳酸含量均降低(P<0.05),且试验组胃液中总酸、游离酸含量高于对照组(P<0.05),乳酸含量低于对照组(P<0.05)。治疗前,2组胃液pH值分布比较,差异无统计学意义(P>0.05)。治疗后,2组pH值分布比较,差异有统计学意义(P<0.05)。治疗前,2组胃窦前壁、胃窦后壁、胃窦大弯、胃窦小弯胃黏膜血流量比较,差异无统计学意义(P>0.05);治疗后,2组上述胃黏膜血流量均增加(P<0.05),且试验组多于对照组(P<0.05)。结论:胃复春胶囊联合西药治疗脾虚型CAG,可改善患者临床症状和病理状态,调节胃液中游离酸、乳酸、总酸度含量及pH值,改善胃黏膜血流量,临床疗效优于单用西药治疗。

瑞巴匹特对胃粘膜保护作用的实验研究

目的：观察瑞巴匹特对空腹大鼠胃粘膜血流量（ＧＭＢＦ）、胃碱分泌的影响及对盐酸乙醇损伤胃粘膜的保护作用。方法：实验分３部分，每部分均包括５组，即对照组、替普瑞酮组及瑞巴匹特３０，１００，３００ｍｇ／ｋｇ组。前两部分分别观察用药后ＧＭＢＦ及胃灌流液ｐＨ值变化，第３部分观察各组动物用药后经０．１５ｍｏｌ／ＬＨＣｌ－４０％乙醇灌胃处理所致的胃粘膜溃疡面积。结果：１００ｍｇ／ｋｇ，３００ｍｇ／ｋｇ瑞巴匹特组ＧＭＢＦ平均升高（１４．５５±４．２９）×１０－２，（２１．１４±６．１９）×１０－２ｍｌｍｉｎ－１ｇ－１；胃灌流液ｐＨ值平均升高０．２５±０．１３及０．４１±０．１５；平均溃疡面积为（１９．６０±４．０９），（５．００±２．７５）ｍｍ２。上述数据与对照组比较，统计学差异显著（Ｐ＜０．０５）。结论：瑞巴匹特可增加ＧＭＢＦ。

艾灸足三里、梁门穴对应激性溃疡大鼠胃黏膜细胞凋亡的干预作用

目的:探讨艾灸足三里、梁门穴对应激性溃疡胃黏膜细胞凋亡的影响,分析其与血浆多巴胺(DA)、胃黏膜内皮素(ET)的关系,揭示艾灸足三里、梁门穴对抗应激性损伤,进而保护胃黏膜的机制.方法:SD大鼠60只随机分为4组,即束缚对照组、模型组、艾灸足三里和梁门穴组、艾灸非穴点对照组,每组15只.束缚水浸应激法造模,免疫组化方法测定细胞凋亡指数(×10-6个/μm2).采用生物信号分析仪检测胃黏膜血流量(GMBF),高效液相色谱法测定血浆DA含量,放射免疫法测定胃黏膜ET含量.结果:预先艾灸足三里、梁门穴可显著降低随后的应激性胃黏膜损伤指数,降低胃黏膜ET和血浆DA含量,增加胃黏膜血流量,降低胃黏膜细胞凋亡指数.造模后,B组UI值(26.80±9.81vs12.00±5.94,P<0.01)、血浆DA(9.97±3.69μg/Lvs4.54±2.61μg/L,P<0.01)、胃黏膜ET(361.469±98.080ng/Lvs149.205±94.1425ng/L,P<0.01)以及凋亡指数(9.65±4.19vs4.36±2.60,P<0.01)显著高于A组,而GMBF低于A组(139.489±33.133mL/minvs377.090±85.840mL/min,P<0.01);C组UI值、凋亡指数显著低于B组和D组(UI:14.10±5.42vs26.80±9.81,26.20±7.23,P<0.01;凋亡指数:3.00±1.58vs9.65±4.19,8.20±5.17,P<0.01),而GMBF高于B组和D组(316.552±85.469mL/minvs139.489±33.133,141.512±58.450mL/min,P<0.01);C组血浆DA含量及胃黏膜ET显著低于B组(DA:4.41±2.48μg/Lvs9.97±3.69μg/L,P<0.01;148.271±69.113ng/Lvs361.469±98.080ng/L,P<0.01),但与D组比较无显著性差异(P>0.05).结论:艾灸足三里、梁门穴预处理可减轻束缚水浸应激所造成大鼠胃黏膜的损伤程度,这一作用可能是通过降低血浆DA和胃黏膜ET含量,增加胃黏膜血流量,抑制细胞凋亡实现的.

