胃电刺激对大鼠胃扩张反应神经元及增食欲素的影响

目的:观察胃电刺激(GES)对大鼠下丘脑腹内侧区(VMH)胃扩张(GD)相关神经元的作用及脑内增食欲素(orexin)表达的影响,初步探讨 GES的中枢作用机制．方法:选用成年Wistar大鼠52只,采用细胞外记录神经元单位放电方法,记录VMH神经元自发放电活动,根据神经元对胃扩张刺激反应的不同,分为胃扩张兴奋性神经元(GD-E) 和胃扩张抑制性神经元(GD-I)．观察3组不同参数的胃电刺激(GES1,GES2,GES3)对VMH 内GD-E和GD-I放电频率的影响:GES1(6 mA, 0．3 ms,40 Hz,2 s-on,3 s-off)为标准参数; GES2的串刺激持续时间减少为0．1 s:GES3的串刺激频率减少至20 Hz,其他参数均同GES1．采用免疫荧光组织化学染色方法和放射免疫分析法观测胃电刺激2 h对大鼠下丘脑外侧区 (LHA)增食欲素-A(orexin-A)阳性神经元和不同脑orexin含量表达的影响．结果:VMH记录的96个神经元中有82个神经元(85．41％)对胃扩张刺激(GD,3-5 mL, 10-30 s)有反应,其中31个(37．8％)为胃扩张兴奋性(GD-E)神经元,51个(62．2％)为胃扩张抑制性(GD-I)神经元．GES1,2,3分别兴奋了 55．0％,17．6％,14．3％的GD-E神经元．GES1对 GD-E神经元的作用明显强于GES2和GES3 (P=0．002,P=0．016)．63．6％,37．9％和51．9％的GD-I神经元分别被GES1,2,3所兴奋,其中 GES2的兴奋作用较弱(P=0．043)．GES1刺激胃窦部2 h,下丘脑LHA orexin-A免疫阳性神经元表达明显减少(6．97±1．51/0．1 mm2 vs 26．62 ±8．30/0．1 mm2,P<0．01):且下丘脑、中脑、延脑和孤束核中orexin免疫反应物(IR)的含量与对照组相比明显减少(112．54±11．58 fmol/ mg vs 185．23±15．22 fmol/mg,P<0．01:71．95 ±8．45 fmol/mg vs 98．48±12．02 fmol/mg． P<0．05;72．36±6．58 fmol/mg vs 101．29± 15．22 fmol/mg．P<0．05;69．12±4．99 fmol/mg vs 89．21±9．23 fmol/mg,P<0．05),但脑桥内 orexin-IR的含量与对照组相比无显著差异．结论:GES可兴奋下丘脑“饱中枢”-VMH内胃扩张反应性神经元,电刺激作用的强弱与 GES刺激的频率和刺激的持续时间有关:脑内 orexin的降低可能也参与了GES的中枢作用机制．     

食欲素受体通路干预海马神经元放电研究

目的采用膜片钳技术研究食欲素受体(OxR)通路对海马CA1区锥体神经元放电的影响。方法将Wistar大鼠取脑,急性分离单个CA1区锥体神经元。选140例神经元,用膜片钳技术记录电活动,根据神经元自身放电频率分为低频和高频,神经元分别用人工脑脊液(低频对照组60例和高频对照组22例),食欲素A受体激动剂(O6012 200nmol/L,低频实验组48例和高频实验组10例),O6012 200nmol/L和选择性OxR1拮抗剂SB334867混合液(低频拮抗组7例和高频拮抗剂组1例)刺激,观察低频实验组28例和高频实验组4例给药前、给药期间和停止给药的电活动变化。结果低频实验组激活58.3%神经元,给药期间神经元放电频率明显高于给药前(5.36±4.01Hz vs 1.43±0.88Hz,P0.05);停止给药后与给药期间和给药前放电频率比较,无统计学差异(P0.05)。高频组激活40.0%神经元,给药期间神经元放电频率明显高于给药前[(6.98±2.45)Hz vs(4.93±2.55)Hz,P0.05],停止给药后与给药期间比较放电频率显著减少(P0.05),停止给药后与给药前比较,无统计学差异(P0.05)。结论海马CA1区锥体神经元上可能存在OxR;激活OxR可兴奋神经元,并介导某些神经活动。     

