狗小肠部分切除对移行性综合肌电的影响

将9只狗的小肠总长度的30％,50％及75％的上端分别切除,观察其对移行性综合肌电(MMC)发生规律和红霉素诱发MMCⅢ相的影响。结果发现,所有小肠部分切除的狗,残余小肠的慢波节律均较小肠完整时相应部位明显减慢;75％上端小肠切除的狗,MMC活动消失。小肠完整的狗,静脉注射红霉素均能使MMCⅢ相提前发生;30％上端小肠切除的狗,红霉素仅在一半的实验中可诱发MMCⅢ相,50％及75％上端切除后,红霉素不能诱发MMCⅢ相。但静脉注射吗啡后在所有动物模型上均能诱发MMCⅢ相。提示小肠MMC的周期活动需要空肠以上小肠的存在,红霉素仅在小肠上端能诱发MMCⅢ相。     

红霉素对狗胃肠道电活动的影响

以移行性综合肌电(MMC)作指标,研究红霉素(EM)消化道副作用与平滑肌电活动的关系。结果发现,在狗消化间期,静脉注射EM50～400μg/kg,在3～7min内即诱发剂量依赖性早发MMCⅢ相。此早发Ⅲ相起于胃、十二指肠,向小肠尾端移行,其锋电发生率、Ⅲ相持续时间和移行速度等均与自发Ⅲ相类似。胃、十二指肠内分别注射EM500μg/kg,经24.5±7.5min和23.7±2.2min才诱发移行性Ⅲ相。双侧膈上迷走神经切除后,EM仍诱发早发Ⅲ相,但其移行速度减慢(p<0.01),阿托品能阻断EM诱发Ⅲ相的发生。EM在Ⅲ相诱发后的70～250min甚至更长时间内仍使MMC周期和Ⅲ相起始紊乱,甚至完全破坏MMG,代之以超速扩布锋电簇活动。EM不影响进食后狗的胃肠电活动。因此,EM消化道反应的发生可能与其被吸收进血液后通过内在胆碱能神经启动早发Ⅲ相及其后较长后效应有关。     

绒毛膜促性腺激素及孕酮对大鼠小肠移行性综合肌电的影响

于去卵巢大鼠小肠的不同部位植入铂金丝单极电极,观察了绒毛膜促性腺激素(HCG)及孕酮对其移行性综合肌电(MMC)的影响。结果为:(1) 静注HCG后,十二指肠及空肠上段出现典型的与妊娠有关的MMC改变,即MMC的周期被间断出现且不规则延长的Ⅱ相所打乱。(2) 肌注孕酮后,十二指肠MMC的Ⅰ相和Ⅱ相时程均显著延长,但MMC的周期性无明显紊乱。(3) 在肌注孕酮的基础上加注HCG后,MMC的变化在特征上与单独注射HCG时相同,在范围上扩大到整个小肠。上述结果提示,在大鼠,HCG可引起典型的与妊娠有关的MMC活动紊乱;当有孕酮存在时,HCG的这一效应进一步增强。     

侧脑室注射Orexin-A对大鼠胃运动的影响

目的:观察侧脑室注射食欲素A(OXA)对大鼠胃运动的作用及作用途径。方法:选取成年雄性大鼠50只,随机分为5组,即生理盐水(NS)组、1μg组、5μg组、10μg组和20μg组。在胃窦和十二指肠植入应力传感器,记录大鼠胃肠自发性运动。通过侧脑室注射OXA,观察胃肠环形肌运动波形的变化和持续时间。选取10只大鼠随机分为2组,一组皮下注射NS+10μg OXA,另一组皮下注射阿托品+10μg OXA,观察OXA对胃肠运动的影响。同理选取10只大鼠分为假手术组+10μg OXA组,迷走神经切断组+10μg OXA组,观察OXA调控大鼠胃肠运动的作用途径。再选取10只大鼠,先注射NS再注射OXA拮抗剂SB334867,观察内源性OXA对胃肠运动的影响。结果:侧脑室注射OXA(1-20μg),大鼠消化间期胃和十二指肠III期收缩波消失,继而出现胃和十二指肠餐后不规则的收缩波。OXA对餐后胃肠运动的影响可被阿托品或切断迷走神经干所阻断(P0.05)。中枢注射选择性OXA受体拮抗剂SB-334867(16μg),可增强胃消化间期III相收缩(P0.05)。结论:中枢注射OXA可能经迷走神经胆碱能通路调控大鼠消化间期的胃肠运动,内源性OXA可能对大鼠消化间期胃肠运动具有抑制作用。     

