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1.
直肠内温度变化影响肠易激综合征患者内脏感觉阈值   总被引:4,自引:2,他引:4  
目的 探讨直肠内温度及压力变化对肠易激综合征(IBS)患者内脏感觉阈值的影响,进一步研究IBS的发病机制。方法 通过直肠球囊内注入空气(压力刺激)、38℃温水、4℃冰水(温度刺激)及脐部放置冰袋加直肠球囊内充气,研究直肠温度和压力变化刺激对初始感觉阈值和排便阈值的影响。结果 (1)直肠球囊内注气后,IBS组患者的初始感觉阈值明显低于对照组,排便阈值差异不明显。IBS组中腹泻型与交替型患者的初始感觉阈值及排便阈值均明显降低;便秘型患者的初始感觉阈值稍低于对照组,排便阈值明显增高。(2)直肠球囊内注入4℃冰水后,除便秘型IBS的排便阈值稍有所增加外,其余患者初始感觉阈值及排便阈值均显著降低,以腹泻型变化最明显。(3)脐部放置冰袋可诱发部分患者产生症状,但对初始感觉阈值和排便阈值无明显影响。结论 直肠温度和压力刺激可明显降低IBS患者的初始感觉阈值和排便阈值,以腹泻型患者最显著。内脏对压力和温度的敏感性增高可能是IBS发病的重要机制之一。  相似文献   

2.
肠易激综合征病人内脏高敏感性的研究   总被引:6,自引:0,他引:6  
目的 比较肠易激综合征(IBS)病人和健康对照者在直肠内温度变化刺激后所产生感觉阈值的差异,探讨IBS内脏敏感性的变化。方法 对46例IBS病人和13例健康对照者,用直肠测压导管依次向球囊内注入38℃温水和4℃冰水,记录相应的初始感觉阈值及排便阈值,注意温度变化刺激对IBS病人症状的影响。结果 ①直肠球囊内温水刺激后,IBS组病人的初始感觉阈值明显低于对照组,排便阈值差异不明显。IBS组中腹泻型与交替型病人的初始感觉阈值及排便阈值均显著降低;便秘型病人的初始感觉阈值稍低于对照组,排便阈值明显增高。②直肠球囊内冰水刺激后,除便秘型IBS的排便阈值稍有所增加外,其余病人初始感觉阈值及排便阈值均显著降低,以腹泻型变化最明显。结论 直肠温度变化刺激可明显降低IBS病人的初始感觉阈值和排便阈值,以腹泻型病人最显著。内脏对温度的敏感性增高,可能是IBS发病的重要机理之一。  相似文献   

3.
饮冰水对肠易激综合征患者内脏感觉的影响   总被引:1,自引:0,他引:1  
肠易激综合征(IBS)患者进冷食和腹部受凉后可出现腹痛、腹胀、腹泻等症状和肠鸣音的改变,但其发生机制尚不清楚。目的:观察IBS患者与对照者饮冰水前后内脏感觉阈值和腹部症状的差异,探讨温度刺激对IBS患者内脏敏感性的影响。方法:测定IBS患者和对照者的初始感觉阈值和排便阈值:予受试者饮4℃冰水220ml,20min后重复上述测定,并连续观察1h受试者的腹痛、腹胀、腹泻等症状和肠鸣音的改变情况。结果:直肠气囊内注入空气后,IBS患者的初始感觉阈值显著低于对照组,排便阈值与对照组无显著差异。饮冰水后,除便秘型IBS,其余各型IBS患者的初始感觉阈值和排便阈值均显著低于对照组.与单纯直肠气囊扩张(即饮冰水前)相比,对照组饮冰水后的初始感觉阈值和排便阈值无明显改变:除便秘型IBS,其余各型IBS患者饮冰水后的初始感觉阈值和排便阈值明显降低。有腹部症状的腹泻型IBS患者饮冰水后的症状轻重与内脏感觉阈值呈直线负相关。结论:饮冰水所致的温度刺激可明显降低IBS患者(除便秘型)的内脏感觉阈值,并与部分腹泻型IBS患者的腹部症状相关,证实’IBS患者的内脏敏感性增高,不同类型IBS患者的内脏感觉功能存在一定差异。  相似文献   

