快动眼睡眠剥夺对丁酸钠诱导的内脏感觉过敏大鼠模型的调节作用

目的研究丁酸钠灌肠对大鼠内脏感觉功能的影响以及快动眼睡眠剥夺对大鼠内脏感觉功能的调节作用。方法大鼠行丁酸钠溶液灌肠（200mmol／L，6次），对照组行生理盐水灌肠。两组大鼠均在第1次灌肠后的第3、6、9、12、15、18天行结直肠气蠼扩张（CRD），观察大鼠的腹壁回撤反射（AWR）测定内脏感觉功能。丁酸钠灌肠大鼠分为快动眼睡眠剥夺组和对照组。在快动眼睡眠剥夺的第24h、48h、72h行CRD，观察大鼠的腹壁回撤反射（AWR）测定内脏感觉功能。结果第3，6、9、12天，在20、40、60、80mmHg的扩张压力下，丁酸钠灌肠组的AWR评分明显高于生理盐水灌肠组（P＜0．05）。而在第15、18天，丁酸钠灌肠组的AWR评分与对照组无显著性差异（P＞0．05）。快动眼睡眠剥夺的第24h，大鼠对80mmHg扩张刺激的AWR评分明显低于对照组（P＜0．05）；而快动眼睡眠剥夺的第48、72h，大鼠对不同程度扩张刺激的AWR评分均明显低于对照组（P＜0．05）。在快动眼睡眠剥夺的第48、72h大鼠的疼痛感觉阈值升高（P＜0．01）。结论丁酸钠溶液反复灌肠可诱导大鼠内脏感觉过敏；快动眼睡眠剥夺可提高模型鼠的内脏疼痛感觉阈值，降低内脏感觉敏感性。     

去甲肾上腺素在快动眼睡眠剥夺降低大鼠内脏感觉功能中的作用

目的 研究去甲肾上腺素(NE)在快动眼(REM)睡眠剥夺降低大鼠内脏感觉功能中的作用.方法 大鼠随机分为实验对照组(YC)、REM睡眠剥夺组(SD)、REM睡眠剥夺后育亨宾干预组(YSD).采用"花瓶技术"对SD组及YSD组进行REM睡眠剥夺48 h,YSD组在48 h时给予腹腔注射育亨宾.造模完成后行结直肠扩张(CRD),观察各组大鼠疼痛感觉阈值,记录大鼠的腹壁肌电图了解腹壁肌的放电次数.采用RT-PCR半定量检测丘脑及肠道组织单胺氧化酶A(MAO-A)和酪氨酸羟化酶(TH)基因表达水平.结果 REM睡眠剥夺48 h时各组大鼠在20、40、60、80 mm Hg(1 mm Hg=0.133 kPa)扩张压力下的腹壁肌放电结果显示:(1)SD组大鼠扩张刺激后的腹壁肌放电次数(178±98、839±323、1331±444、1703±478)显著低于YC组(413±171、1400±245、2070±386、2510±469),且疼痛感觉压力阈值显著增高(P＜0.05);(2)YSD组大鼠扩张刺激后的腹壁肌放电次数(415±212、1490±227、2129±435、2381±399)明显高于SD组,且疼痛感觉压力阈值显著降低(P＜0.05);(3)SD组REM睡眠剥夺48 h后,丘脑及肠道中MAO-A mRNA的水平明显低于YC组(P＜0.05),而TH mRNA的表达显著增高(P＜0.05).结论 REM睡眠剥夺降低大鼠的内脏感觉功能与NE合成增加及代谢减少有关,α2受体拮抗剂可提高大鼠的内脏感觉功能.     