甘草提取物的抑菌作用及其对小鼠免疫功能的影响

目的 研究甘草提取物的最低抑菌浓度及其对小鼠免疫功能的影响.方法 以大肠埃希菌和金黄色葡萄球菌为供试菌.结果 甘草提取物对大肠埃希菌和金黄色葡萄球菌的最低抑菌浓度均为12 mg/mL.甘草提取物能提高小鼠的免疫功能,当甘草提取物浓度为100μg/mL时,与对照组相比,小鼠脾脏T淋巴细胞增殖率为(32.62±1.06)％,B淋巴细胞增殖率为(28.20±1.68)％;腹腔巨噬细胞的增殖率为(40.19 ±2.38)％;腹腔巨噬细胞吞噬能力提高(24.20 ±0.01)％;NK细胞杀伤活力提高(15.83 ±1.02)％;IL-1、IL-2的体外诱生增殖率分别为(12.34±0.72)％、(23.78±1.87)％.结论 甘草提取物能抑制大肠埃希菌和金黄色葡萄球菌的生长,且抑制作用呈剂量依赖性.     

脑室和静脉注射吗啡对狗移行性综合肌电的影响

用10只狗作慢性实验,沿胃窦、小肠缝植8对银-氯化银双极电极,观察脑室和静脉注射吗啡对移行性综合肌电(migrating myoelectric complex,MMC)的影响。结果:(1)在十二指肠MMC周期时程的43％以后,静脉注射吗啡能诱发MMCⅢ相活动提前发生;在42％以内则无效应。(2)静脉注射3,000μg吗啡后,MMC周期延长,胃窦慢波频率减少;静脉注射300μg吗啡,对MMC周期时程和胃窦慢波频率无影响。(3 )脑室注射吗啡后,胃、小肠慢波首先发生自下而上的逆行性抑制,随之各部位峰电活动增多,十二指肠还发生痉挛性收缩的峰电活动,动物伴有呕吐的前驱症状和呕吐,MMC周期延长,胃窦慢波频率减少。(4)切断双侧膈上迷走神经后,脑室注射吗啡对胃和小肠肌电活动影响消失,但呕吐及其前驱症状仍然发生。     

甘草多糖的抗肿瘤活性及对免疫功能的影响

从甘草残渣中提取分离得到甘草多糖,采用血清溶血素及抗体生成细胞水平实验、碳粒廓清实验、S180荷瘤小鼠实验测定其免疫和抗肿瘤作用.结果表明,甘草多糖能促进小鼠血清溶血素IsM和ISG的生成,提高抗体生成细胞水平和胸腺、脾脏指数,增强巨噬细胞的吞噬活性,抑制肿瘤细胞S180的生长,与对照组比较均有显著性差异,提示甘草多糖具有免疫增强和肿瘤抑制作用.     

性类固醇激素受体ER、AR和PR在牛蛙胃肠胰的定位

本文用免疫组织化学技术检测及光密度定量分析,研究4种性类固醇激素受体在牛蛙(Rana catesbeiana)胃肠胰内的定位及表达的强弱,探讨4种性类固醇激素在牛蛙胃肠胰中的功能。染色结果显示,4种性类固醇激素受体在牛蛙胃肠胰内都有分布,雌雄之间分布差异较小。雌激素受体α(ERα)主要分布在牛蛙胃腺、直肠固有层和胰腺中;雌激素受体β(ERβ)主要分布在食道上皮、直肠固有层和胰腺中;雄激素受体(AR)主要分布在食道上皮、直肠固有层和胰腺中;孕激素受体(PR)主要分布在空肠、食道上皮和胰腺中。光密度检测结果显示,雌激素受体α(ERα)在牛蛙胃和直肠中阳性反应最强,在胰腺中相对较弱。雌激素受体β(ERβ)在牛蛙直肠中阳性反应最强,胰腺和食道次之。雄激素受体(AR)在食道中阳性反应相对较强,其他部位都较弱。孕激素受体(PR)在空肠中的阳性反应较强,其他部位都较弱。雌激素受体α(ERα)在胃中以及雄激素受体(AR)在食道和直肠中的免疫阳性反应均是雌性牛蛙强于雄性牛蛙,雌激素受体β(ERβ)在胰腺中的免疫阳性反应是雄性牛蛙强于雌性牛蛙。4种性类固醇激素受体中,雌激素受体α(ERα)和雌激素受体β(ERβ)在牛蛙胃肠胰中的分布最多,雄激素受体(AR)、孕激素受体(PR)的分布相对较少。性类固醇激素受体主要分布在食道、胃、直肠和胰腺中,其中,分布最多的部位是胃和直肠。4种性类固醇激素受体在牛蛙胃肠胰内的分布表明,性类固醇激素对牛蛙消化功能特别是胃和直肠的功能具有多方面的调节作用。     

