钙离子在大鼠结肠平滑肌运动中作用机制的研究

目的 应用束缚应激大鼠实验模型,研究离体结肠平滑肌的收缩运动及其影响因素,探讨鸟苷素在结肠运动中的作用。方法 建立束缚应激大鼠动物模型,制备离体结肠平滑肌环行肌及纵行肌肌条,应用张力换能器,测定其肌张力。应用放射配基法测定结肠组织及血浆中鸟苷素含量。结果 束缚应激刺激可诱发大鼠排便增加,该动物模型是较好的模拟人ＩＢＳ的实验动物模型。束缚应激大鼠离体结肠平滑肌的张力升高,对Ｋ＾＋、Ｃａ＾２＋、乙酰胆     

马来酸曲美布汀对束缚应激大鼠离体结肠平滑肌张力的调节作用机制

目的 研究曲美布汀对离体结肠平滑肌收缩及舒张运动的作用机制。方法 建立束缚应激诱发排便异常大鼠动物模型，制备离体结肠平滑肌环行肌及纵行肌肌条，应用张力换能器测定其肌张力。结果 束缚应激大鼠平滑肌肌条在基础状态时，曲美布汀可增加环行肌肌条张力，且随着浓度的递增平滑肌肌条张力有增加倾向。低于10^-7g／ml曲美布汀可增加纵行肌肌条张力，但高于10^-6g／ml时则降低肌条张力。曲美布汀可降低K^ 及乙酰胆碱作用下的束缚应激大鼠环行肌及纵行肌肌条张力，随着浓度的递增曲美布汀舒张平滑肌的作用有增加倾向。在Ca^2 作用下，10^-8g／ml曲美布汀增加束缚应激大鼠纵行肌及环行肌肌条张力，但高于10^-7g／ml时降低肌条的张力。结论 曲美布汀具有抑制和兴奋平滑肌双重作用，作用特点是调节平滑肌收缩与舒张运动，纠正肠管平滑肌运动异常。     

匹维溴胺对大鼠内脏高敏感形成和蛋白酶激活受体2表达的影响

目的 观察匹维溴胺对大鼠内脏高敏感形成及蛋白酶激活受体2(PAR2)表达的影响.方法 采用慢性避水应激法(WAS)构建内脏高敏感大鼠模型.Wistar大鼠随机分为假避水应激组、避水应激组和匹维溴胺治疗组(30 mg·kg~(-1)·d~(-1)),每组12只.观察每组大鼠应激时的排便颗粒数,并以结直肠扩张时的内脏运动反射(VMR)幅度值为指标观察内脏敏感性的变化.采用Western印迹和免疫荧光法检测结肠黏膜上皮PAR2的表达.结果 应激组大鼠排便颗粒数高于假避水应激组[(8.104±2.75)颗比(4.13±1.36)颗,P<0.001],匹维溴胺干预能减少应激时的排便颗粒数[(5.87±1.78)颗,P<0.001].避水应激后大鼠对60 mmHg(1 mmHg=0.133 kPa)压力扩张刺激的VMR幅度值(8.64±2.88)高于假避水应激组(3.805±1.04,P<0.001),匹维溴胺治疗可降低模型大鼠的VMR幅度值(6.09±0.77,P=0.02).与假避水应激组相比,避水应激上调结肠PAR2表达(相对灰度值分别为0.32±0.04和0.70±0.06,累积A值分别为77.16±10.74及279.085±100.91,P<0.001),匹维溴胺治疗抑制了PAR2的表达上调(相对灰度值0.53±0.06,累积A值180.59±25.75,P<0.05).结论 匹维溴胺能通过降低结肠黏膜上皮PAR2的表达而抑制内脏高敏感的形成与维持.     