电针足三里在血容量失血大鼠口服补液时对胃排空率、血浆一氧化氮及胃动素的影响

目的:研究电针足三里对40%血容量失血大鼠早期口服葡萄糖-电解质液(GES)时胃排空率、血浆一氧化氮(NO)及胃动素(MTL)的影响.方法:♂SD大鼠24只,随机分为假手术+口服GES组(GES组,n = 8)、失血+口服GES+电针足三里组(H+GES/EA,n = 8)、失血+口服GES+非经非穴组(H+GES/SEA,n = 8).用氯胺酮-速眠新Ⅱ肌注复合麻醉后,行右侧颈总动脉插管,按全身血容量的40%分两次间隔15min放血制作失血性休克模型,GES组不予放血.于失血后0.5 h及1 h分两次灌胃给予总计2倍失血量的GES.H+GES/EA组和H+GES/SEA组大鼠用自制布袋固定,于第2次灌胃后在清醒状态下电针刺激足三里穴(频率2-100 HZ,强度2-3 mA,时间1 h)和非经非穴处皮肤(足三里外侧旁开0.5 cm,频率2-100 HZ,强度2-3mA,时间1 h).失血后4 h腹主动脉抽血处死动物,酚红法测定胃排空率,检测血浆NO和MTL水平.结果:失血后4 h,H+GES/EA组胃排空率比H+GES/SEA组提高了21.6%,比GES组降低了17.6%( P<0.05).H+GES/EA组血浆NO水平显著低于H+GES/SEA组(90.2±8.3 vs 103.9±12.5,P<0.05),而显著高于GES组(90.2±8.3 vs 53.6±6.9,P<0.01);MTL含量显著高于H+GES/SEA组(101.3±18.7 vs 73.7±14.1,P<0.01),而显著低于GES组(101.3±18.7 vs132.26±24.1,P<0.01).结论:电针足三里能显著降低血浆NO水平,提高MTL含量,改善40%血容量失血大鼠早期口服补液时胃排空率.     

山楂叶总黄酮对慢性脑缺血大鼠轴突过度再生抑制因子A及其受体表达的影响

目的探讨山楂叶总黄酮对慢性脑缺血大鼠的轴突过度神经再生抑制因子A(neurite outgrowth inhibitor,NogoA)及NogoA受体(NgR1)表达的影响。方法 SPF级雄性成年SD大鼠48只,随机分为假手术组、模型组、山楂叶总黄酮组[山楂叶总黄酮140mg/(kg·d)]、银杏叶片组[银杏叶提取物65mg/(kg·d)],每组12只,后3组采用双侧颈总动脉永久性结扎法制备慢性脑缺血模型后第30天开始灌胃,连续30d。HE染色观察海马CA1区神经元形态和密度;Western blot法和免疫组织化学法分别检测NogoA和NgR1蛋白表达。结果与模型组比较,山楂叶总黄酮组大鼠NogoA蛋白[(18.3±0.54)×10-3 vs(46.3±5.81)×10-3,P<0.01]和NgR1蛋白(0.68±0.08 vs 0.82±0.15,P<0.05)表达明显降低,分别降低了(38.88±9.22)%和(17.07±5.34)%;海马CA1区神经元密度显著增加[(20.28±4.68)个/mm2 vs(15.47±5.61)个/mm2,P<0.05]。山楂叶总黄酮组NogoA蛋白与银杏叶片组比较无显著差异(P>0.05),2组海马CA1区神经元密度[(20.28±4.68)个/mm2 vs(21.62±4.24)个/mm2]也无统计学差异(P>0.05)。结论山楂叶总黄酮对慢性脑缺血大鼠的神经功能具有保护作用,其机制可能与下调NogoA和NgR1蛋白表达,促进中枢神经再生有关。     