内源性阿片肽系统在快眼动睡眠剥夺所致大鼠内脏感觉降低中的作用

背景：内脏感觉过敏是功能性胃肠病的重要病理生理机制之一。快动眼（REM）睡眠剥夺可降低大鼠内脏感觉，但具体机制不清。目的：研究内源性阿片肽系统是否参与构成REM睡眠剥夺所致大鼠内脏感觉降低的机制。方法：24只雄性Sprague-Dawley大鼠随机分为实验对照组、睡眠剥夺组和睡眠剥夺加阿片受体拮抗剂纳洛酮干预组（纳络酮组）。采用花瓶技术制作REM睡眠剥夺大鼠模型。睡眠剥夺持续48h后行结直肠扩张，记录腹壁肌电图，观察疼痛感觉阈值。以反映内脏感觉功能的变化。采用逆转录聚合酶链反应（RT-PCR）测定大鼠结直肠和丘脑阿片受体恤、KmRNA表达的变化。结果：给予不同压力扩张刺激后，睡眠剥夺组腹外斜肌放电次数显著低于实验对照组，疼痛感觉阈值高于实验对照组（P〈0．05）；纳洛酮组放电次数显著高于睡眠剥夺组，疼痛感觉阈值低于睡眠剥夺组（P〈0．05），与实验对照组相比则均无显著差异。与实验对照组相比，睡眠剥夺组结直肠阿片受体KmRNA表达上调（P〈0．05），丘脑K受体mRNA表达无明显变化。上述部位μ受体mRNA表达均无明显变化。结论：REM睡眠剥夺降低大鼠内脏感觉的作用与内源性阿片肽和阿片受体K表达上调有关。     

外周内源性大麻素系统在快眼动睡眠剥夺所致大鼠内脏感觉降低中的作用

背景：内脏感觉过敏是功能性胃肠病的重要病理生理机制之一．快眼动（REM）睡眠剥夺可降低大鼠内脏感觉,但具体机制尚不明。目的：研究外周内源性大麻素系统在REM睡眠剥夺所致大鼠内脏感觉降低中的作用。方法：24只雄性Sprague—Dawley大鼠随机分为实验对照组、睡眠剥夺组和利莫那班干预组。采用花瓶技术制作REM睡眠剥夺大鼠模型。睡眠剥夺48h后行结直肠扩张（CRD）,记录腹壁肌电图,以反映内脏感觉功能的变化。采用逆转录聚合酶链反应（RT—PCR）和蛋白质印迹法分别测定大鼠肠道组织中1型大麻素（CBl）受体、脂肪酰胺水解酶（FAAH）和单酰基甘油脂酶（MAGL）mRNA和蛋白表达。结果：予不同扩张压力（40、60和80mmHg）后,睡眠剥夺组大鼠腹外斜肌放电次数显著低于实验对照组（P〈0．05）;利莫那班干预组放电次数显著高于睡眠剥夺组（P〈0．05）,但与实验对照组无明显差异。与实验对照组相比,睡眠剥夺组大鼠肠道CB1受体mRNA表达上调（P〈0．05）,结肠FAAH和MAGLmRNA和蛋白表达显著下调（P〈0．05）。结论：REM睡眠剥夺降低大鼠内脏感觉的作用与外周内源性大麻素代谢降低有关。     

急性和慢性束缚应激对大鼠内脏敏感性的影响

目的了解急性和慢性求缚应激对大鼠内脏敏感性的影响和持续时间。方法成年SD大鼠随机分为3组：对照组（没有束缚应激），急性部分束缚应激组（单次2h的束缚应激）和慢性部分束缚应激组（连续束缚应激3天，每天2h），通过腹壁回撤反应（AWR）评分评估应激前后不同时间点大鼠对结直肠扩张（CRD）的内脏敏感性。结果①在扩张压力20mmHg和40mmHg时，急慢性束缚应激组的AWR评分均显著高于应激前基础水平（Od）（P〈0．05），但在60，80mmHg压力时各组的AWR评分均无显著差异；②急性束缚组在应激后24h和应激后第7天，AWR评分显著下降（P〈0．05）；③慢性束缚组在末次应激后24h，AWR评分仍维持增高水平，但在第7天时AWR评分回到基础水平。结论急性和慢性束缚应激郜可以导致大鼠内脏敏感性增高，但其作用可能是短暂的。     

快速眼动睡眠剥夺及恢复睡眠对大鼠海马和皮质神经元型一氧化氮合酶mRNA表达的影响

目的研究快速眼动(REM)睡眠剥夺和睡眠恢复对大鼠海马及皮质区神经元型一氧化氮合酶(nNOS)转录水平表达的影响。方法将大鼠分为两组,分别为REM睡眠剥夺组(SD组)和对照组(空白对照组:CC组和环境对照组:TC组)采用改良多平台睡眠剥夺法建立大鼠REM睡眠剥夺模型,获取海马及皮质组织,采用半定量逆转录-聚合酶链式反应(RT-PCR),测定REM睡眠剥夺13、、5及7天、恢复睡眠6、12、24及48 h大鼠皮质、海马nNOS mRNA的表达。结果CC组和TC组海马及皮质nNOS mRNA表达无显著性差异。REM睡眠剥夺1天和3天组nNOS mRNA表达增多,睡眠剥夺5天组nNOS mRNA表达明显升高,睡眠剥夺7天组nNOS mRNA达到峰值(0.691±0.008,P<0.01),睡眠恢复后6 h、12 h和24 h组nNOS mRNA表达仍高于TC组。结论大鼠REM睡眠剥夺增加皮质、海马nNOS mRNA的表达。     

