芦荟全汁对便秘小鼠结肠肌电生理变化的影响

目的 观察芦荟对便秘小鼠的结肠肌电生理变化的影响.方法 用复方地芬诺酯混悬液对小鼠进行灌胃建立便秘模型,后用芦荟全汁对小鼠进行灌胃,从而探讨芦荟全汁对便秘小鼠结肠肌电生理变化的影响.结果 三组小鼠的结肠慢波表现为近似于正弦波样曲线.对照组频率(43.52±0.71次/min),便秘组频率(47.80±2.66次/min),与对照组相比,便秘组小鼠的结肠慢波频率增快,两组相比较有极显著差异;芦荟组频率(44.45±1.31次/min),与便秘组相比,芦荟组小鼠的结肠慢波频率减慢(P＜0.01);与对照组相比,便秘组小鼠的结肠慢波频率变异系数增大(P＜0.01);与便秘组相比,芦荟组小鼠的结肠慢波频率变异系数减慢(P＜0.01);与对照组相比,便秘组小鼠的结肠慢波振幅减少(P＜0.01);与便秘组相比,芦荟组小鼠的结肠慢波振幅升高(P＜0.01);与对照组相比,便秘组小鼠的结肠慢波振幅变异系数增大(P＜0.01);与便秘组相比,芦荟组小鼠的结肠慢波振幅变异系数减小(P＜0.01).结论 芦荟全汁能有效地改善便秘小鼠结肠运动功能.     

便秘小鼠结肠肌的电生理变化

目的观察便秘小鼠结肠肌的电生理变化。方法用复方地芬诺酯混悬液对小鼠进行灌胃建立便秘模型,然后测定其小肠结肠段的肌电,并分析其电生理活动变化。结果与对照组比较,便秘组慢波肌电频率明显增快(P<0.01);结肠肌电慢波频率的变异系数明显增大(P<0.01);结肠肌电慢波振幅明显减少(P<0.01);结肠肌电慢波振幅变异系数明显增大(P<0.01)。结论便秘小鼠结肠肌电慢波频率及振幅的异常改变可能是导致结肠传输减慢的重要原因。     

内吗啡肽对泻剂结肠大鼠结肠肌电活动的影响

目的研究内吗啡肽对泻剂结肠大鼠结肠肌电活动的影响,探讨慢传输性便秘的发病机制。方法建立泻剂结肠动物模型,测定内吗啡肽1和内吗啡肽2对大鼠结肠肌电活动的影响。结果泻剂组大鼠结肠慢波频率和振幅分别为(28.19±7.51)次/min和(0.076±0.018)mV,与对照组比较[(36.05±8.94次/min)和(0.600±0.310)mV]明显降低;内吗啡肽1、内吗啡肽2以浓度依赖方式抑制泻剂结肠的慢波肌电活动,振幅明显降低,频率[(2 8.18±7.51)次/min3无明显变化,内吗啡肽1的作用强于内吗啡肽2。注射内吗啡肽不能阻断乙酰胆碱对结肠的兴奋作用。阿片受体拮抗剂纳洛酮(naloxone)能逆转内吗啡肽的抑制作用。结论内吗啡肽参与了泻剂结肠大鼠结肠肌电活动和结肠动力的调控,可能是慢传输性便秘发病的重要因素之一。     

大黄酸对便秘小鼠肠道传输功能和结肠肌电及结肠黏膜水通道蛋白3表达的影响

目的探讨大黄酸对便秘小鼠肠道传输功能、结肠肌电及结肠黏膜水通道蛋白(AQP)3表达的影响。方法 90只小鼠随机分为对照组、便秘组和大黄酸组。用复方地芬诺脂片复制小鼠便秘模型后,大黄酸组用大黄酸灌胃治疗。测量3组首便时间,6 h排便数量,大便性状,小肠推进率,结肠肌电信号和结肠黏膜AQP3的表达。结果便秘组首粒排便时间较对照组显著延长(P<0.01),6 h内排便粒数显著减少(P<0.01),小肠推进率显著降低(P<0.01);大黄酸组首次排便时间较便秘组显著缩短(P<0.01),6 h内排便粒数显著增加(P<0.01),小鼠小肠推进率显著提高(P<0.01)。3组结肠慢波近似于正弦波样曲线,便秘组结肠慢波较不规则。与对照组相比,便秘组结肠慢波频率显著减慢(P<0.05)。与便秘组相比,大黄酸组结肠慢波频率显著增快(P<0.05)。与对照组相比,便秘组结肠慢波频率变异系数显著增大(P<0.05);与便秘组相比,大黄酸组结肠慢波频率变异系数显著降低(P<0.05);与对照组相比,便秘组结肠慢波振幅显著降低(P<0.05);与便秘组相比,大黄酸组结肠慢波振幅显著升高(P<0.05)。与对照组相比,便秘组结肠慢波振幅变异系数显著增大(P<0.05);与便秘组相比,大黄酸组结肠慢波振幅变异系数显著减小(P<0.05)。便秘组结肠AQP3平均光密度值及阳性面积表达率明显高于对照组,大黄酸组结肠AQP3平均光密度值及阳性面积表达率明显低于便秘组(均P<0.05)。结论大黄酸能够有效地提高便秘小鼠的肠道传输功能,减少便秘小鼠结肠黏膜AQP3的表达,对缓解便秘具有显著疗效。     