4.
目的研究肠易激综合征(IBS)患者对直肠内冷、温两种不同温度扩张试验的反应,以探讨IBS的可能发病机制。方法门诊随机选择腹泻型IBS(D—IBS)21例,便秘型IBS(C—IBS)15例,对照者33例,随机应用冷刺激(3℃水)或温刺激(35℃水)进行球囊灌注扩张,记录诱发受试对象产生便意和腹痛时的球囊内容量及压力。结果①无论予以冷、温何种刺激,D—IBS患者及C—IBS患者便意容量阈值(DSVT)及腹痛容量阈值(APVT)较对照者均明显降低,其中在D—IBS患者又稍低于C—IBS患者,但两者之间无显著性差异;而两种刺激下虽然在D—IBS患者及C—IBS患者中便意压力阈值(DSPT)及腹痛压力阈值(APPT)均较对照者稍低,但三者之间无显著性差异。②在D—IBS患者中,予以冷刺激后患者便意容量阈值(DSVT)及便意压力阈值(DSPT)均较温刺激时明显升高,而对于腹痛容量阈值(APVT)及腹痛压力阈值(APPT)影响不明显;在C—IBS患者中,予以冷刺激后,患者便意容量阈值(DSVT)明显升高,但便意压力阈值(DSPT)无明显变化,而对于腹痛容量阈值(APVT)及腹痛压力阈值(APPT)影响不明显;在对照者中,虽然予以冷刺激后便意及腹痛容量及压力阈值均较温刺激时稍高,但均无统计学差异。③IBS患者较对照者的容量/压力比值普遍降低,但D-IBS组与C—IBS组两者之间无显著性差异;在IBS患者中,无论D—IBS还是C—IBS,予以冷刺激后。诱发患者产生便意所需的球囊内容量/压力比值明显升高,而对于腹痛的产生影响不明显;在对照者两种温度刺激诱发出受试对象产生便意及腹痛的球囊内容量/压力比值均无统计学差异。结论①IBS患者较对照者的内脏敏感性明显增高。②直肠内温度变化对IBS患者的非伤害性内脏感觉的产生有显著的影响,而对伤害性内脏感觉的产生影响不明显。③IBS患者的直肠顺应性减低。  相似文献   

5.
肠易激综合征患者内脏高敏感性的研究   总被引:2,自引:0,他引:2  
目的:比较肠易激综合征(IBS)患者和健康对照者在直肠内温度变化刺激后所产生感觉阈值的差异,并探讨IBS内脏敏感性的变化。方法:对46例IBS患者和13例健康对照者,用直肠测压导管依次向球囊内注入38℃温水和4℃冰  相似文献   

6.
周克伦  于征 《山东医药》2011,51(7):70-71
目的进一步明确肠易激综合征(IBS)临床特点及其发病机制。方法分别测定30例IBS患者(观察组)与30例健康志愿者(对照组)直肠容量感觉阈值,包括初始感觉阈值(FSV)、排便感觉阈值(DSV)、最大耐受阈值(MTV);荧光分光光度计测定血清5-羟色胺(5-HT)水平。分析直肠容量感觉阈值与5-HT的相关性。结果观察组直肠容量感觉阈值均明显低于对照组;5-HT水平明显高于对照组,P均〈0.05。直肠容量感觉阈值与5-HT水平呈负相关,P均〈0.05。结论直肠容量感觉阈值降低是IBS腹痛发生的主要原因;可能与5-HT升高有关。  相似文献   

7.
肠易激综合征与内脏高敏感性关系研究   总被引:5,自引:0,他引:5  
多数肠易激综合征(IBS)患者都存在内脏感觉异常。临床上这些病人常表现为对腹部触诊及内镜检查的疼痛或不适反应增强,在结直肠扩张时内脏感觉阈值降低。本文就IBS与内脏敏感性增高相关的各种证据进行回顾,探讨内脏敏感性增高与IBS的关系。  相似文献   

8.
肠易激综合征内脏感觉过敏大鼠脊髓诱发电位的研究   总被引:5,自引:0,他引:5  
背景:内脏感觉过敏是肠易激综合征(IBS)的主要发病机制之一,临床上缺乏客观、无创的内脏敏感性检测方法。目的:建立直肠球囊扩张下脊髓诱发电位(SEP)的检测方法,并通过IBS内脏感觉过敏大鼠与正常大鼠的比较以及雌雄大鼠之间的比较,取得IBS存在内脏感觉过敏的客观证据。方法:通过直肠球囊有节律的充气、放气,给予直肠一定频率的反复刺激,记录诱发得到的脊髓相应节段(L6~S2)的SEP。结果:实验组雌雄大鼠分别与对照组同性别大鼠相比,SEP各波潜伏期显著缩短(P<0.05),峰间波幅显著增高(P<0.01)。实验组雌性大鼠的各波潜伏期显著短于雄性大鼠(P<0.05),峰间波幅也低于雄性大鼠(P<0.05);对照组雌性与雄性大鼠的各波潜伏期和峰间波幅无显著差异。结论:通过有节律的直肠球囊扩张,能诱发得到重复性好、易识别的SEP,可作为内脏敏感性的客观依据。  相似文献   