维生素K3通过延迟整流钾通道影响豚鼠结肠平滑肌收缩

目的研究维生素K3对豚鼠结肠平滑肌肌条自发性收缩频率和平均张力的影响,和对细胞膜延迟整流钾通道的影响,并初步探讨其治疗肠痉挛的机制。方法将豚鼠处死后取5cm左右长的结肠,用张力换能器测量(40,100,400)μmol/L维生素K3对肌条收缩频率和平均张力的影响,再将肌条消化得到单个豚鼠结肠平滑肌细胞,用K(v)电级内液充灌玻璃微电级,分别用台氏液和含40μmol/L,100μmol/L,400μmol/L的维生素K3的台氏液灌流。以-40mV为钳制电压钳制细胞,20mV为阶跃,检测K(v)。每检测1个浓度维生素K3后均用台氏液洗脱1min。结果40μmol/L,100μmol/L,400μmol/L维生素K3可减弱豚鼠结肠平滑肌的收缩频率和平均张力(40,100,400)μmol/L,维生素K3相对正常组的频率分别下降了(21.4±2.16)%,(42.3±3.24)%,(66.5±3.67)%(P<0.05),张力分别减少了(23.6±2.64)%,(46.7±2.96)%,(69.7±3.23)%(P<0.05)。40μmol/L,100μmol/L,400μmol/L维生素K3作用下延迟整流钾电流的峰值相对正常组分别增加了(44.04±4.36)%,(92.05±6.34)%,(115.89±6.41)%,(P<0.05)。结论维生素K3能浓度依赖性的减弱平滑肌条的收缩频率和平均张力,并增强延迟整流钾通道的开放,这可能是其治疗胃肠痉挛的机制之一。     

四种胃肠激素在糖尿病胃动力障碍中的作用

目的通过对糖尿病大鼠模型离体胃窦平滑肌自发性收缩运动的研究,探讨血浆和胃窦组织中生长抑素(SS),血管活性肠肽(VIP),胃动素(MTL),P物质(SP)等在糖尿病胃动力障碍中的作用。方法建立糖尿病大鼠模型,制备实验组和对照组大鼠离体胃窦环行肌及纵行肌肌条,应用张力换能器测定其静息张力、平均振幅、收缩频率等运动指标;用放免法同批测定两组大鼠血浆和胃窦组织中SS,VIP,MTL和SP含量。结果①糖尿病组胃窦肌条自发收缩运动的多项指标均较对照组明显降低(P<0.01);②糖尿病组血浆中SS、VIP、MTL增加,SP降低;胃窦组织中SS增加,MTL和SP降低,VIP无变化;③血浆和胃组织SS与胃运动指标呈负相关;血浆VIP与MTL与胃运动指标呈负相关;血浆和胃组织SP和胃运动指标无明显相关性。结论①糖尿病多伴有胃运动功能障碍;②血浆和胃组织中胃肠激素含量变化在糖尿病胃动力障碍的发病中有一定作用。     

P物质NK1受体对大鼠结肠动力的调节作用

[目的]探讨P物质(substance P,SP)不同受体对大鼠结肠动力的调节作用。[方法]取大鼠近端结肠制备纵行肌(LMS)及环形肌(CMS)肌条,用张力换能器及多通道生理信号采集处理系统观察SP及其受体拮抗剂对SP诱导的LMS和CMS收缩活动的影响。[结果]SP显著促进大鼠结肠LMS和CMS自发性收缩活动[LMS:正常(0.85±0.06)g∶SP(1.02±0.05)g;CMS:正常(0.22±0.03)g∶SP(0.81±0.07)g,P0.01];CMS孵育河豚毒素TTX后加入SP收缩幅度显著增加[正常(1.15±0.11)g∶SP(2.25±0.18)g,P0.05];NK1受体特异性阻断剂L-703孵育肌条后加入SP,平滑肌收缩无显著增强,NK2受体特异性阻断剂GR159孵育后,SP能显著诱导平滑肌收缩增强(P0.05)。[结论]NK1和NK2受体均参与SP对结肠动力的调节,且对CMS的调节过程中,NK1受体发挥更重要的作用,SP对LMS的调节可能主要通过肠神经系统。     