中枢5-羟色胺系统在快速动眼期睡眠剥夺导致大鼠内脏感觉降低中的作用

我们既往的研究证实睡眠剥夺导致大鼠内脏感觉降低，但机制尚不清楚。5-羟色胺（5-HT）是一种与睡眠密切相关的神经递质，同时中枢5-HT系统作为下行抗伤害性作用的主要神经递质之一，在内脏感觉敏感性的调节方面起着重要作用。本实验选取5-HT1A受体及5-HT特异性转运体（SERT）作为反映中枢5-HT系统功能的指标。通过比较睡眠剥夺大鼠和睡眠剥夺加中枢给予5-HT受体拮抗剂二甲麦角新碱干预大鼠的内脏感觉，来证实睡眠剥夺降低内脏感觉敏感性和中枢5-HT系统之间的关系。另通过观察5-HT1A受体和SERT在不同部位的表达变化来反映快速动眼期（REM）睡眠剥夺后中枢5-HT系统的改变。     

丁酸钠溶液灌肠对大鼠内脏感觉的影响

对于肠易激综合征（IBS）内脏感觉功能异常的研究，需建立合适的动物模型。目的：以丁酸钠溶液灌肠建立大鼠结肠感觉过敏模型，观察其内脏感觉功能和结肠黏膜改变。方法：16只大鼠随机分为实验组和对照组。实验组予1 ml 200mmol／L丁酸钠溶液灌肠，对照组予1 ml 0.9％NaCl溶液灌肠，每天2次，连续3d。分别于灌肠前和实验开始后第3、6、9、12、15、18d行结直肠扩张（CRD），观察腹壁回撤反射（AWR）评分和内脏感觉压力闽值，以反映内脏感觉功能。实验结束后处死大鼠，行结肠黏膜大体形态观察和组织学检查。结果：实验第3-12d．实验组不同CRD压力下AWR评分均显著高于对照组（P〈0.05），疼痛感觉压力阈值显著低于对照组（P〈0.05）；第15-18d，上述指标恢复至初始状态。实验结束后,实验组与对照组结肠黏膜大体形态和组织学改变均无明显差异。结论：丁酸钠溶液反复灌肠可诱导大鼠结肠感觉过敏，内脏感觉功能恢复后，结肠黏膜改变同步恢复。该模型可用于IBS病理生理机制的研究。     

替加色罗对内脏感觉过敏大鼠模型的抗伤害性感觉作用

目的　了解结直肠机械刺激对大鼠内脏感觉功能的影响以及替加色罗对大鼠内脏感觉功能的调节作用。方法　 8～ 2 1日龄大鼠每天行结直肠扩张 (CRD组 ,压力 6 0mmHg) ,对照组仅用导管在肛门周围轻微接触。 8～ 1 0周龄时用自制气囊扩张大鼠降结肠和直肠 ,观察动物的腹壁回撤反射(AWR)以测定内脏感觉。选取 8～ 1 0周龄的雄性大鼠分为CRD组、对照组和溶媒对照组 ,观察腹腔注射替加色罗前后的AWR评分。结果　扩张压力与AWR评分显著相关 (P <0 .0 1 ) ;CRD组在 4 0、6 0、80mmHg的压力扩张下 ,AWR评分明显高于对照组 (1 .96± 0 .1 6比 1 .36± 0 .1 6、2 .82± 0 .1 3比 2 .1 7± 0 .1 4、3.2 1± 0 .1 4比 2 .5 9± 0 .1 4 ,P <0 .0 1 ) ;在 4 0、6 0、80mmHg扩张压力下 ,CRD组的AWR评分在用替加色罗后较用药前明显降低 (1 .95± 0 .5 0比 1 .32± 0 .5 5、3.0 5± 0 .4 8比 2 .32± 0 .5 4、3.2 5± 0 .6 3比 2 .77± 0 .5 1 ,P <0 .0 5 ) ;对照组和溶媒对照组的AWR评分在用药前后差异无显著性。结论　新生大鼠给予结直肠机械刺激在成年后可导致慢性内脏感觉过敏 ;替加色罗通过提高对结直肠扩张的疼痛阈值 ,具有抗伤害性感觉作用     