葛根素对大鼠应激性胃黏膜损伤的保护作用

目的:研究葛根素对大鼠应激性胃黏膜损伤的保护作用。方法:采用浸水束缚应激法建立大鼠应激性胃溃疡模型。气囊法记录胃运动,激光多普勒血流计测定胃黏膜血流量,比色法测定胃黏膜组织一氧化氮(NO)和内皮素(ET)含量,并观察胃黏膜组织病理学变化。结果:葛根素可以明显减轻浸水应激引起的胃黏膜损伤;抑制胃运动亢进,尤其是降低胃运动指数、收缩时间百分比和高强度收缩次数;增加胃黏膜血流量;同时增加胃黏膜NO含量,并降低ET含量;胃黏膜组织损害程度显著减轻。结论:葛根素对应激性胃黏膜损伤具有明显的保护作用,其作用机制可能是通过舒张胃黏膜血管,升高胃黏膜NO水平,同时抑制胃运动亢进,增加局部胃黏膜血流量而产生作用。

大鼠重度脑外伤后胃粘膜血流、胃泌酸的动态变化

目的：探讨大鼠重度脑外伤后胃粘膜血流（ＧＭＢＦ）、胃泌酸动态变化及与急性胃粘膜损伤的相关性。方法：将４９只雄性ＳＤ大鼠随机分为７组，即对照组、液压打击重度颅脑伤后３０ｍｉｎ，１，２，４，８及１６ｈ组。观察各组动物的ＧＭＢＦ、胃液ｐＨ值及粘膜损伤面积。结果：与对照组相比，伤后３０ｍｉｎＧＭＢＦ明显升高（Ｐ＜０．０１），１ｈ后明显持续降低（Ｐ＜０．０１）；伤后３０ｍｉｎ后胃液ｐＨ持续降低（Ｐ＜０．０１），直至伤后１６ｈ开始明显高于对照组（Ｐ＜０．０１）；致伤３０ｍｉｎ后随时间延长，胃粘膜损伤面积逐渐增加，与ＧＭＢＦ及ｐＨ值呈明显负相关。结论：大鼠重度脑外伤所致胃粘膜血流降低、胃酸分泌亢进与胃粘膜损伤程度有明显相关性。

应激性溃疡大鼠血浆、胃粘膜内皮素水平变化及其意义

目的：探讨内皮素１（ＥＴ－１）在应激性溃疡形成与发展中的意义。方法：采用大鼠冷束缚应激溃疡模型（ＣＲＳ），动态检测应激前及应激后１，３，６，９，１２ｈ各时相血浆、胃粘膜组织ＥＴ－１含量、胃粘膜血流量（ＧＭＢＦ）及溃疡指数（ＵＩ）的变化。结果：应激后血浆、胃粘膜组织ＥＴ－１含量均较应激前明显升高，其中血浆ＥＴ－１含量于６ｈ达峰值，以后虽有所下降，但１２ｈ内仍高于正常（Ｐ＜０．０５）。而胃粘膜组织ＥＴ－１含量在应激后１２ｈ内持续显著上升（Ｐ＜０．０１）；同时ＧＭＢＦ明显降低（Ｐ＜０．０１），ＵＩ明显增加（Ｐ＜０．０１）。胃粘膜ＥＴ－１与ＵＩ呈显著正相关（ｒ＝０．９８４，Ｐ＜０．０１），与ＧＭＢＦ呈显著负相关（ｒ＝－０．８４２，Ｐ＜０．０５）。结论：内源性ＥＴ－１可能参与了应激性溃疡的形成与发展，其作用机制可能是通过减少ＧＭＢＦ，进而引起胃粘膜的缺血。