羟基积雪草苷干预神经元退变的机制研究

目的 探讨羟基积雪草苷(madecassoside,MC)对慢性铝中毒所致小鼠海马神经元损伤的干预作用及机制.方法 按葡萄糖酸铝(400mg AI3+kg)给予NIH小鼠灌胃90d建立铝中毒神经元损伤小鼠模型.通过跳台和Moms水迷宫实验、生化实验、HE染色和免疫组化染色技术,观察MC大小剂量(每天30、60mg/kg)同步给药90d对小鼠学习记忆能力、脑丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性、海马神经元病理形态学、海马Caspase-3和cox-2蛋白表达的影响.结果 与模型组相比,30和60mg/kg剂量MC可明显延长铝中毒小鼠跳台潜伏期(31.40±22.04 vs 124.10±74.38和138.80±90.85)(P＜0.05),减少跳台错误次数(3.00±1.15 vs 1.60±0.69和1.40±0.84)(P＜0.05),缩短第5天寻找平台潜伏期(36.2±11.2 vs 18.5±7.3和19.4±9.9)(P＜0.05)的时间;明显减少脑内MDA含量(nmol/mg prot)(3.73±0.38 vs 2.50±0.42和2.59±0.47)(P＜0.05),提高脑内SOD酶活性(U/mg prot)(362.8±37.6 vs 445.7±23.9和425.5±38.8);大小剂量的MC均能明显减轻铝中毒小鼠海马神经元损伤,下调海马神经元Caspase-3(0.255±0.079 vs 0.090±0.026和0.132±0.049)(P＜0.05)和COX-2(0.099±0.006 vs 0.038±0.004和0.045±0.008)(P＜0.05)蛋白表达.结论 MC可通过提高抗氧化应激、阻遏神经元凋亡和抗炎作用,减轻海马神经元损伤.     

卡巴胆碱对烫伤大鼠口服补液时小肠TNF-α及水通道蛋白-1的影响

目的:研究拟胆碱药卡巴胆碱对烫伤大鼠口服补液时小肠TNF-α及水通道蛋白-1(AQP-1)表达的影响.方法:♂Wistar大鼠50只,随机分为假烫(N)、单纯烫伤(S)、肠内葡萄糖-电解质液(GES)、肠内卡巴胆碱组(CAR)和肠内葡萄糖-电解质液 卡巴胆碱组(GES/CAR)5组(n=10).大鼠背部用沸水造成35%TBSA烫伤.N,GES和GES/CAR组于伤后30 min开始补液.免疫组化法测定肠组织AOP-1的表达,ELISA法检测肠组织TNF-α含量,酚红法测定大鼠小肠对水的吸收率.结果:S组大鼠小肠AQP-1与N组比明显降低(90.3±1 8.4 vs 4851.6±654.5,P<0.01);CAR,GES和GES/CAR组AQP-1与S组相比均显著增加(1806.1±110.1,2272.3±113.8,3322.0±595.9 vs 90.3±18.4.均P<0.01).给予卡巴胆碱组(CAR,GES/CAR)与未给予卡巴胆碱组(S,GES)相比肠组织TNF-α含量明显下降(0.9±0.3,1.0±0.47 vs 1.8±0.3,1.9±0.2,P<0.05).GES/CAR,CAR及S组AOP-1表达量与TNF-α含量成负相关(r=-0.9030,-0.9602,-0.9866,均P<0.05).GES/CAR组水吸收率较GES组明显升高(21.0%±0.1%vs 12.7%±0.1%,P<0.05).结论:卡巴胆碱可抑制促炎因子TNF-α的释放,上调小肠AQP-1表达,改善大鼠烫伤早期肠道对水的吸收.     

脂联素对心脏神经节丛的影响

目的探究脂联素对心脏神经节丛(GP)的影响。方法 12只成年雄性比格犬随机分为实验组(n=6)和对照组(n=6)。3%戊巴比妥钠全身麻醉后经右侧开胸暴露心脏右前神经节丛(ARGP),实验组将0.1 mL脂联素(0.1 mg/mL)注射至ARGP,对照组注入等量生理盐水。分别于基础状态和注射后20 min测定ARGP功能和神经活性。其中,电压递增式高频电刺激ARGP引起窦性心率(SR)下降的程度反映ARGP功能。使用微电极记录ARGP神经元放电频率和振幅以反映ARGP神经活性。实验结束后留取ARGP组织行免疫荧光染色以检测神经元上脂联素受体的表达情况。结果免疫荧光显示ARGP神经元上存在脂联素受体1和脂联素受体2表达。实验组给予脂联素后可显著减轻不同电压下刺激ARGP引起的SR下降[2 V:(23.3±4.3)%vs(14.4±5.6)%;3 V:(43.3±5.1)%vs(30.9±5.1)%;4 V:(57.3±5.2)%vs(47.9±8.0),P均<0.05]。给予脂联素后神经元放电频率[(40±5) impulses/min vs (32±3) impulses/min,P<0.05]和振幅[(0.036±0.006) mV vs (0.026±0.004)mV,P<0.05]均下降。对照组干预前后各指标无显著差异。结论脂联素可抑制心脏神经节丛功能和活性。     

