目的：研究回肠Na+/胆酸转运体（IBAT）抑制剂SC-435喂养后，豚鼠胃肠移行性复合波（MMC）与胆酸池大小的变化。方法：60只豚鼠分别给予正常饮食和IBAT抑制剂SC-435饮食2周、4周、8周。喂养结束后，评估胆囊动力并将4对电极植入胃窦、12指肠、空肠、回肠。7d后，记录MMC并测量胆酸池大小。结果：IBAT抑制剂喂养后，胆囊动力在4周与8周组下降。胆酸池在4周组减小17.11%（P<0.05），8周组减小48.35%（P<0.05）。MMC起源部位发生改变：胃窦起源（37%）和十二指肠起源（46%）减少而空肠起源（17%）增多。与对照组相比，MMC周期延长（4周组1.16倍，P<0.05；8周组1.38倍，P<0.05）而波幅降低（4周组降低10.58%，P<0.05；8周组降低49.17%，P<0.05）。在对照组与2周组之间，所有MMC参数无统计学意义差异。结论：IBAT抑制剂SC-435减小胆酸池并抑制MMC运动；MMC与胆酸肠肝循环有关，与胆酸池大小改变一致。

目的 探讨大鼠杏仁核胃动素受体分布及杏仁核基底外侧核胃动素受体与外源性胃动素结合或者毁损后对十二指肠消化间期移行性复合肌电活动（MMC）的影响及其作用机制。方法 采用免疫组织化学、中枢立体定位杏仁核微量注射、杏仁核毁损、多道生理记录仪监测十二指肠MMC的方法，探讨大鼠杏仁核胃动素受体的作用。结果 杏仁核各亚核团都有胃动素受体分布，以杏仁内侧核分布最多；杏仁基底外侧核也有较多分布，后部多于前部；分布较少的核团是杏仁基底内侧核、杏仁中央核、杏仁基底外侧核；杏仁核基底外侧核胃动素受体与外源性胃动素结合后可以使十二指肠MMC时相变短。峰电振幅增加，峰电频率增快；膈下迷走神经切断术可完全阻断这种效应；阿托品、酚妥拉明、普萘洛尔不能阻断这种效应；抗胃动素血清只能部分阻断这种效应；杏仁基底外侧核核团毁损对十二指肠MMC：影响不明显。结论 杏仁核各亚核团都有胃动素受体分布，杏仁内侧核是胃动素受体分布最多的部位。杏仁核微量注射胃动素可以使十二指肠MMC：的时相、峰电振幅和峰电频率发生变化，这种作用可能是通过杏仁核一下丘脑一脑干一迷走神经通路实现的。提示杏仁核胃动素受体在对十二指肠MMC的中枢性调节中发挥着重要作用。

目的 探讨海马微量注射胃动素对十二肠消化间期移行性复合肌电活动（mogratomgmyoclectricalcomplex，MMC）的影响及作用机制。方法 采用中枢立体定位海马微量注射。多道生理记录仪监测十二指肠MMC的方法。观察海马微量注入胃动素（0.3nmol）对十二指肠MMc的影响。结果 海马微量注入胃动素可以使十二指肠MMC时相明显变短。峰电振幅增加峰电频率增快但对峰电时相无明显影响：膈下迷走神经切断术可完全阻断海马胃动素对十二指肠MMC的影响；阿托品、酚妥拉明、普萘洛尔不能阻断海马胃动素对十二指肠MMC的影响；抗胃动素血清只能部分阻断海马胃动素对十二指肠MMC的影响。结论 海马外源性胃动素可以使十二指肠MMC的时相、峰电振幅和峰电频率发生变化这种作用可能是通过海马下丘脑脑干迷走神经通路由非肾上腺素能非胆碱能神经元作用于十二指肠平滑肌或者促进胃动素的释放而实现的。海马在十二指肠MMC的调节中发挥着重要作用。

目的 研究门脉高压犬小肠微循环超微结构的改变。方法 行缩窄门静脉主干1/2加丝线慢性栓塞术建立犬肝前性门脉高压症模型，观察小肠黏膜上皮和黏膜及黏膜下层微循环超微结构的改变。结果 肝前性门脉高压犬小肠黏膜及黏膜下微循环超微结构改变的特征为：血管数量增多，直径增大；微动脉腔小、壁厚，胶原纤维增生、紊乱，内皮细胞受损；微静脉腔大、壁薄，基膜及内皮细胞受损；毛细血管内皮细胞受损，白细胞浸润；肠黏膜上皮细胞、基底膜受损，回肠平滑肌细胞核畸形。结论 门脉高压犬小肠黏膜及黏膜下微循环超微结构出现明显改变。