PGE1对大鼠在体小肠肌电活动的影响

PGEs exhibit a variety of actions on gastrointestinal motility.The study,therefore,has been performed to determine the effect of PGE1 on conscious rats intestinal myoelectric activity and the relation of the PGE1 action with cholinergic M receptor and adrenergic α and β receptors.     

人及大鼠胃、小肠CGRP的定位研究

本实验选用成年健康男性尸体和成年雄性Wistar大鼠各4例,死后迅速取胃、小肠各段组织.用免疫组织化学PAP法,对CGRP在人及大鼠胃、小肠中的分布进行了研究.结果表明:胃粘膜内可见CGRP免疫反应阳性的内分泌细胞,其数量人多于大鼠;胃、小肠各段均可见CGRP免疫反应阳性神经纤维分布;大鼠小肠粘膜下层及内环、外纵肌间可见单个存在的CGRP免疫反应阳性神经细胞.这些结果表明,胃和小肠中的CGRP有两种来源,即来源于神经和内分泌细胞.文内还对CGRP在胃和小肠中的可能功能进行了讨论.     

Effects of intracerebroventricular administration of neurotensin,substance P and calcitonin on gastrointestinal motility in normal and vagotomized rats

The effects of intracerebroventricular (ICV) vs. intravenous (IV) injection of neurotensin, substance P and calcitonin on intestinal myoelectrical activity were examined in fed rats. ICV administered neurotensin and calcitonin restored the ‘fasted’ pattern of intestinal activity, i.e. the migrating myoelectric complex (MMC) at a dose as low as 12 and 0.2 pmol, respectively, whereas substance P only reduced significantly ($\text{P < 0.01}$) the duration of the postprandial pattern when injected ICV (48 pmol).Administered systemically at doses 100 times higher than the smallest active doses by the ICV route, calcitonin induced a fasted pattern, while neurotensin and substance P did not modify the fed pattern.The effects of ICV administration of neurotensin and calcitonin were abolished after vagotomy but the shortening effect of substance P on the duration of the postprandial pattern was still present.It is concluded that these three neuropeptides act centrally to control the pattern of intestinal motility in fed rats by shortening the ‘fed’ pattern for substance P and by restoring the MMC pattern for calcitonin and neurotensin, this last effect being mediated by the vagus.     

Chronic kidney disease after 5/6 nephrectomy disturbs the intestinal microbiota and alters intestinal motility

Organ–organ crosstalk is involved in homeostasis. Gastrointestinal symptoms are common in patients with renal failure. The aim of this study was to elucidate the relationship between gastrointestinal motility and gastrointestinal symptoms in chronic kidney disease. We performed studies in C57BL/6 mice with chronic kidney disease after 5/6 nephrectomy. Gastrointestinal motility was evaluated by assessing the ex vivo responses of ileum and distal colon strips to electrical field stimulation. Feces were collected from mice, and the composition of the gut microbiota was analyzed using 16S ribosomal RNA sequencing. Mice with chronic kidney disease after 5/6 nephrectomy showed a decreased amount of stool, and this constipation was correlated with a suppressed contraction response in ileum motility and decreased relaxation response in distal colon motility. Spermine, one of the uremic toxins, inhibited the contraction response in ileum motility, but four types of uremic toxins showed no effect on the relaxation response in distal colon motility. The 5/6 nephrectomy procedure disturbed the balance of the gut microbiota in the mice. The motility dysregulation and constipation were resolved by antibiotic treatments. The expression levels of interleukin 6, tumor necrosis factor-α, and iNOS in 5/6 nephrectomy mice were increased in the distal colon but not in the ileum. In addition, macrophage infiltration in 5/6 nephrectomy mice was increased in the distal colon but not in the ileum. We found that 5/6 nephrectomy altered gastrointestinal motility and caused constipation by changing the gut microbiota and causing colonic inflammation. These findings indicate that renal failure was remarkably associated with gastrointestinal dysregulation.     