快速眼动睡眠剥夺后大鼠皮质及海马神经元突触相关蛋白神经颗粒素表达的变化

目的:探讨不同时间的快速眼动(REM)睡眠剥夺对大鼠皮质及海马各区神经颗粒素分子表达变化的影响及意义。方法:Sprague-Dawley大鼠70只,随机分为睡眠剥夺组(SD)、实验环境对照组(TC)和空白对照组(CC)。其中SD组又分为12h、1d、3d、5d、7d共5个时点组。采用改良多平台(MMPM)睡眠剥夺法进行REM睡眠剥夺,运用免疫荧光染色共聚焦显微镜观察REM睡眠剥夺后不同时点大鼠皮质及海马各区的神经颗粒素表达的分布规律和时空变化;同时结合蛋白印迹(Western blot)技术对皮质及全海马神经颗粒素蛋白作选择性半定量分析。结果:神经颗粒素主要分布于正常大脑皮质Ⅱ、Ⅲ层的神经元胞体和树突、海马CA1～CA3锥体细胞层和齿状回颗粒细胞层内。REM睡眠剥夺12h后大鼠皮质神经颗粒素的表达即开始减少,与对照组比较有显著性差异,直至第7d均呈下降趋势;海马结构中神经颗粒素表达未见显著变化。蛋白印迹实验印证了这一结果。结论:REM睡眠剥夺能引起大鼠大脑皮质神经颗粒素表达减少,且随睡眠剥夺时间的延长而渐趋明显,这可能是REM睡眠剥夺引起大脑神经元突触可塑性改变,进而影响大鼠学习记忆功能损害的机制之一。     

焦虑大鼠内脏敏感性增高以及行直结肠扩张后血清皮质酮的变化及意义

目的内脏高敏感性是肠易激综合征( 1BS)症状最重要的病理生理机制之一,焦虑可能与内脏高敏的发生密切相关。本研究旨在探讨焦虑对大鼠直结肠敏感性的作用以及血清皮质酮与内脏高敏的关系。方法Wistar大鼠随机分为对照组和焦虑组两组,通过对大鼠行空瓶刺激2周建立以焦虑为主要表现的慢性情绪应激模型。造模期间,观察大鼠的攻击、探究和修饰三种行为,对其进行情绪性行为学分析。造模结束后,以腹部回缩反射(AWR)评分为指标观察大鼠对直结肠气囊扩张(CRD)的反应性,评估内脏敏感性。然后将两组各随机分为扩张组和非扩张组,对扩张组行CRD ,并取血清,对血清皮质酮定量测定。结果空瓶刺激期间,同对照组相比,焦虑组探究、攻击行为明显增多,修饰行为减少(P <0 0 1)。焦虑组在2 0mmHg、40mmHg、60mmHg和80mmHg的扩张压力下的AWR评分均显著高于对照组(P <0 0 1)。焦虑组与对照组相比血清皮质酮水平明显升高(P <0 0 1) ,但各组扩张后皮质酮水平较扩张前仅有轻微升高,无显著差异(P >0 0 5 )。结论焦虑对IBS内脏高敏起一定作用,其发挥作用的机制可能并非单一通过下丘脑_垂体_肾上腺皮质系统(HPA轴)来实现,推测还可能与脑内单胺类神经递质NE浓度的改变有关。     

ZD 7288,an HCN channel blocker,attenuates chronic visceral pain in irritable bowel syndrome-like rats

AIM:To investigate the effects of ZD 7288,a hyperpolarization-activated cyclic nucleotide-gated(HCN)channel blocker,on rats with chronic visceral pain.METHODS:Rats with visceral hypersensitivity were generated using neonatal colon irritation during postnatal days 8-15 as described previously.Visceral hypersensitivity was evaluated using electromyographic(EMG)responses of abdominal external oblique muscles to 20-80 mmHg colorectal distentions(CRD).Abdominal withdrawal reflex(AWR)scores and pain thresholds were also detected in adult rats.Different doses of ZD7288(25,50,and 100 nmol/L)were intrathecally administered in rats to study the role of spinal HCN channel in chronic visceral hypersensitivity.RESULTS:EMG responses to 20-80 mmHg CRD and AWR scores under 20-60 mmHg CRD significantly increased in rats with visceral hypersensitivity compared to control rats(P<0.05).The pain threshold in rats with visceral hypersensitivity significantly decreased compared to control rats(P<0.05).Treatment with50-100 nmol/L ZD 7288 significantly inhibited EMG responses(16%-62%,80-20 mmHg CRD,P<0.05)and AWR scores(24%-37%,40-20 mmHg CRD,P<0.05;12%-61%,80-20 mmHg CRD,P<0.05,respectively),and significantly increased pain thresholds(32%-77%,P<0.05).CONCLUSION:Spinal HCN channels may play an important role in chronic visceral hypersensitivity.     