钙稳态失衡在致结肠平滑肌收缩性改变中的作用

目的　探讨应激大鼠结肠平滑肌收缩时细胞内外钙离子 (Ca2 +)利用异常、细胞内钙稳态失衡在导致其收缩性改变中的作用。方法　建立寒冷 束缚应激大鼠排便异常的动物模型 ;测定离体结肠环形平滑肌收缩张力 ;差速离心制备结肠平滑肌肌浆网 ,测定肌浆网Ca2 + ATP酶活性。结果　应激大鼠结肠平滑肌收缩活性明显增强 ,并受Ca2 +通道阻滞剂显著抑制。应激大鼠结肠平滑肌肌浆网Ca2 + ATP酶活性降低 5 6 % (P <0 .0 5 )。结论　应激大鼠结肠环形平滑肌收缩活性显著增强 ,可能和肌细胞收缩时细胞外Ca2 +内流增加 ,肌浆网贮存Ca2 +释放减少、Ca2 + ATP酶活性降低等因素导致细胞内钙稳态失衡有关     

钙离子在CNP抑制Ach增强胃窦环行平滑肌收缩效应中的作用

目的 探讨细胞内外钙离子在C型钠尿肽(CNP)对乙酰胆碱(Ach)引起的大鼠离体胃窦环行平滑肌收缩效应中的作用.方法 利用浴槽孵育离体大鼠胃窦环行肌肌条,用离体平滑肌张力记录装置记录平滑肌肌条收缩活动,观察钙离子对Ach引起的大鼠离体胃窦环行平滑肌收缩效应的影响.结果 CNP对Ach引起的胃平滑肌自发性收缩增强效应有明显的抑制作用,在用无钙灌流液灌流后,CNP仍能抑制Ach引起的收缩效应.而用胞内钙离子释放抑制剂(TMB-8)后,CNP不能抑制Ach引起的收缩效应.结论 CNP抑制Ach引起的胃平滑肌自发性收缩增强效应与胞内钙释放有关.     

早期母婴分离对成年大鼠内脏感觉和肠道炎症的影响

背景：心理-社会因素在肠易激综合征（iBs）的发病机制中起重要作用,但早期生活事件如母婴分离对内脏敏感性的负性影响尚存在争议。目的：探讨早期母婴分离对成年大鼠内脏感觉和肠道黏膜炎症的影响。方法：37只新生雄性Sprague．Dawley幼鼠随机分为正常对照组、母婴分离组、急性避水应激组。母婴分离组幼鼠出生第2d开始进行母婴分离,持续至出生后第3周。2月龄时大鼠接受结肠气囊扩张,行腹壁回撤反射（AWR）评分和腹壁肌电测定;观察结肠组织病理学变化,以甲苯胺蓝染色法测定肥大细胞（MC）计数和脱颗粒率;以EHSA法测定结肠组织IL-1β和类胰蛋白酶含量。结果：母婴分离组结肠组织学评分、MC计数、IL-1β和类胰蛋白酶含量均显著高于避水应激组、正常对照组（P〈0．05）。当结肠内气囊压力为40、60、80mmHg时,母婴分离组和避水应激组AWR评分和腹壁肌电幅值均显著高于正常对照组（P〈0．05）,且母婴分离组AWR评分和腹壁肌电幅值与上述各项炎症指标均呈正相关（P〈0．05）。结论：早期母婴分离和急性避水应激均可导致内脏感觉过敏,早期母婴分离还可诱导肠道黏膜低度炎症,这种低度炎症可能与内脏感觉过敏相关。     