加味四逆散对肝硬化大鼠异常胃电图的作用观察

[目的]观察加味四逆散对肝硬化大鼠异常胃电图的作用,并对其机制进行初步探讨。[方法]Wister雄性大鼠48只随机分为正常、模型、西药和中药组,每组12只。除正常组外,其他3组大鼠均给予腹腔注射40%CCl4花生油2.5 ml/kg,每周2次造模,连续造模11周。造模后2周中药组用加味四逆散灌胃治疗,西药组以西沙比利灌胃治疗;正常、模型组则给予等体积0.85%氯化钠灌胃。实验11周末次给药后,检测大鼠胃电图。[结果]模型组慢波节律、主频率、主功率、快波频率明显低于正常组（P〈0.05,〈0.01）,胃电慢波振幅无明显改变;中药组慢波节律、主频率、主功率、快波频率与模型组比较明显增强（P〈0.05,〈0.01）,胃电慢波振幅无明显改变,胃电波接近正常水平,与西药组比较慢波节律及快波频率均有明显差异（P〈0.05,〈0.01）;西药组主频率、快波频率与模型组比较明显增强（P〈0.05）,主功率、慢波节律与模型组比较无统计学意义（P〉0.05）。[结论]加味四逆散能明显改善实验性肝硬化大鼠的胃电波异常,提示有明显促胃动力作用。     

多潘立酮在增强结肠运动中的作用

目的 观察多潘立酮对结肠的促动力作用,并与莫沙必利及西沙必利比较.方法 ①在体实验:将40只大鼠分为对照组、多潘立酮组、莫沙必利组和西沙必利组,每组10只.在各组大鼠近端结肠和远端结肠埋植应力传感器,记录清醒大鼠结肠运动.②离体实验:在恒温灌流肌槽中,采用张力传感器测定多巴胺和多巴胺+多潘立酮对大鼠离体结肠肌条的收缩活动.结果 在体实验:①清醒大鼠在消化间期的静息状态下,结肠呈现节律性相位收缩活动.②多潘立酮可明显增加结肠的收缩活动,使近端结肠和远端结肠平均振幅分别比对照组增加84.61%±7.26%和76.37%±8.47%,呈剂量-效应关系.同等剂量的莫沙必利对近端结肠和远端结肠平均振幅分别比对照组增加50.32%±8.16%和45.13%±7.16%.莫沙必利对结肠的促动力作用明显低于多潘立酮.而同等剂量的西沙必利对近端结肠和远端结肠平均振幅分别比对照组增加92.55%±8.37%和81.27%±9.95%,其促动力作用与多潘立酮相同.离体实验:①灌流多巴胺(40 mg/ml)可明显抑制离体结肠肌条收缩活动,较Krebs-Ringer液对照组减少91.56%±10.24%.②多潘立酮可阻断多巴胺对离体结肠肌条的舒张作用.结论 多潘立酮可明显增强结肠动力,其作用明显优于莫沙必利,并与西沙必利作用相同.多潘立酮增强结肠动力作用是通过抗多巴胺作用实现.     