失血性休克大鼠模型的改进及胃黏膜血流量的测定

目的探讨失血性休克大鼠模型的建立及胃黏膜血流量的测定。方法16只健康雄性SD大鼠随机分为两组:对照组(n=8)、失血性休克组(n=8)。失血性休克组使用颈动脉失血-颈静脉失血回输的方式制备失血性休克大鼠模型。维持平均动脉压40mmHg1h后复苏,复苏后2h动物模型制作成功。使用激光多普勒血流仪测定大鼠胃黏膜血流量;采用光镜及透射电镜观察胃黏膜损伤情况。结果失血性休克组胃黏膜血流量较对照组明显降低,差异非常显著(P<0·01),胃黏膜细胞坏死、脱落、溶解,局部溃疡形成。结论失血性休克大鼠胃黏膜血流量明显降低,存在广泛的胃黏膜损伤。

补中益气汤的药理作用研究——抗实验性胃溃疡作用与机理

补中益气汤对应激性溃疡,幽门结扎性溃疡、利血平性溃疡模型均有良好的保护作用,对乙酸法胃溃疡模型有明显促进溃疡愈合的作用。其作用机理与该方抑制胃分泌,抑制胃运动、增加胃粘膜血流量以及一定的中枢抑制作用有关。

早期肠道营养改善烧伤大鼠胃组织血液灌流的实验研究

目的 探讨早期肠道喂养改善烧伤大鼠胃组织血液灌流的机制。方法 采用 3 0 %TBSAⅢ度烧伤大鼠模型 ,随机分为正常对照 (C)、单纯烧伤 (B)和烧伤加肠道营养 (EF)组。分别检测伤前及伤后 3、6、1 2、2 4、48h胃组织中内皮素 (ET)、一氧化氮(NO)、血管活性肠肽 (VIP)含量及胃粘膜血流量 (GMBF)。结果 烧伤后胃组织中ET、NO、VIP及ET/NO、ET/VIP比值均呈上升趋势 ,而GMBF则显著低于伤前。EF组中ET含量及ET/NO、ET/VIP比值明显低于B组 ,而NO、VIP及IMBF则高于B组 ,ET/NO、ET/VIP同GMBF呈显著负相关 (r1 =- 0 93 ,P <0 0 1 ;r2 =- 0 89,P <0 0 1 )。结论 早期肠道喂养改善烧伤后胃组织缺血状况的机制可能与食物对胃肠道神经的刺激 ,导致NO、VIP释放增加 ,并适度降低ET含量有关。

胃粘膜血流量对大鼠胃粘膜适应性细胞保护作用的影响

采用氢气清除法测定胃粘膜血流量（ｇａｓｔｒｉｃｍｕｃｏｓａｌｂｌｏｏｄｆｌｏｗ，ＧＭＢＦ），观察大鼠胃内灌注低浓度盐酸酒精（０．１５ｍｏｌ／ＬＨＣｌ＋１５％ＥｔＯＨ）后灌注高浓度盐酸酒精（０．６ｍｏｌ／ＬＨＣｌ＋１５％Ｅｔｏｌｌ）对ＧＭＢＦ和胃粘膜损害的影响，以及ＧＭＢＦ在适应性细胞保护中的作用。结果如下：（１）先用低浓度盐酸酒精作为弱刺激灌注随之以高浓度盐酸酒精作为强刺激灌注，引起胃粘膜适应性保护现象，它表现为：大体损伤和损伤深度分别比单独强刺激组减少４７．０９％和４４．５７％（Ｐ＜０．０１，Ｐ＜０．０５）；与此同时，ＧＭＢＦ亦出现适应性增强反应，即比单独强刺激组增加２８．０２％（Ｐ＜０．０５）；（２）近胃动脉灌注血管加压素后，ＧＭＢＦ的适应性增强反应被阻断，对胃粘膜的适应性保护作用也消失；（３）静脉注射消炎痛后，ＧＭＢＦ的适应性增强反应被阻断，对胃粘膜的适应性细胞保护作用消失，粘膜损伤程度加重。上述结果表明：低浓度盐酸酒精作为弱刺激引起的适应性细胞保护作用与ＧＭＢＦ增加反应增强有关；减弱或阻断这一增强效应可使适应性细胞保护作用消失；内源性前列腺素参与适应性细胞保护作用可能部分与ＧＭＢＦ增加有关。