Establishment of model of visceral pain due to colorectal distension and its behavioral assessment in rats

AIM: To establish a visceral pain model via colorectal distension (CRD) and to evaluate the efficiency of behavioral responses of CRD by measuring the score of abdominal withdrawal reflex (AWR) in rats. METHODS: Thirty-eight male SD rats weighing 180-240g were used to establish the visceral pain model. The rat was inserted intra-anally with a 7 cm long flexible latex balloon under ether anesthesia, and colorectal distensions by inflating the balloon with air were made 30 min after recovering from the anesthesia. Five AWR scores (AWRO to AWR4) were used to assess the intensity of noxious visceral stimuli. It was regarded as the threshold of the minimal pressure (kPa). For abdominal flatting was induced by colorectal distension. RESULTS: A vigorous AWR to distension of the descending colon and rectum was found in 100% of the awake rats tested. The higher the pressure of distension, the higher the score of AWR. The distension pressures of 0, 2.00, 3.33, 5.33 and 8.00 kPa produced different AWR scores (P<0.05). The pain threshold of AWR was constant for up to 80 min after the initial windup (first 1-3 distensions), the mean threshold was 3.69±0.35 kPa. Systemic administration of morphine sulfate elevated the threshold of visceral pain in a dosedependent and naloxone reversible manner. CONCLUSION: Scoring the AWR during colorectal distensions can assess the intensity of noxious visceral stimulus. Flatting of abdomen (AWR 3) to CRD as the visceral pain threshold is clear, constant and reliable. This pain model and its behavioral assessment are good for research on visceral pain and analgesics.     

金荞麦提取物对IBS大鼠脊髓镇痛的干预机制

目的:观察金荞麦(Fagopyrumcymosum,Fag)提取物对肠易激综合征(irritablebowelsyndrome,IBS)样结肠刺激(colonirritation,CI)模型内脏高敏感性的改善作用以及对动物脊髓背角内5-HT及其受体的影响.方法:采用结肠刺激新生期乳大鼠来制作IBS样CI模型.CI大鼠成年后给予口服Fag2wk,并用腹壁撤退反射(AWR)评分来评价给药后CI大鼠内脏高敏感性的变化,取大鼠脊髓用免疫组织化学法观察5-HT免疫染色,用蛋白印迹法检测5-HT1A受体(5-HT1AR)、5-HT3A受体(5-HT3AR)表达.结果:和对照组比,CI组大鼠AWR评分明显增高(20mmHg:0.625±0.518vs1.333±0.778;30mmHg:0.750±0.463vs1.667±0.888;40mmHg:1.125±0.641vs2.000±0.739;50mmHg:1.500±0.926vs2.583±0.793;60mmHg:2.125±0.991vs3.083±0.669;均P<0.05);且脊髓内5-HT染色度增加(11.250±4.833vs21.125±7.827,P<0.01),5-HT3A受体表达升高(179.038±29.786,P<0.01),5-HT1A受体则表达降低(64.523±16.873,P<0.01);高剂量Fag可降低CI大鼠AWR评分(20mmHg:0.250±0.002;30mmHg:0.875±0.044;40mmHg:1.250±0.036;50mmHg:1.875±0.050;60mmHg:2.625±0.037;均P<0.05),并下调脊髓内5-HT(13.375±5.579,P<0.05)和5-HT3AR的表达(114.200±20.983,P<0.05),上调5-HT1AR的表达(93.008±13.523,P<0.05);低剂量Fag则对CI大鼠的影响不明显.结论:Fag对IBS样CI大鼠有镇痛作用,并通过调节其脊髓内5-HT及其受体来改善痛觉过敏.     