9.
内脏感觉功能障碍与肠易激综合征   总被引:14,自引:1,他引:13  
肠易激综合征 (IBS)是一组以腹痛或腹部不适为主 ,伴大便习惯的改变和排便异常 ,但缺乏生化和病理学变化证据的临床症候群。目前认为 ,IBS的发病主要与胃肠道运动功能障碍、内脏感觉过敏和精神心理因素等有关[1] 。本文就IBS的内脏感觉过敏机制综述如下。1 胃肠道内脏感觉过敏与脑肠轴1.1 内脏感觉过敏的定义 内脏感觉过敏是指内脏对各种刺激 (物理、化学刺激等 )感知的阈值降低 ,对正常的非伤害性刺激表现出疼痛或不适 ,即痛觉异常 ;或对伤害性刺激表现出更强的疼痛或不适反应 ,即痛觉过敏。1.2 内脏感觉过敏与周围神经 胃肠道感…  相似文献   

10.
据认为因胃肠道局部内脏感觉改变所致的症状是功能性肠病的一个重要发病机制。然而,患有某种胃肠功能性症状的病人常伴有胃肠道其他部位的症状,提示内脏感觉的增强可能是一种全胃肠道的现象。作者测定了12例肠易激综合征(IBS)和10例功能性消化不良(FD)患者在球囊扩张直肠时的初始感觉(IP)、便意(DD)和紧迫感(U)的阈值以及球囊扩张食管时的初始感觉和不适感的阈值,另测定了他们的躯体感觉阈值,并与正常人进行了比较。 结果:12例IBS患者中3例有上消化道症状,10例FD患者中4例有与结肠相关的症  相似文献   

11.
Background Visceral hypersensitivity has been shown to be present in irritable bowel syndrome (IBS). This study sought to investigate rectal sensitivity and abdominal symptoms in IBS patients before and after 220 ml cold water intake. Methods A total of 60 IBS patients and 18 healthy controls participated in this study. Both the perception thresholds and defecation thresholds to rectal balloon distension were measured. Then, all subjects were asked to drink 220 ml 37°C warm water or 4°C cold water, and these steps were repeated 20 min later. Symptoms including abdominal pain/discomfort, bloating, and diarrhea were recorded during the study. Results Compared with the controls, the thresholds of initial sensation to rectal balloon distention in IBS patients were significantly lower while the defecation thresholds were higher in constipation-predominant IBS patients. After drinking cold water, the perception thresholds in IBS patients and the defecation thresholds in diarrhea-predominant IBS patients were further decreased. However, warm water intake did not change the perception thresholds significantly in either IBS patients or controls. A negative linear correlation was found between the symptoms and the visceral perception thresholds in diarrhea-predominant IBS patients who showed significant symptoms after cold water intake. Conclusion The results indicated that cold water intake leads to lowered visceral perception thresholds in IBS patients that were inversely relevant to the abdominal symptoms in symptomatic diarrhea-predominant IBS patients. The alteration of rectal sensitivity and abdominal symptoms following cold water stimulation provided further objective evidence for visceral hypersensitivity in IBS patients.  相似文献   

12.
BACKGROUND AND AIM: Visceral hypersensitivity has been shown to be present in irritable bowel syndrome (IBS). The current study sought to compare the characteristics of visceral perception thresholds after rectal thermal and pressure stimuli between IBS patients and healthy subjects. METHODS: A total of 46 patients with IBS were diagnosed using Rome II criteria. Thirteen healthy individuals participated in the study. Rectal visceral perception thresholds were examined in patients with IBS and in normal controls after thermal and pressure stimuli. Subjects were asked to report the sensation type, location, and spread. RESULTS: Compared with healthy subjects, IBS patients demonstrated significantly initially lower perception thresholds and defecation thresholds to rectal thermal and pressure stimuli, particularly in patients with diarrhea-predominant IBS. Ice stimuli on the abdominal wall had varied effects on symptoms in patients with IBS and did not affect perception thresholds. CONCLUSIONS: Visceral perception thresholds were decreased significantly after rectal thermal and pressure stimuli in patients with IBS. Visceral hypersensitivity may be one of the important pathogenic mechanisms in IBS.  相似文献   