17β-雌二醇对去卵巢豚鼠结肠平滑肌的作用

目的:观察17β-雌二醇对去卵巢豚鼠结肠平滑肌的作用.方法:将豚鼠分为A组(去卵巢7 d)、B组(去卵巢+雌二醇3 d)、C组(去卵巢+雌二醇7 d).利用张力换能器记录豚鼠离体结肠平滑肌肌条对胆囊收缩素(cholecystokinin,CCK)的反应.结果:加入CCK后,三组平滑肌肌条收缩幅度均增加.增加幅度分别为0.096 g±0.015 g、0.134 g±0.026 g、0.179 g±0.027 g.B、C两组增加幅度较A组更为明显(P＜0.05),差别有统计学意义.结论:雌二醇能增强结肠平滑肌对CCK的敏感性.     

Effect of areca on contraction of colonic muscle strips in rats

AIM: To investigate the effects of areca on the contractileactivity of isolated colonic muscle strips in rats andmechanism involved.METHODS: Each strip (LMPC, longitudinal muscle ofproximal colon; CMPC, circular muscle of proximal colon;LMDC, longitudinal muscle of distal colon; CMlC, circularmuscle of distal colon. ) was suspended in a tissue chambercontaining 5 mL Krebs solution (37 ℃), bubbledcontinuously with 950 mL@ L-1 O2 and 50 mL@ L-1 CO2 . Themean contractile amplitude (A), the resting tension (T),and the contractile frequency (F) were simultaneouslyrecorded on recorders.RESULTS: Arsca dose dependently increased the meancontractile amplitude, the resting tension of proximal anddistal colonic smooth muscle strips in rats ( P ＜ 0.05). Italso partly increased the contractile frequency of colonicsmooth muscle strips in rats ( P ＜ 0.05). The effects werepartly inhibited by atropine (the resting tension of LMPCdecreased from 0. 44 ± 0. 12 to 0. 17 ± 0.03; the restingtension of LMDC decreased from 0.71 ± 0.14 to 0.03 ± 0.01;the mean contractile amplitude of LMPC increased from -45.8 ± 7.2 to -30.5 ± 2.9; the motility index of CMDC decreasedfrom 86.6± 17.3 to 32.8 ± 9.3; P＜ 0.05 vs areca), but theeffects were not inhibited by hexamethonium (P＞ 0.05).CONCLUSION: Areca stimulated the motility of isolatedcolonic smooth muscle strips in rats. The stimulation ofareca might be relevant with M reoeptor partly.     

Human colonic smooth muscle: spontaneous contractile activity and response to stretch.

The length dependence of the spontaneous contractile activity of human colonic muscle was assessed in vitro. Muscle obtained from the right colon was more distensible than that of the left colon. This was true for all muscle layers. Maximum spontaneous active stress was exerted by both circular and longitudinal muscle layers of the right colon at greater degrees of stretch (p less than 0.001) than those of the left colon. The contractile frequency of longitudinally oriented strips increased with length. The contractile frequency of intertaenial longitudinally oriented strips from the right colon was lower (p less than 0.001) than that of strips from the left colon. The contractile frequency of circularly-oriented strips from the right colon (6.25 +/- 0.38 min) was higher (p less than 0.001) than that of strips from the left colon (3.35 +/- 0.35 min). The human colon appears to consist of two distinct areas based on the mechanical behaviour of the smooth muscle during spontaneous contraction.     

慢性间歇性缺氧对大鼠胸骨舌骨肌收缩能力及疲劳指数的影响

目的 探讨慢性间歇性缺氧对大鼠上气道扩张肌即胸骨舌骨肌收缩性能的影响。方法 取健康雄性SD大鼠12只，随机分为正常对照组和慢性间歇性缺氧组，采用电刺激法，测定等长收缩胸骨舌骨肌肌条在不同条件下收缩性能及疲劳指数的变化。结果 慢性间歇性缺氧可造成大鼠胸骨舌骨肌在10和20Hz刺激下肌张力明显较对照组下降，两者比较差异有显著性；其肌肉的颤搐和强直性张力、颤搐／强直性张力比虽有所下降，但差异无显著性；此外，慢性间歇缺氧能显著增加胸骨舌骨肌的疲劳度。结论 慢性间歇性缺氧能够降低上气道扩张肌的张力，增加上气道肌的疲劳，使上气道抗疲劳能力下降，从而使其在抵抗上气道在吸气时负压的作用下降，可能参与了睡眠呼吸暂停的发病过程，加重或诱发呼吸暂停。     