Electroacupuncture alleviates stress-induced visceral hypersensitivity through an opioid system in rats

AIM:To investigate whether stress-induced visceral hypersensitivity could be alleviated by electroacupuncture(EA) and whether EA effect was mediated by endogenous opiates.METHODS:Six to nine week-old male SpragueDawley rats were used in this study.Visceral hypersensitivity was induced by a 9-d heterotypic intermittent stress(HIS) protocol composed of 3 randomly stressors,which included cold restraint stress at 4?℃ for 45 min,water avoidance stress for 60 min,and forced swimming stress for 20 min,in adult male rats.The extent of visceral hypersensitivity was quantified by electromyography or by abdominal withdrawal reflex(AWR) scores of colorectal distension at different distention pressures(20 mmHg,40 mmHg,60 mmHg and 80 mmHg).AWR scores either 0,1,2,3 or 4 were obtained by a blinded observer.EA or sham EA was performed at classical acupoint ST-36(Zu-San-Li) or BL-43(Gao-Huang) in both hindlimbs of rats for 30 min.Naloxone(NLX) or NLX methiodide(m-NLX) was administered intraperitoneally to HIS rats in some experiments.RESULTS:HIS rats displayed an increased sensitivity to colorectal distention,which started from 6 h(the first measurement),maintained for 24 h,and AWR scores returned to basal levels at 48 h and 7 d after HIS compared to pre-HIS baseline at different distention pressures.The AWR scores before HIS were 0.6 ± 0.2,1.3 ± 0.2,1.9 ± 0.2 and 2.3 ± 0.2 for 20 mmHg,40 mmHg,60 mmHg and 80 mmHg distention pressures,respectively.Six hours after termination of the last stressor,the AWR scores were 2.0 ± 0.1,2.5 ± 0.1,2.8 ± 0.2 and 3.5 ± 0.2 for 20 mmHg,40 mmHg,60 mmHg and 80 mmHg distention pressures,respectively.EA given at classical acupoint ST-36 in both hindlimbs for 30 min significantly attenuated the hypersensitive responses to colorectal distention in HIS rats compared with sham EA treatment [AWRs at 20 mmHg:2.0 ± 0.2 vs 0.7 ± 0.1,P = 4.23 711 E-4;AWRs at 40 mmHg:2.6 ± 0.2 vs 1.5 ± 0.2,P = 0.00 163;AWRs at 60 mmHg:3.1 ± 0.2 vs 1.9 ± 0.1,P = 0.003;AWRs at 80 mmHg:3.6 ± 0.1 vs 2.4 ± 0.2,P = 0.0023;electromyographic(EMG) at 20 mmHg:24 ± 4.7 vs 13.8 ± 3.5;EMG at 40 mmHg:60.2 ± 6.6 vs 30 ± 4.9,P = 0.00 523;EMG at 60 mmHg:83 ± 10 vs 39.8 ± 5.9,P = 0.00 029;EMG at 80 mmHg:94.3 ± 10.8 vs 49.6 ± 5.9,P = 0.00 021].In addition,EA at the acupuncture point BL-43 with same parameters did not alleviate visceral hypersensitivity in HIS rats.EA in healthy rats also did not have any effect on AWR scores to colorectal distention at distention pressuresof 20 and 40 mmHg.The EA-mediated analgesic effect was blocked by pretreatment with NLX in HIS rats [AWR scores pretreated with NLX vs normal saline(NS) were 2.0 vs 0.70 ± 0.20,2.80 ± 0.12 vs 1.50 ± 0.27,3 vs 2.00 ± 0.15 and 3.60 ± 0.18 vs 2.60 ± 0.18 for 20 mmHg,40 mmHg,60 mmHg and 80 mmHg;P = 0.0087,0.0104,0.0117 and 0.0188 for 20,40,60 and 80 mmHg,respectively].Furthermore,EA-mediated analgesic effect was completely reversed by administration of m-NLX,a peripherally restricted opioid antagonist(EMG pretreated with m-NLX vs NS were 30.84 ± 4.39 vs 13.33 ± 3.88,74.16 ± 9.04 vs 36.28 ± 8.01,96.45 ± 11.80 vs 50.19 ± 8.28,and 111.59 ± 13.79 vs 56.42 ± 8.43 for 20 mmHg,40 mmHg,60 mmHg and 80 mmHg;P = 0.05 026,0.00 034,0.00 005,0.000 007 for 20 mmHg,40 mmHg,60 mmHg and 80 mmHg,respectively).CONCLUSION:EA given at classical acupoint ST-36 alleviates stress-induced visceral pain,which is most likely mediated by opioid pathways in the periphery.