血容量失血40%大鼠早期口服补液时胃排空率的变化及其影响因素

目的:观察40%血容量失血大鼠模型早期口服补液时胃排空(GE)率的变化及其与血浆一氧化氮(NO)、胃动素(MTL)水平的关系.方法:♂ SD大鼠24只,随机分为假手术 葡萄糖-电解质溶液(GES)组(GES组,n=8)、单纯失血组(H组,n=8)、失血 GES组(H GES组,n=8).氯胺酮-速眠新Ⅱ肌注复合麻醉发后,行右侧颈总动脉插管,H组和H GES组按全身血容量的40%分2次间隔15 min放血,GES组不予放血.GES组和H GES组大鼠在手术或失血后0.5 h及1 h分2次灌胃给予总计2倍预计放血量的GES.失血后4 h腹主动脉取血处死动物,检测血浆NO和MTL水平,酚红法测定胃排空率.结果:失血后4 h H GES组胃排空率显著低于GES组(62.4%±11.4% VS 92.4%±12.5%,P＜0.01).H GES组血浆NO水平显著高于GES组与H组(105.7±13.2 μmol/L VS 53.6±6.9μmol/L,75.4±10.5 μmol/L,均p＜0.01),MTL含量显著低于GES组与H组(72.5±14.3 ng/L VS 132.3±24.1 ng/L,95.7±15.5 ng/L,均P＜0.01).胃排空率与血浆NO水平呈负相关,与MTL水平呈正相关(P＜0.01).结论:大鼠40%血容量失血早期口服补液时胃排空率降低,其机制可能为失血性休克时血浆NO水平升高,KMTL水平降低等因素有关.     

米诺环素对慢性脑低灌注大鼠海马神经元β位点剪切酶1和β淀粉样蛋白表达的影响

目的观察不同剂量米诺环素对慢性脑低灌注大鼠海马神经元β位点剪切酶1(BACE1)和β淀粉样蛋白(Aβ)表达的影响。方法选择SD大鼠144只,随机分为假手术组、对照组、慢性脑低灌注组(模型组)、米诺环素低剂量组、中剂量组、高剂量组,每组24只。采用双侧颈总动脉永久结扎建立大鼠慢性脑低灌注模型,低、中、高剂量组在慢性脑低灌注模型的基础上分别给予5mg/(kg·d)、50mg/(kg·d)、500mg/(kg·d)的米诺环素连续灌胃。观察时间点分别为造模后1、2、3个月,采用免疫组织化学法检测海马CA1区神经元BACE1和Aβ表达。结果模型组1、2、3个月BACE1和Aβ表达较假手术组、对照组、低剂量组、中剂量组、高剂量组明显增加(P<0.05)。高剂量组2、3个月BACE1表达较低剂量组明显降低[(1.40±1.77)个/视野vs(10.50±4.83)个/视野,(1.25±1.24)个/视野vs(12.35±2.57)个/视野,P<0.05],3个月BACE1表达较中剂量组明显降低[(1.25±1.24)个/视野vs(12.00±1.02)个/视野,P<0.05]。结论米诺环素能抑制慢性脑低灌注大鼠海马神经元BACE-1和Aβ表达,高剂量米诺环素对BACE-1抑制作用明显。     

电刺激小脑顶核对AD大鼠海马神经元c—Rel和Bcl—xl表达的影响

目的 研究电刺激小脑顶核(FNS)对阿尔茨海默病(AD)大鼠学习记忆能力及脑内海马神经元c-Rel和Bcl-xl表达的影响.方法 40只SD大鼠随机分成4组:Aβ1-40微量注射组(AD组)、假手术组(SC组)、Aβ1-40微量注射+电刺激小脑顶核组(FNS组)和Aβ1-40微量注射+电刺激齿状核组(DNS组),采用Morris水迷宫检测电刺激小脑顶核对AD大鼠认知功能的影响;通过HE染色、电镜观察电刺激小脑顶核对AD大鼠的海马神经元形态的影响;采用免疫组化法观察电刺激小脑顶核对AD大鼠海马神经元c-Rel和Bcl-xl的表达的影响.结果 与SC组比较,AD组、FNS组和DNS组每天隐匿平台逃避潜伏期明显延长(P＜0.05)、海马CA1区的Bcl-xl和c-Rel阳性细胞OD值差异显著(均P＜0.05); FNS组与AD组比较,大鼠每天逃避潜伏期明显缩短(P＜0.05),FNS组海马CA1区Bcl-xl和c-Rel阳性细胞OD值为(0.46±0.04、0.65±0.09),较AD组阳性细胞OD值明显增高(P＜0.05),但齿状核刺激(DNS)组与AD组比较大鼠每天逃避潜伏期和海马CA1区Bcl-xl和c-Rel阳性细胞OD值无显著差异(P＞0.05).结论 电刺激小脑顶核能通过增强C-Rel及Bcl-xl的表达,抑制海马神经元的凋亡,改善AD大鼠学习记忆能力.     