Role of melatonin in reducing water avoidance stress-induced degeneration of the gastrointestinal mucosa

We investigated the role of melatonin on water avoidance stress (WAS)-induced degeneration of the gastric, ileal and colonic mucosa. Wistar albino rats were exposed to acute WAS (aWAS group) or chronic WAS (cWAS group). Before exposing animals to acute (aWAS + mel group) or chronic WAS (cWAS + mel group), 10 mg/kg melatonin was injected i.p. The stomach, ileum and colon samples were investigated under light and scanning electron microscope. Malondialdehyde (MDA) and glutathione (GSH) levels were also determined. In both aWAS and cWAS groups, the epithelium of stomach showed ulceration in some areas, dilatations of the gastric glands and degeneration of gastric glandular cells; prominent congestion of the capillaries after WAS was apparent. In the cWAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. MDA levels were increased and GSH levels were decreased in all tissues in both the aWAS and cWAS groups. The morphology of gastric, ileal and colonic mucosa in both aWAS + mel and cWAS + mel groups showed that the indole significantly reduced degeneration of the gastrointestinal mucosa. Decreased MDA and increased GSH levels were observed in the WAS + mel groups. Based on the results, melatonin treatment significantly prevented WAS induced degenerative morphological and biochemical changes of gastrointestinal mucosa.     

Effects of nociceptin/orphanin FQ on rats with cathartic colon

AIM To demonstrate the change and effect of nociceptin/orphanin FQ in the colon of rats with cathartic colon.METHODS The cathartic colon model was established by feeding rats rhubarb for 3 mo, the changes of colonic electromyography were investigated by both suspension muscle strips test and serosal recordings of colonic myoelectrical activity. Immunohistochemical staining (S-P methods) and image analysis were used to determine the changes of nociceptin/orphanin FQ in the proximal colon and distal colon of rats with cathartic colon.RESULTS Suspension muscle strips test in vitro showed OFQ (10-9-10-6 mol/L) concentration dependently caused an immediate tonic contraction in the isolated colon. But the increase of tension in cathartic colon was less than control groups (P＜0.01). Intravenous administration of OFQ (1μg/kg) caused phasic contractions in the proximal colon, while the amplitude of phasic contractions caused by OFQ in cathartic colon was much lower than that in the control groups (2.58 ± 0.41 vs 4.16± 0.53, t= -2.6, P = 0.012). OFQ was highly expressed in the myenteric plexus of the rat colon but not in the muscle cells. The immunoreactivity of OFQ in the proximal colon in cathartic colon rats decreased significantly compared with the control group (P = 0.001).CONCLUSION Colonic smooth muscle of cathartic colon showed low sensitivity to the stimulation of OFQ, suggesting that it might be caused by the abnormal distribution of OFQ or the abnormalities of receptors, leading to the disorganization of dynamic and incoordinated contractions.     