13.
AIM: Visceral hypersensitivity has been found to be present in irritable bowel syndrome (IBS). The current study sought to study visceral afferent hypersensitivity in IBS patients and obtain further objective evidence of alterations in intestinal afferent pathways in IBS patients by cerebral evoked potentials (CEP). METHOD: We studied 30 female IBS patients and 12 female healthy subjects. Rectal perception thresholds to balloon distention were measured and CEP was recorded in response to rhythmic rectal distention (two distention series, each of 100 repetitions at a frequency of 1 Hz) at the volume of perception thresholds. All subjects were then asked to drink 220 mL 4 degrees C ice water and the above steps were repeated 20 min later. RESULTS: Rectal distention led to recognizable and reproducible CEP. Compared to healthy subjects, IBS patients demonstrated significantly shorter N1, P1 and N2 latencies (P < 0.05). After drinking ice water, IBS patients exhibited further shortened N1, P1 and N2 latencies (P < 0.05), but drinking did not alter the latencies of healthy controls and the amplitudes of both IBS patients and healthy controls. CONCLUSION: The shorter latency of cerebral potentials evoked by rectal distention and ice water stimulation in IBS patients provided further objective evidence for defective visceral afferent transmission in IBS patients.  相似文献   

14.
目的 探讨一氧化氮 (NO)在肠易激综合征 (IBS)发病机制中的作用 ,并从基因水平揭示NO含量改变的原因。方法  (1)应用电子气压泵及灌注导管测压仪研究 2 5例腹泻型IBS患者及 15例正常志愿者的肛门、直肠压力、直肠顺应性、乙状结肠和直肠运动指数以及直肠对容量刺激的感觉阈值 ;(2 )应用硝酸还原酶法测定两组肠黏膜NO的含量 ;(3)NADPH黄递酶组化法和计算机图像分析系统对两组肠黏膜肌层一氧化氮合酶 (NOS)阳性神经纤维作定量分析 ;(4)采用荧光定量PCR(FQ PCR)方法对神经型一氧化氮合酶 (nNOS)的基因表达进行定量分析。结果  (1)肠道测压 :IBS患者的直肠静息压、肛管上部静息压、收缩压、松弛压、肛管下部静息压、收缩压、松弛压和直肠顺应性与正常人比较 ,差异无显著性 (P >0 .0 5 ) ;患者乙状结肠和直肠运动指数明显高于正常人 (P <0 .0 5 ) ;(2 )直肠内脏感觉阈值 :最低感觉阈值、排便阈值和疼痛阈值明显低于正常人 (P <0 .0 5 ) ;(3)肠黏膜NO含量 :患者结肠黏膜NO含量显著低于正常人 ,并且患者的NO含量与运动指数成负相关 ,与感觉阈值、排便阈值、疼痛阈值呈正相关 (P <0 .0 5 ) ;(4)NADPH组化染色 :IBS患者黏膜肌层NOS阳性神经纤维的面积和平均吸光度较正常人显著减少 (P <0 .0 5 ) ;(5 )NOS mRNA  相似文献   

15.
Visceral hypersensitivity has emerged as a key hypothesis in explaining the painful symptoms of irritable bowel syndrome (IBS), and it has been proposed as a “biologic marker” for the condition. Visceral hypersensitivity can be influenced by peripheral and central mechanisms affecting pain perception. The optimal method for its assessment in humans has not been determined. Current techniques include stimulation via the computerized barostat and electrical stimulation, response measures including the lower limb reflex, and brain imaging modalities such as functional MRI and positron emission tomography. It has been shown that IBS patients have decreased sensory thresholds to colonic and rectal balloon distention by barostat. Studies using electrical stimulation and the RIII lower limb reflex have further confirmed enhanced visceral perception in IBS. Evidence from more recent neuroimaging studies suggests that IBS patients have abnormal activation of brain circuits involved in emotional and cognitive modulation of sensory information, resulting in ineffective pain modulation; these circuits may have a pathophysiologic role in enhancing visceral perception. There are few effective pharmacologic treatments that relieve IBS symptoms, and improved understanding of brain-gut interactions and factors relating to enhanced visceral perception may guide us in developing more efficacious treatments.  相似文献   

16.
目的 通过比较直肠扩张后脑诱发电位(CEP)的改变,探讨肠易激综合征(IBS)患者内脏高敏感性的发生机制,旨在进一步获得IBS感觉传入通路异常的客观依据。方法 根据罗马Ⅱ标准选择女性IBS患者10例,其中腹泻型6例,便秘型2例,腹泻-便秘交替型2例,另设7例女性健康志愿者为对照组,对其进行直肠气囊扩张,首先测出每例受试者感觉阈值,用1.5倍该阈值空气体积作为刺激(频率1Hz,连续100次,休息10分钟,重复一次),启动并记录两组受试者CEP的变化。结果 直肠节律性机械扩张引出可识别、可复制的CEP。与健康对照者相比,IBS患者N_1,P_1,N_2潜伏期明显缩短(P<0.05),同时,峰间波幅有增大趋势,但无统计学意义(P>0.05)。结论 IBS患者经直肠扩张后产生的CEP的改变证实了其内脏高敏感性及内脏传入通路的异常。  相似文献   