胃微生态与胃癌的研究进展

胃微生态平衡是人体健康的重要前提,幽门螺杆菌(Helicobacter pylori,Hp)是目前已发现的与胃癌相关的关键病原体之一,普遍存在于人胃黏膜上皮。Hp感染可引起胃内其他菌群的改变,还可引起长期慢性的胃黏膜损伤,导致一系列胃黏膜上皮恶性进展和胃癌的发生。本文就胃微生态与Hp感染的关系、Hp感染在胃癌发生中的作用、胃内其他菌群在胃癌发生中的作用及微生态制剂在胃癌治疗的作用进行综述。进一步揭示Hp感染对胃微生态平衡的影响,胃微生态平衡和Hp感染在胃癌发生发展中的作用及微生态制剂在胃癌治疗中的意义。     

The electrophoretic pattern of normal human gastric juice and of the gastric juice of patients with gastric ulcer and gastric cancer

This study reports the electrophoretic pattern of the proteins in human gastric juice of control patients and patients with gastric ulcer and gastric carcinoma. Autodigestion was prevented by intragastric neutralization. The statistical limits of normal are defined and the changes found in the gastric juice of gastric ulcer and gastric patients with gastric carcinoma described.     

胃起搏对胃动力紊乱犬胃排空及胃肌电活动的影响

目的　研究胃起搏对胃动力紊乱犬胃排空及胃电参数的影响。方法　采用双侧迷走神经干切断术联合应用胰高血糖素建立胃动力紊乱犬模型 ;采用 4导联胃肠电系统微机分析仪记录胃肠浆膜肌电活动 ;99mTc 植酸钠标记的半固体试餐 ,单光子计算机断层显像技术 (SPECT)检测胃半排空时间(GEt1/ 2 ) ;采用适宜起搏参数从胃体、胃窦在腹部投影部位输入起搏信号驱动胃电节律。结果　迷走神经干切断术后犬的GEt1/ 2 为 (79.4 2± 1.91)min ,较术前 (5 6 .35± 2 .99)min明显延迟 (P <0 .0 0 1) ,但行胃起搏治疗后GEt1/ 2 为 (6 4 .94± 1.75 )min ,较治疗前明显加快 (P <0 .0 0 1) ;胃起搏治疗前迷走神经干切断犬餐后的胃电频率为 (0 .0 81± 0 .0 0 7)Hz、胃电幅度为 (2 .32± 0 .35 )mV、慢波的传播速度为 (4 .0 6± 0 .4 0 )cm/s ,均较正常对照犬显著降低 [(0 .0 90± 0 .0 0 6 )Hz ,(4 .2 5± 0 .12 )mV ,(6 .92± 0 .2 4 )cm/s,(P <0 .0 5 ) ],治疗后其餐后胃电频率 (0 .0 92± 0 .0 0 5 )Hz、胃电幅度 (3.97± 0 .19)mV和慢波的传播速度 (5 .5 7± 0 .4 8)cm/s均明显高于治疗前 (P <0 .0 5 )。结论　采用适宜起搏参数输入起搏信号可完全触发胃电慢波 ,改善胃电参数 ,纠正药物导致的异常胃电节律 ,加速胃排空 ,恢     

Hemodynamics of the gastric mucosa and gastric ulceration in rats and in patients with gastric ulcer

The microcirculation is the fundamental nutrient supply and waste removal system of all tissues. Recent improvements in spectrophotometric technique have made possible the noninvasive assessment of oxygen supply and utilization in the gastric mucosa. The authors have utilized such methods to assess gastric mucosal hemodynamics. The technique permitted further clarification of the roles of the gastric microcirculation, mucosal oxygenation, and acid secretion in the pathogenesis of stress ulcers in the stomach of rats. Furthermore, it provided important information on the function of gastric mucosal hemodynamics in the healing of gastric ulcers in man. The technique is described along with the authors' correlation studies between spectrophotometric data and other techniques for measuring gastric blood flow (hydrogen gas clearance and aminopyrine clearance methods and direct electromagnetic flowmeter techniques) and the prevention of ulcerogenesis.     