应激状态下大鼠胃黏膜适应性细胞保护作用的研究

目的 :探讨心理、一氧化氮合酶 (NOS)及胃黏膜血流量 (GMBF)与应激状态下大鼠胃黏膜适应性细胞保护相互作用及意义。方法 :采用高压恒流脉冲刺激器复制胃黏膜损伤模型 ,将 72只雄性 SD大鼠随机分为对照组、规则光组及不规则光组 3组 ,分光光度法检测 NOS活性 ,动态检测 GMBF及 Nils L ambecht法判定胃黏膜损伤指数 (II)。结果 :在两个应激组中 ,NOS均升高 ,GMBF均下降后回升 ,而黏膜损伤均渐趋减轻。在规则组中 ,II与 GMBF呈显著负相关 ,在不规则组中 ,II与 NOS和 GMBF均呈显著负相关 ,而 NOS与 GMBF呈显著正相关。结论 :NOS、GMBF及心理共同参与了胃黏膜适应性细胞保护反应。

穴注黄芪、当归注射液对实验性慢性萎缩性胃炎胃粘膜血流的影响

目的 :探讨穴注黄芪、当归注射液对慢性萎缩性胃炎 (CAG)胃粘膜血流的影响。方法 :采用N 甲基 N 硝基亚硝基胍 (MNNG)诱发大鼠CAG。随机将 70只大鼠分为正常组、模型 1组( 40 μg/mLMNNG造模 )、模型 2组 ( 60 μg/mLMNNG造模 )、穴注 1组 ( 40 μg/mLMNNG造模+穴注 )与穴注 2组 ( 60 μg/mLMNNG造模 +穴注 )。穴注组均于造模第 1 0周开始以黄芪、当归注射液等份混合注入“足三里”穴。造模第 3 1周时观察各组大鼠胃粘膜病理及胃粘膜血流的改变。结果 :随造模浓度的增加 ,大鼠胃粘膜血流量下降 ,胃粘膜损伤加重 ,二者呈负相关 ;同时胃粘膜肠化及异增程度加重 (P均 <0 0 5)。穴注组可明显增加胃粘膜血流量 ,减轻胃粘膜损伤 (P <0 0 5)。结论 :局部血流量减少是胃粘膜损伤与萎缩发生、进展至胃癌前病变的重要原因 ;穴注法可能通过改善胃粘膜血供、促进组织修复而防治CAG。

党参及其有效成分抗胃粘膜损伤作用与机制研究——Ⅵ、党参部位提取物Ⅶ-Ⅱ对胃分泌、胃血流与胃肠运动的影响

党参部位提取物Ⅶ-Ⅱ十二指肠内给药能明显抑制幽门结扎大鼠胃液与胃酸分泌,降低胃液分泌量、总酸度和总酸排出量,在10～40克生药/公斤体重剂量下量效依赖关系良好;本品10、20克生药/公斤体重口服给药使幽门结扎大鼠胃粘膜中性红清除率有所下降,此作用可能与药物对胃液分泌的抑制作用有关;小鼠口服本品对甲基橙胃排空运动无明显影响,但对家兔离体十二指肠自发活动呈现轻度抑制,并能明显拮抗乙酰胆碱所致的家兔离体肠管的强直性收缩。