电针足三里穴对不完全性肠梗阻大鼠小肠肌电活动的影响

目的:探讨电针足三里穴对肠梗阻大鼠小肠肌电活动的影响.方法:采用非贯穿肠管的方式,末端回肠套环建立不完全性肠梗阻大鼠模型,将大鼠随机分为:空白对照组(n=10)、假手术组(n=10)、肠梗阻组(IO组,n=10)、肠梗阻+电针组(14dIO+EA组,n=10,21dIO+EA组,n=10).造模成功后空白对照组、假手术组、IO组均未给予电针治疗措施,IO+EA组连续给予电针14d、21d电针治疗措施.最后1次电针后2h,分别测体质量后打开腹腔,肉眼观察回肠组织形态学的改变,BL-420F生物机能实验系统测定回肠肌电.结果:IO组大鼠体质量较空白对照组和假手术组显著降低(P<0.01),IO+EA组大鼠体质量较IO组显著升高(P<0.01).回肠肌电慢波活动改变情况:14dIO组振幅(mV)低于空白对照组(0.11±0.03vs0.35±0.06,P<0.01),且频率(%)、振幅(%)变异系数均明显高于空白对照组和假手术组(27.71±10.54vs14.08±4.22,22.00±6.24;75.54±8.59vs15.84±1.49,20.67±7.57,均P<0.01);电针实验治疗IO+EA组大鼠14...     

胃肠宁合剂对大鼠胃排空功能和胃电活动及血浆胃动素含量的影响

目的:观察胃肠宁合剂对大鼠胃排空、胃电活动和血浆胃动素含量的影响.方法:12周龄的Wistar大鼠128只随机分为正常对照、多潘立酮(商品名为吗丁啉)对照、胃肠宁小剂量及大剂量4组,每组32只.连续给药6 d后,用比色分光光度法测定胃液体和固体排空功能,用放免法检测其血浆胃动素,在给予上述各组药物的同时,用四道生理记录仪检测大鼠胃十二指肠电活动.结果:正常对照、吗丁啉对照、胃肠宁小剂量及大剂量组的胃液体排空率分别为(8.6±1.5)%、(12.1±2.9)%、(18.6±3.1)%和(22.2±5.8)%,各组间比较差异均有统计学意义(均P<0.05);胃固体排空率分别为(9.2±0.7)%、(12.7±1.2)%、(19.8±3.7)%和(20.0±3.2)%,正常对照组、吗丁啉对照组和胃肠宁小剂量组之间差异均有统计学意义(P<0.05,＜0.01),但胃肠宁小剂量组和大剂量组间差异无统计学意义(P>0.05);血浆胃动素含量分别为(149.4±15.8)、(185.1±21.7)、(230.4±12.4)和(298.9±19.5)pg/ml,各组间差异均有统计学意义(P<0.05,＜0.01);胃肠平滑肌电活动频率分别为(3.71±0.19)、(4.10±0.35)、(4.70±0.23)和(5.30±0.32)次/min,振幅分别为(3.37±0.46)、(3.86±0.31)、(4.34±0.43)和(5.42±0.53)mV,各组间慢波频率和振幅间差异均有统计学意义(P<0.05,＜0.01).结论:胃肠宁合剂具有促进胃液体、固体排空,提高血浆胃动素含量及增强胃十二指肠慢波频率和振幅的作用.     

房性并行心律并发多部位的干扰

患者女性,30岁,1983年11月健康体检时发现心律不齐,心电图报告为窦性心动过缓,频发房性早搏伴室内差异性传导。图1系Ⅱ导联连续记录的心电图。一、P波有两种形态:1.圆钝型P波,振幅0.10mV,宽0.08秒,P-R0.13秒,P-P0.88秒,频率68次/分,判断为窦性P波;2.尖峰型P′波,以早搏形式出现,配对时间不固定,振幅0.15mV,宽0.06秒,P-R0.12—0.20秒,可确认是房性异位P波;有时重叠于前一次心动的T波上,部分P′波未下传。各异位P′波之间的最大公约数为1.37±0.03秒。二、QRS波群大致可分三种形态:1.R型,振幅约0.9mV,时限0.08秒,大多在窦P后出现,个别出现在P′波之后,2.高R型,出现在房性异位P′波之后,振幅1.2—2.1mV,时限0.08秒;3.宽R型,振幅0.9mV,时限0.12秒,全部出现在与T波重叠的P′波之后。后两种皆属室内差异传导。     