Human gastric myoelectric activity and gastric emptying following gastric surgery and with pacing.

Postoperative gastric myoelectric activity, gastric emptying, and clinical course were correlated in 17 patients at high risk of developing gastroparesis after gastric surgery. In addition, an attempt was made to pace the stomach with an electrical stimulus and determine the effect of pacing on early postoperative gastric emptying. Gastric dysrhythmias (bradygastria, slow wave frequency < 2 cycles/min; tachygastria, slow wave frequency > 4 cycles/min) persisted beyond the first postoperative day in 6 patients (35%). Delayed gastric emptying was identified by a radionuclide meal in 15 patients (88%), but symptoms of gastroparesis developed in only 6 of 15 (40%). Patients with postoperative gastroparesis had more frequent dysrhythmias than asymptomatic patients (67% vs. 18%), but these differences were not significant, although we cannot exclude a type II statistical error. Gastric rhythm was entrained in 10 of 16 patients (63%). Pacing increased the gastric slow wave frequency (3.1 vs. 4.1 cycles/min; P < 0.01) but did not improve gastric emptying (gastric retention at 60 minutes, 86% +/- 6% for control and 90% +/- 2% for paced). In conclusion, gastric dysrhythmias do not appear to play a major role in the development of postsurgical gastroparesis. Although gastric rhythm could be entrained in the majority of patients, pacing did not improve gastric emptying overall.     

The relationship between gastric microbiota and gastric disease

Traditionally, the stomach was believed to be a sterile organ unsuitable for microbiota growth. However, the discovery of H. pylori subverted this conception. With the development of molecular techniques, an abundance of microbiota of great diversity was found in the stomach. In addition, various lines of evidence suggest that the gastric microbiota plays a critical role in the development and progression of the gastric disease.The gastrointestinal microbiome plays an important role in various physiologic and pathologic processes.     

Endoscopy,gastric ulcer,and gastric cancer

The practice of following benign-appearing gastric ulcers until healing was critically evaluated in a retrospective manner by reviewing all gastric ulcers that were followed with serial endoscopy and all gastric cancers diagnosed at the University of Alabama at Birmingham. The stated purpose of following ulcers to healing is to detect those gastric cancers that may be masquerading as benign ulcer and were not correctly diagnosed at initial endoscopy. Over a five-year period, 148 gastric ulcers were followed with serial endoscopy and in no case was an unsuspected carcinoma found at follow-up endoscopy. In addition, of 67 gastric cancers diagnosed between 1979 and 1986, 62 were suspected of being malignant by the endoscopist at initial examination for an accuracy of 92%. The accuracy rate based solely on biopsy and/or brush cytology was 94%. When endoscopic and biopsy and/or cytology impressions were combined, only one case of gastric carcinoma was not suspected. The overall accuracy was 99%. These results suggest that if either the endoscopic impression or the biopsy and cytology is suspicious for malignancy, then follow-up endoscopy until healing should be done. On the other hand, if, at the initial examination, the ulcer appears benign and biopsy plus cytology are negative, then serial endoscopy has a low benefit relative to its cost.     

Relationship between gastric mucosal hemodynamics and gastric motility

Continuous measurement of gastric mucosal hemodynamics (the index of mucosal hemoglobin concentration, the index of oxygen saturation and blood flow) in rats showed oscillatory changes. The mechanism of the oscillations was investigated using a probe specially designed for simultaneous measurement of hemodynamics and intragastric pressure. A hemodynamics-measuring probe for either reflectance spectrophotometry or laser-Doppler flowmetry was tied to a pressure microtransducer, inserted through an incision in the forestomach, and brought into gentle contact with the corpus mucosa. Synchronous oscillatory changes (4-6 cycles/min) in hemodynamics and motility were observed in the resting state (mean blood pressure: 120 mmHg). During moderate hemorrhagic hypotension (mean: 81 mmHg), oscillations in the hemodynamics increased in both amplitude and frequency, while motility remained constant. Oscillations in the hemodynamics were also affected by fluctuations in blood pressure and by topical application of norepinephrine to the corpus serosa. In water-immersion restraint rats, changes in the oscillations in the hemodynamics and motility were virtually synchronous; frequency decreased and amplitude increased. These findings suggest that oscillatory changes in gastric mucosal hemodynamics are regulated not only by gastric motility but also by arteriolar vasomotion of the gastric wall.