AIM: To investigate the bile acid pool size after cholecystectomy whether or not correlated to the gastrointestinal migrating myoelectric complex (MMC) in guinea pigs. METHODS: Gallbladder motilities were assessed before cholecystectomy. Furthermore, we continuously monitored interdigestive gastrointestinal motilities using bipolar electrodes in conscious guinea pigs before and after surgery at 4 wk in standard diet group and high cholesterol diet (cholesterol gallstone) group. Total bile acid pool sizes were measured by isotope dilution method at meantime. RESULTS: After cholecystectomy, there were parallel falls in duration of phase I, Ⅱ, Ⅲ and MMC cycle duration but increase in amplitude in the guinea pigs with normal gallbladder function, and in the guinea pigs with cholesterol stones. However, There were not significantly differences. On the other hand, the bile acid pool was definitely small in the GS guinea pigs compared to normal guinea pigs and became slightly smaller after cholecystectomy. Similarly, bile acid in gallbladder bile, fecal bile acid was slightly increased in GS guinea pigs after cholecystectomy, to the same degree as normal. These differences, however, were not significant. CONCLUSION: It is concluded that in the guinea pigs with normal gallbladder function, and in the guinea pigs with cholesterol stones: (1) Cholecystectomy produce a similar but less marked trend in bile acid pool; and (2) MMC are linked to enterohepatic circulation of bile acids, rather than surgery, which is consistent with changes of the bile acid pool size. As a result, gastrointestinal dyskinesia is not involved in occurrence of postcholecystectomy syndrome.

目的 探讨高胆固醇饮食（HCD）能否引起胆囊胆固醇结石和对胆囊运动的影响及其机制。方法 用实体解剖、B超观察HCD组、正常对照组的胆囊成石情况；测定两组的胆囊运动功能；用放免法测定空腹及脂肪餐后血浆胆囊收缩素（CCK）水平；用比色法测定胆汁中胆固醇浓度；观察胆囊病理学改变。结果 HCD组的胆固醇结石成石率、胆汁胆固醇浓度显著高于正常对照组（P<0.05）；HCD组的脂肪餐后CCK水平、胆囊排空功能低于正常对照组（P<0.05）；HCD组有9例出现胆囊炎症性病理改变；正常对照组仅1例出现黏膜水肿。结论 高胆固醇饮食可以造成家兔的胆囊胆固醇结石，成石的原因可能与胆囊运动功能障碍、胆固醇代谢紊乱、血浆ccK水平降低、胆囊炎症以及它们之间的相互作用有关。

近年发现，生长抑素及其类似物能够抑制肿瘤细胞增殖，诱导肿瘤细胞凋亡，不仅能抑制具有神经内分泌功能肿瘤的增殖，对普通的实体瘤亦有抑制作用，现已初步应用于临床。其生物学活性是通过靶细胞膜上的特异性受体介导，不同组织受体表达量及种类不同，抑瘤效果也不同。肝癌和胰腺癌是消化系统两大恶性肿瘤，对其治疗及防治具有重要意义。