17.
目的研究便秘型肠易激综合征患者结肠、直肠动力,直肠感觉功能.方法用结肠传输试验检测结肠传输时间,并用结肠传输指数分型,用肛门直肠测压方法测定便秘型IBS直肠静息压,肛管静息压,肛门括约肌最大缩榨压,模拟排便时,直肠收缩压,肛门括约肌剩余压,直肠对容量扩张刺激的初始感觉阈值,最大耐受容量,直肠顺应性.结果便秘型IBS患者全结肠及各节段结肠传输时间均高于对照组,便秘型IBS患者肛管静息压,直肠静息压与对照组无差异(P>0.05),肛门括约肌最大缩榨压低于正常对照组,最大耐受容量及直肠顺应性均明显高于对照组(P<0.01),且发现不同传输类型的便秘型IBS肛门直肠测压表现不同.结论便秘型IBS患者存在结肠、肛门直肠动力及直肠感觉功能异常,结肠传输试验与肛门直肠测压相结合,可体现不同传输类型便秘型IBS肛门直肠动力学病因机制.  相似文献   

18.
OBJECTIVE: Due to a lack of reliable biological markers, the diagnosis of irritable bowel syndrome (IBS) is based on symptom criteria. The possible physiological correlates of these criteria are not known. Our aims were to identify correlations of currently used IBS symptom criteria with distinct alterations in visceral perception. METHODS: Forty-two IBS patients (51% women) with a mean age of 39.5+/-1.4 yr, were included; 64% of patients were recruited from advertisement and 36% were clinic referrals. Patients completed a bowel symptom questionnaire, which included the Rome criteria and symptom severity ratings. Rectal discomfort thresholds were evaluated in all patients and in 19 controls, using a nonbiased tracking protocol consisting of phasic rectal balloon distensions before (PreTh) and after (PostTh) repetitive, high-pressure sigmoid distensions. We assessed the effect of each Rome criteria and symptom severity on PreTh and PostTh. RESULTS: IBS symptom severity was reported as moderate in 38.1% and as severe in 61.9% of patients. Overall, lower thresholds were observed in IBS patients than in controls (PreTh: 28.2+/-1.7 vs. 36.3+/-2.8 mm Hg, p<0.05; PostTh: 25.3+/-1.5 vs. 34.2+/-2.7 mm Hg, p<0.01). When assessing the effect of Rome criteria on rectal thresholds, we found that patients with hard/lumpy stools had lower thresholds than those without them, whereas patients with loose watery stools had higher thresholds than those who lacked them (both p<0.05). The lowering of rectal discomfort thresholds after sigmoid stimulation was observed regardless of the presence or absence of any Rome criteria or symptom severity. CONCLUSION: Although a decrease in rectal discomfort thresholds after sigmoid stimulation is seen in IBS regardless of specific symptoms, baseline and postsigmoid stimulation thresholds are lower in IBS patients with constipation-related symptoms.  相似文献   

19.
AIM: To investigate the role of endogenous pain modulatory mechanisms in the central sensitization implicated by the visceral hypersensitivity demonstrated in patients with irritable bowel syndrome (IBS). Dysfunction of modulatory mechanisms would be expected to also result in changes of somatic sensory function.
METHODS: Endogenous pain modulatory mechanisms were assessed using heterotopic stimulation and somatic and visceral sensory testing in IBS. Pain intensities (visual analogue scale, VAS 0-100) during suprathreshold rectal distension with a barostat, cold pressor stimulation of the foot and during both stimuli simultaneously (heterotopic stimulation) were recorded in 40 female patients with IBS and 20 female healthy controls.
RESULTS: Rectal hypersensitivity (defined by 95% Cl of controls) was seen in 21 (53%), somatic hypersensitivity in 22 (55%) and both rectal and somatic hypersensitivity in 14 of these IBS patients. Heterotopic stimulation decreased rectal pain intensity by 6 (-11 to -1) in controls, but increased rectal pain by 2 (-3 to +6) in all IBS patients (P 〈 0.05) and by 8 (-2 to +19) in IBS patients with somatic and visceral hypersensitivity (P 〈 0.02).
CONCLUSION: A majority of IBS patients had abnormal endogenous pain modulation and somatic hypersensitivity as evidence of central sensitization.  相似文献   

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