实验性脾虚证结肠动力肌胃肠肽和一氧

目的观察大鼠在脾虚和应激状态下结肠动力及结肠组织内P物质(SP)、血管活性肠肽(VIP)和神经型一氧化氮合酶(nNOS)改变及治疗后变化.方法实验随机分为五组正常组、脾虚组、自然恢复组、治疗组、冷应激组;其中治疗组以加味四君子汤治疗.实验采用银球三电极和高灵敏度应变片传感器同步记录结肠电-机械活动,即结肠运动、慢波和快波,并采用Ag-AgCl电极记录结肠体表电活动.信号由计算机系统软件采集并分析;放射性免疫方法测定SP,VIP;用免疫组织化学方法显示结肠组织内nNOS.结果脾虚组同正常组相比,结肠组织SP含量增高[(18.31±2.37)ng@g-1,(1.45±0.43)ng@g-1,P<0.05],VIP含量降低[(3.43±1.12)ng@g-1,(6.48±2.56)ng@g-1,P<0.05],结肠肌层中nNOS阳性神经细胞和神经纤维增多,运动频率降低[(3.6±1.1)min-1,(5.8±2.6)min-1,P<0.05].加味四君子汤治疗后各指标基本恢复正常.应激组同正常组相比,SP含量增高[(28.41±11.56)ng@g-1,P<0.05],运动振幅增高(1.6g±0.6g,0.9g±0.4g,P<0.05),体表结肠电活动与慢波的相关性比较,脾虚组和应激组均低于正常组(P<0.05)结论①脾虚状态下结肠SP、VIP含量及nNOS发生改变,结肠动力紊乱,但体内仍存在调节稳态的机制;nNOS升高VIP则降低.②加味四君子汤对脾虚结肠动力紊乱有一定调理作用.③冷束缚应激时SP升高,结肠动力紊乱以振幅升高为主.④体表结肠电活动与慢波的峰值频率相关性在各组间发生的变化,提示脾虚和冷应激皆为包括肌肉和神经系统在内的全身病变,对体表电活动产生影响.     

Effect of cisapride on relapse of esophagitis

The effect of a prokinetic agent, cisapride, on the relapse of reflux esophagitis was investigated in a randomized, double-blind trial conducted in 443 patients whose esophagitis had previously been healed with an acid antisecretory drug. Patients received cisapride, 20 mg at night, cisapride 10 mg twice daily, or placebo for 12 months or until endoscopic relapse was confirmed endoscopically. In 88% of all patients (respectively 133, 132, and 124), endoscopic data were available at discontinuation of treatment. In comparison with placebo, the two cisapride regimens prolonged both the time to endoscopically confirmed relapse (Kaplan-Meier analysis;P=0.001) and the time to symptomatic relapse (P=0.012). The life-table endoscopic relapse rates at 12 months were 51% for placebo, 32% for cisapride 20 mg at night (P=0.005), and 34% for cisapride 10 mg twice daily (P=0.02). Patients with more severe esophagitis before healing relapsed more rapidly during maintenance therapy, regardless of the treatment regimen. Adverse events were infrequent in all three groups. These findings indicate that maintenance treatment with the prokinetic drug cisapride prevents the relapse of esophagitis after it has been healed by acid antisecretory therapy.This work was supported by the Janssen Research Foundation and the Swiss National Foundation. Grant SNF 32-26369.89.     

Treatment of chronic constipation with cisapride and placebo.

The effect of cisapride (20 mg bid), a new prokinetic drug, on bowel habits and laxative consumption was studied in patients with idiopathic painless constipation and chronic laxative intake. After a four week base line period, spontaneous defection (frequency without laxative intake) and total defecation (total frequency) were measured. Patients with a spontaneous defecation of less than three stools per week entered the treatment period and were randomly assigned to double blind treatment with either cisapride (n = 64) or placebo (n = 62). After eight weeks of treatment, a four week run out phase on single blind placebo medication was conducted. Cisapride and placebo increased spontaneous stool frequency from 1.1 +/- 0.2 SEM to 3.0 +/- 0.2 per week (p less than 0.001) and from 1.2 +/- 0.1 to 1.5 +/- 0.2 (p greater than 0.05), respectively. Laxative consumption was decreased from 3.6 +/- 0.3 to 1.8 +/- 0.2 doses/week by cisapride (p less than 0.001) and from 3.3 +/- 0.3 to 2.8 +/- 0.3 by placebo (p less than 0.05). Both drugs improved constipation as assessed by the patient by means of a visual analogue scale, but cisapride did so to a larger extent than placebo. The effects of cisapride partly outlasted active medication by at least four weeks. It is concluded that cisapride improves bowel habits in patients with idiopathic constipation and reduces laxative consumption.     