Involvement of dopamine in the central effect of neurotensin on intestinal motility in rats

The effects of intracerebroventricular (ICV) administration of neurotensin (NT) before a meal on intestinal postprandial motility were examined in conscious rats chronically fitted with intraparietal Nichrome electrodes in the duodeno-jejunum. The effects were compared with those of two analogues, [D-Tyr¹¹]NT and [D-Trp¹¹]NT, resistant to degradation by brain peptidases. NT (10 μg ICV) delayed the occurrence of postprandial disruption of duodenal motility and blocked it on the jejunum. [D-Tyr¹¹]NT and [D-Trp¹¹]NT (1 μg ICV) elicited the same effects but at a ten-fold lower dose. NT administered peripherally just before a meal significantly lengthened the duration of the postprandial motor pattern. The central effect of NT on the fed pattern involved dopaminergic neurons as it was mimicked by dopamine, blocked by haloperidol and partly antagonized by either sulpiride or (+) SCH 23390. It is concluded that: 1) both D₁ and D₂ receptors are involved in the blocking effect of the postprandial disruption induced by central NT; 2) that [D-Tyr¹¹]NT and [D-Trp¹¹]NT are potent agonists at NT receptors in the brain.     

大鼠下丘脑外侧区内微量注射胃动素对胃窦运动和迷走背核复合体神经元电活动的影响

采用清醒大鼠胃运动记录和玻璃微电极记录神经元活动的实验方法 ,研究下丘脑外侧区 (lateralhy pothalamicarea,LHA)微量注射胃动素 (motilin) ,对清醒大鼠胃窦运动和对麻醉大鼠迷走背核复合体 (dorsalvagalcomplex ,DVC)中胃扩张敏感神经元电活动的调节作用。LHA内微量注射胃动素 (0 37nmol/ 0 5 μl)可使胃窦运动增强 76 2 9± 4 0 9% (P <0 0 1)。DVC中 6 0个胃扩张 (gastricdistention ,GD)敏感神经元中 ,39(6 5 % )个GD刺激引起电活动增强 ,2 1(35 % )个电活动减弱 ,分别称之为GD兴奋型神经元和GD抑制型神经元。双侧LHA微量注射胃动素 0 37nmol/ 0 5 μl,14个GD抑制型神经元中有 12个单位放电频率增加 4 4 35± 7 89% (P <0 0 1) ;2 4个GD兴奋型神经元中有 15个单位放电频率减少 7 17± 7 89% (P <0 0 5 )。结果提示 ,中枢胃动素可能通过LHA-DVC-迷走神经实现对胃窦运动的调控     

Effects of ginsenoside on pacemaker potentials of cultured interstitial cells of Cajal clusters from the small intestine of mice

Ginsenoside, one of the active ingredients of Panax ginseng, has a variety of physiological and pharmacological actions in various organs. However, little is known about the effects of ginsenosides on gastrointestinal (GI) motility. We studied the modulation of pacemaker potentials by ginsenoside in the interstitial cells of Cajal (ICCs) using the whole-cell patch clamp technique in the current clamp mode. Among ginsenosides, we investigated the effects of ginsenoside Rb1, Rg3 and Rf. While externally applied Rb1 and Rg3 had no effects on pacemaker potentials, Rf caused membrane depolarization. The application of flufenamic acid or niflumic acid abolished the generation of pacemaker potentials and inhibited the Rf-induced membrane depolarization. Membrane depolarization induced by Rf was not inhibited by intracellular application of guanosine 5′-[β-thio]diphosphate trilithium salt. Pretreatment with a Ca²⁺-free solution, thapsigargin, a Ca²⁺-ATPase inhibitor of the endoplasmic reticulum, U-73122, a phospholipase C inhibitor, or 2-APB, an IP3 receptor inhibitor, abolished the generation of pacemaker potentials and suppressed Rfinduced actions. However, treatment with chelerythrine and calphostin C, protein kinase C inhibitors, did not block Rf-induced effects on pacemaker potentials. These results suggest that ginsenoside Rf modulates the pacemaker activities of ICCs and therby regulates intestinal motility.     