Taurine Ameliorates Water Avoidance Stress–Induced Degenerations of Gastrointestinal Tract and Liver

We investigated the role of taurine, is a potent free radical scavenger, on water avoidance stress (WAS)-induced degeneration of the gastric, ileal, and colonic mucosa and liver parenchyma. Wistar albino rats were exposed to chronic WAS (WAS group) 2 hr daily for 5 days. After exposing animals to chronic WAS (WAS + taurine group), 50 mg/kg taurine was injected IP for 3 days. Control animals received vehicle solution only. The stomach, ileum, colon, and liver samples were investigated under light microscope for histopathologic changes. To demonstrate the topography of the luminal mucosa of the stomach, ileum, and colon, scanning electron microscope was used and for hepatocyte ultastructure transmission electron microscope was used. Malondialdehyde (MDA, a biomarker of oxidative damage) and glutathione (GSH, a biomarker of protective oxidative injury) levels were also determined in all tissues. In the WAS group, the stomach epithelium showed ulceration in some areas, dilatations of the gastric glands, and degeneration of gastric glandular cells; prominent congestion of the capillaries was apparent. In the WAS group, severe vascular congestion was observed along with degeneration of ileal and colonic epithelium. Prominent vascular congestion and dilated sinusoids, activated Kupffer cells, dilated granular endoplasmic reticulum membranes, and focal pyknotic nuclei were observed in liver parenchyma. MDA levels (stomach, P < 0.01; ileum, colon, and liver P < 0.05) were increased and GSH levels (P < 0.01) were decreased in all tissues in the WAS group compared with the control group. The morphology of gastric, ileal, and colonic mucosa and liver parenchyma in the WAS + taurine group (stomach and ileum, P < 0.05; colon and liver, P < 0.01) showed a significant amelioration when compared to the WAS group. Increased MDA and decreased GSH levels in the WAS group were ameliorated with taurine treatment. Based on the results, taurine supplementation effectively attenuates the oxidative damage of gastrointestinal mucosa and liver because of WAS induction possibly by its antioxidant effects.     

Role of nitric oxide in the impairment of circular muscle contractility of distended, uninflamed mid-colon in TNBS-induced acute distal colitis in rats

AIM: To evaluate the role of nitric oxide (NO) in the motor disorders of the dilated uninflamed mid-colon (DUMC) from trinitrobenzene sulfonic acid (TNBS)-induced acute distal colitis in rats. METHODS: Colitis was induced in male Sprague-Dawley rats by a single intracolonic administration of TNBS. Control rats received an enema of 0.9% saline. The rats were killed 48 h after TNBS or saline administration. Macroscopic and histologic lesions of the colon were evaluated. Myeloperoxidase (MPO) and nitric oxide synthase (NOS) activity were measured on the colonic tissue. In TNBS rats, we evaluated spontaneous and evoked contractile activity in circular muscle strips derived from DUMC in comparison to the same colonic segment of control rats, both in the presence and in the absence of a non-selective NOS isoforms inhibitor N-nitro-L-arginine (L-NNA). Pharmacological characterization of electric field stimulation (EFS)-evoked contractile responses was also performed. RESULTS: In TNBS rats, the distal colon showed severe histological lesions and a high MPO activity, while the DUMC exhibited normal histology and MPO activity. Constitutive NOS activity was similar in TNBS and control rats, whereas inducible NOS activity was significantly increased only in the injured distal colon of TNBS rats. Isometrically recorded mechanical activity of circular muscle strips from DUMC of TNBS rats showed a marked reduction of the force and frequency of spontaneous contractions compared to controls, as well as of the contractile responses to a contracting stimulus. In the presence of L-NNA, the contractile activity and responses displayed a significantly greater enhancement compared to controls. The pharmacological characterization of EFS contractile responses showed that a cooperative-like interaction between cholinergic muscarinic and tachykinergic neurokinin 1 and 2 receptors mediated transmission in DUMC of TNBS rats vs a simple additive interaction in controls. CONCLUSION: The results of this study show that, during TNBS-induced acute distal colitis, circular muscle intrinsic contractile mechanisms and possible enteric neural excitatory activity are inhibited in the distended uninfiamed mid-colon. Suppression of NO synthesis markedly improves spontaneous and evokes muscle contractions, in spite of any evident change in local NO activity.     