Treatment of postoperative paralytic ileus with cisapride

The effect of cisapride on postoperative colonic motility was studied in 40 patients undergoing cholecystectomy under randomized, double-blind conditions. The patients received 10 mg of cisapride or placebo by intravenous injection starting on the day of surgery and repeated every 12 h until the 3rd postoperative day. The return of propagative motility in the colon was visualized by means of radiopaque markers and serial abdominal radiographs. Cisapride induced a significantly earlier return of propulsive motility in the right colon, as indicated by the propagation of markers from the ascending colon to the transverse colon (p less than 0.05). Radiopaque markers reached the descending colon (p less than 0.05) and the rectosigmoid colon (p less than 0.05) significantly earlier in the cisapride group than in controls. The first passage of feces occurred significantly earlier in cisapride-treated patients than in controls (p less than 0.05). The first passage of gas after surgery did not differ significantly between the groups. Our results suggest that cisapride can be used to induce earlier return of propagative motility in the colon after major abdominal surgery.     

铝碳酸镁和西沙必利对胆汁反流性胃炎的疗效及胃内胆汁的影响

目的 探讨铝碳酸镁对胆汁反流性胃炎疗效及胃内２４小时胆汁的影响。方法 ３０例胆汁反流性胃炎,经胃内２４小时胆汁监测证实,并随机分为３组。一组服用西沙必利５ｍｇ,３次／ｄ;一组服用铝碳酸镁１．０ｇ,３次／ｄ;一组同时服用西沙必利和铝碳酸镁。治疗４周后观察腹痛,腹胀,呕吐胆汁等症状变化,并复查胃内２４小时胆汁监测。结果 治疗后３组患者症状减轻（Ｐ〈０．０１）,有效率分别为９０％、１００％和１００％。２     

Effects of cisapride on postcibal jejunal motor activity

In the jejunum of fasting humans, cisapride induces a phase 2-like, highly propagative motor pattern. This study investigated cisapride's effects on the fed pattern of the jejunum. Starting 5 min after a phase 3 of the migrating motor complex, 18 healthy men received 5 or 10 mg cisapride or placebo orally in random double-blind fashion and ingested meals containing 1000 and 4200 kJ, respectively. Jejunal pressures were recorded pneumohydraulically with five catheter orifices 10–30 cm aborad the ligament of Treitz. After the 4200-kJ meal, total number and number of propagated contractions as well as area under the curve increased significantly more than after 1000 kJ. Following the 1000-kJ but not the 4200-kJ meal, 10 mg cisapride increased total number of contractions, number of propagated contractions, mean amplitude, and area under curve significantly more than placebo. Fed-pattern duration increased with the meal's caloric content but was not influenced systematically by cisapride. In conclusion, cisapride stimulates jejunal motor activity and induces a propagative pattern after a 1000-kJ but not after a 4200-kJ meal, suggesting that it can produce no further stimulation when motor activity is near maximally enhanced already.     

Electrogastrography in patients with gastroparesis and effect of long-term cisapride

Abnormalities in the gastric pacemaker potentials occur in patients with impaired gastric emptying. It is unclear if treatment effects the underlying rhythm or if normalization of dysrhythmias is important. We examined the effect of cisapride using surface electrogastrograms and radionuclide gastric emptying studies of patients with idiopathic and diabetic gastroparesis. Twelve of 14 patients had abnormal baseline electrogastrograms. After six months of cisapride, four patients had normalization of their electrical activity and six had improvement. Patients with idiopathic gastroparesis had an increase in gastric emptying at 120 min from 48.9±3.8% (baseline) to 70.9±6.0% (six months), P =0.009. Patients with diabetes mellitus had a similar improvement. Patients who had normalization of the electrogastrogram had a greater gastric emptying rate than patients with continued dysrhythmias. Thus, dysrhythmias are important in the etiology for gastroparesis, but other factors need to be examined.This work was in part supported by the Measey Foundation, by NIH grant R01-DK389641-01 A1, and by the Janssen Research Foundation.     

Intestinal pseudoobstruction secondary to amyloidosis responsive to cisapride

Summary A case of chronic intestinal pseudoobstruction secondary to systemic amyloidosis in a patient with multiple myeloma is described. Gastrointestinal symptoms and indices of nutrition improved markedly after commencing treatment with cisapride, which may have been responsible for relatively prolonged survival compared with similar reported cases.