短链脂肪酸对肠道动力影响的研究进展

人体的肠道不仅仅是消化吸收场所,也是大量微生物生存的家园.肠道作为人体最大的储菌库,其多种生理功能离不开复杂多变的肠道菌群和菌群代谢物(如短链脂肪酸等)的参与.短链脂肪酸是肠道菌群发酵膳食纤维产生的一类重要的信号分子,研究发现短链脂肪酸除参与维持人体肠道黏膜免疫屏障、调节体液及电解质平衡以及为肠上皮细胞提供能量外,...     

Sperm motility in the horseshoe crab. III. Isolation and characterization of a sperm motility initiating peptide

Sperm motility in Limulus is initiated by a sperm motility initiating factor (SMI) that emanates from Limulus eggs. This report describes the partial purification of SMI (greater than 230-fold purification with respect to protein content) with 40% recovery. SMI appears to be a hydrophobic peptide of 500–2,000 MW. Although probably not purified to homogeneity, SMI is estimated to be active at a concentration of less than 0.2 μM.     

Central effects of growth hormone-releasing factor (GRF) on intestinal motility in dogs: involvement of dopaminergic receptors

The effects of intracerebroventricular (ICV) and intravenous (IV) administration of human pancreatic growth hormone-releasing factor (hpGRF) on gastro-intestinal motility were examined in fasted and fed conscious dogs equipped with chronically implanted strain-gauges on the antrum and the jejunum. During the fasted state, hpGRF injected ICV at 0.1 micrograms . kg-1 or IV at 0.5 micrograms . kg-1 did not affect the cyclic occurrence of the migrating motor complex (MMC). This pattern was normally disrupted for 8-10 hours by a daily standard meal. Injected ventricularly (0.1 micrograms . kg-1) but not intravenously (0.5 micrograms . kg-1) 10-15 min after the daily meal, hpGRF significantly reduced (p less than 0.01) the duration of the jejunal fed pattern (2.0 +/- 1.4 vs. 8.4 +/- 1.1 hours for control) but not that of the stomach. This effect persisted when hpGRF (0.1 micrograms . kg-1 ICV) was administered after indomethacin (2 mg . kg-1 IM), naltrexone (0.1 mg . kg-1 IV) or domperidone (1 mg . kg-1 IV) but was abolished by a previous IV injection of metoclopramide (1 mg . kg-1). It was concluded that hpGRF is able to act centrally to control the pattern of jejunal motility in fed but not in fasted dog, its effect being probably mediated through dopaminergic pathways.     

Central muscarinic control of the pattern of small intestinal motility in rats

The effects of central and peripheral administration of muscarinic agonists and antagonists on small intestinal motility were examined in conscious rats chronically fitted with electrodes implanted in the duodeno-jejunal wall and a cannula in a cerebral lateral ventricle. Intracerebroventricular (i.c.v.) administration of either atropine or pirenzepine at doses from 1 to 10 micrograms, 15 min before a 3 and 6 g lab chow meal significantly reduced the duration of the postprandial disruption of the migrating myoelectric complexes (MMC). The reduction was significantly greater for atropine, a mixed M1 and M2 muscarinic receptor antagonist, than for pirenzepine, an antagonist with a high affinity for M1 receptors. At a higher dose (10 micrograms) intra peritoneal (i.p.) administration of atropine or pirenzepine did not modify the postprandial disruption of MMC. Oxotremorine (10 ng) a M2 agonist, but not McNeil A343 (5 micrograms), a selective M1 agonist, given i.c.v. in fasted rats disrupted for 1.5 h the MMC pattern. At the same doses given i.p. oxotremorine and McNeil A343 disrupted the MMC for 15 and 45 min respectively. We conclude that the postprandial changes in the small intestinal motility involve muscarinic receptors, mainly of M2 subtype, at the level of the central nervous system.