Involvement of parasympathetic pelvic efferent pathway in psychological stress-induced defecation

AIM:To investigate the role of the pelvic nerve pathway in stress-induced acceleration of colorectal transit and defecation in rats.METHODS:Surgical transection of rectal nerves(rectal branches of the pelvic nerve),vagotomy(Vag) or adrenalectomy(Adx) were performed bilaterally in rats.Number of fecal pellet output of these rats was measured during 1-h water avoidance stress(WAS).To evaluate the colonic transit,rats were given phenol red through the catheter indwelled in the proximal colon and subjected to WAS.After WAS session,entire colon and rectum were isolated and distribution of phenol red was measured.Distal colonic and rectal transit was evaluated using glass bead.Rats were inserted the glass bead into the distal colon and evacuation rate of the bead was measured.Neural activation was assessed by immunohistochemical staining of c-Fos and PGP9.5 in colonic whole-mount preparations of longitudinal muscle myenteric plexus(LMMP).RESULTS:In the sham-operated rats(sham op),WAS significantly increased defecation and accelerated colorectal transit with marked elevation of plasma corticosterone level.Compared with sham-operated rats,increase in the excretion of fecal pellets during WAS was significantly reduced by rectal nerve transection(RNT)(sham op:6.9 ± 0.8 vs RNT:4.3 ± 0.6,P < 0.05) or Vag(sham op:6.4 ± 0.8 vs Vag:3.7 ± 1.1,P < 0.05),although corticosterone level remained elevated.Adx-rats significantly increased the defecation despite the lower corticosterone level.Distribution pattern of phenol red showed RNT inhibited distal colonic and rectal transit accelerated by WAS,while Vag inhibited proximal colonic transit.Suppression of distal colonic and rectal transit by RNT was further confirmed by the bead evacuation rate(sham op:80.0% vs RNT:53.8%).WAS significantly increased the number of c-Fos-immunoreactive neural cells in the LMMP of the proximal and distal colon,whereas c-Fos expression was decreased by RNT in the distal colon(sham op:9.0 ± 2.0 vs RNT:4.4 ± 1.0,P < 0.05) and decreased by V     

Action of progesterone on contractile activity of isolated gastric strips in rats

AIM: To study the effect of progesterone on contractile activity of isolated gastric strips in rats.METHODS: Wistar rats were sacrificed to remove whole stomach. Then, the stomach was opened and the mucosal layer was removed. Parellel to either the circular or the longitudial fibers, muscle strips were cut from fundus, body,antrum and pylorus. Each muscle strip was suspended in a tissue chamber containing 5 mL Krebs solution. Then the motility of gastric strips in tissue chambers was simultaneously recorded. The preparations were subjected to 1 g load tension and washed with 5 ml Krebs solution every 20 min. After 1 h equilibration, progesterone or antagonists were added in the tissue chamber separately. The antagonists were added 3 min before using progesterone (50 μmol. L-1).RESULTS: Progesterone decreased the resting tension of fundus and body longitudinal muscle (LM) (P＜0.05). It inhibited the mean contractile amplitude of body and antrum LM and circular muscle (CM), and the motility index of pyloric CM (P＜0.05). The inhibition of progesterone on the mean contractile amplitude could be partially blocked by phentolamine in LM of the stomach body (the mean contractile amplitude of body LM decreased from -7.5±5.5to -5.2±4.5 P＜0.01), and by phentolamine or indomethacin in CM of body (The inhibition of progesterone on the mean contractile amplitude of body CM decreased from -5.6±3.0to -3.6±2.7 by phentolamine and from -5.6±3.0 to -3.5±2.5by indomethacin, P＜0.01). Hexamethonium, propranolol and L-NNA (inhibitor of NO synthetase) didn′t affect the action of progesterone (P＞0.05).CONCLUSION: The study suggested that progesterone can inhibit the contractile activity of isolated gastric strips in rats and the mechanism seems to be a direct one except that the action on gastric body is mediated through prostaglandin and adrenergic α receptor partly.