AIM: To investigate the mRNA expression of gammaaminobutyric acid A (GABAA) receptor subunits α1, β1, γ2 in different parts of the brain of rats with hepatic encephalopathy. METHODS: Twelve adult male Sprague-Dawley rats were randomly divided into two groups: (1) hepatic encephalopathy model group (n=6), which was induced by intraperitoneal injection of thioacetamide (TAA, 350 mg/kg) for three consecutive days; (2) control group (n=6), in which the rats were treated with same dose of normal saline solution. After the freeze slice of cerebrum was made, in situ hybridization was used to detect the mRNA of GABAA receptor subunits α1, β1, and γ2 in rat cerebral cortex, basal nuclei, substantia nigra and hippocampi. Image data were collected and analyzed quantitatively by QWin550CW model image signal gather and analysis system. RESULTS: In rats with hepatic encephalopathy, mRNA expression levels of GABAA receptor subunits α1, β1 increased significantly in basal nuclei, substantia nigra pars compacta, substantia nigra pars reticularis and hippocampi (144.7±15.67/184.14±4.41, 60.61±33.66/113.07±32.44, 87.71±21.25/128.40±18.85, 122.34±5.56/161.60±4.56, 123.29±5.21/140.65±4.15, 123.40±4.42/140.09±4.52, 124.76±4.18/140.09±4.12, 141.62±15.09/182.80±5.20, 69.13±30.74/134.21±43.76, 87.87±25.16/151.01±19.49, 122.14±6.30/162.33±3.92, 122.81±5.09/137.19±7.12, 123.00±4.63/138.11±5.92, 125.75±2.43/138.81±6.10, P<0.01), but did not change in the cerebral cortex compared to the control group. Similar changes were found in the mRNA expression levels of GABAA receptor subunit γ2, which increased significantly in basal nuclei, substantia nigra pars compacta, substantia nigra pars reticularis (136.81±26.41/167.97±16.23, 51.00±36.14/113.18±36.52, 86.35±20.30/126.90±19.74, P<0.01), CA1 of hippocampal (162.15±9.05/178.62±6.45, P<0.05), and no changes were found in the cerebral cortex and CA2, CA3, CA4 of hippocampi. CONCLUSION: In rats with hepatic encephalopathy, mRNA expression levels of GABAA receptor subunits α1, β1, γ2 increase significantly in basal nuclei, substantia nigra and hippocampi, suggesting that the changes of mRNA expression levels in GABAA receptor subunits may contribute to the pathogenesis of hepatic encephalopathy.

目的 通过研究胃肠激素与消化间期移行性复合运动（MMc）的关系，探讨MMc发生及其调节机制。方法 应用胃十二指肠测压技术对30例健康志愿者的消化间期胃十二指肠运动的特征进行研究，并在检测过程中分别于MMCI、Ⅱ和Ⅲ相采集静脉血行胃动素（MTL）、生长抑素（SS）、P物质（SP）及一氧化氮（NO）的血浆浓度检测。结果 MMC周期为112.7min±37.2min，MMCI相最长，Ⅱ相次之、Ⅲ相最短，MMCⅢ相多起源于胃窦，也可起源于十二指肠。MMC多向远端移行，偶见逆向传导。MMCⅢ相血浆MTL为921.7pg/ml±109.8pg/m1，SP为10.9pg/m1±7.2pg/ml，明显多于I相（分别为334.7pg/ml±58.1pg/ml，11.3pg/ml±8.8pg/m1）和Ⅱ相（分别为370.0pg/ml±69.2pg/ml，11.0pg/m1±10.0pg/m1），差异有统计学意义（P<0.05）。血浆SS、NO水平各时相相比差异无统计学意义（P>0.05）。结论 MTL、SP可能与MMCⅢ相的诱发有关。血浆SS、NO水平可能对胃肠MMC无直接作用。

目的 探讨杏仁核微量注射胃动素对十二指肠消化间期移行性复合肌电活动（migrating myoelectrical complex， MMC）的影响及作用机理。方法 采用中枢立体定位杏仁核微量注射，多道生理记录仪监测十二指肠MMC的方法，观察尾静脉给予阿托品（50μg/kg）、酚妥拉明（200μg/kg）、普萘洛尔（100μg/kg）及抗胃动素血清（1:50）和膈下迷走神经切断术后，杏仁核微量注入胃动素（0.37nmol）对十二指肠MMC的影响。结果 杏仁核微量注入胃动素可以使十二指肠MMC时相明显变短[（586.3±42.0）svs（694.0±36.2）s]，峰电振幅增加[（294.7±43.2）μVvs（255.1±23.5）μV]，峰电频率增快[（23.1±0.6）次/minvs（18.2±0.4）次/min]，但对峰电时相无明显影响，峰电频率的变化率要大于峰电振幅的变化率[（54.3±5.6）%vs（22.4±4.3）%]；膈下迷走神经切断术可完全阻断杏仁核胃动素对十二指肠MMC的影响；阿托品、酚妥拉明、普萘洛尔不能阻断杏仁核胃动素对十二指肠MMC的影响；抗胃动素血清只能部分阻断杏仁核胃动素对十二指肠MMC的影响。结论 杏仁核外源性胃动素可以使十二指肠MMC的时相、峰电振幅和峰电频率发生变化，这种作用可能是通过杏仁核-下丘脑-脑干-迷走神经通路，由非肾上腺素能非胆碱能神经元作用于十二指肠平滑肌或者促进胃动素的释放而实现的。