Cajal间质细胞与慢传输型便秘

慢性便秘中近一半属于慢传输型便秘,其病因复杂,机制尚不明了。研究证实Cajal间质细胞是胃肠道的起搏细胞,产生慢波和传导电兴奋,参与神经递质的调节。近期研究表明慢性便秘患者结肠组织中Cajal间质细胞数量减少,形态及其网状结构改变,这在慢传输型便秘发病中具有重要的病理生理学意义。     

Cajal间质细胞与慢传输型便秘

Cajal间质细胞是胃肠道神经系统(ENS)的一种非神经但又与神经密切相关的特殊间质细胞。近年的研究表明Cajal间质细胞(ICC)可能是肠道慢波的起搏者，并参与了NANC神经肌肉信息传递过程，有潜在的控制胃肠道动力的作用，而且与人类胃肠道运动性疾病以及胃肠道肿瘤的发病机制有关。慢传输型便秘(STC)就是胃肠运动性疾病中的一种，它是以结肠动     

Cajal间质细胞与慢传输型便秘之间关系研究进展

0引言 Cajal间质细胞（ICC）是分布于胃肠道平滑肌和神经细胞之间的一类特殊细胞,它具有产生慢波,传导电兴奋和参与神经递质调节的重要功能。     

大鼠胃肠道不同部位Cajal间质细胞与慢传输型便秘的关系

目的观察慢传输型便秘(slow transit constipation,STC)大鼠模型胃肠道Cajal间质细胞(interstitial cell of cajal,ICC)的分布特点与含量改变,全面评估ICC在STC发病机制中的作用。方法 24只健康Wistar大鼠随机分成便秘组和对照组,分别饲喂含复方苯乙哌啶的混悬液和生理盐水,每5 d记录1次大鼠大便粒数、大便干质量及大鼠体质量。饲养90 d后停药1周,测定胃肠道传输功能并通过免疫组化的方法测定ICC的特异性标志物c-kit+细胞在胃窦、小肠、结肠的分布情况与含量变化。结果便秘组日均粪便粒数少于对照组(P<0.01),平均每粒粪便质量大于对照组(P<0.05);便秘组首粒黑便排出时间长于对照组(P<0.05);与对照组比较,便秘组胃窦部位c-kit+细胞数量无明显变化(P>0.05)。而c-kit+细胞在便秘组大鼠小肠、结肠的数目均少于对照组(P<0.05)。结论在STC模型中,胃窦ICC变化不明显,小肠ICC数量有减少趋势,可能对STC有一定影响,结肠部位ICC数量明显减少,可能是慢传输型便秘大鼠的主要病理生理机制。     

肠神经系统与慢传输型便秘

慢传输型便秘(STC)病因未明,多因素与其发病相关.肠神经系统(ENS)可独立调节肠道功能,其在慢传输型便秘中的改变具有重要意义.此文就此予以阐述,为STC临床治疗提供依据.     

慢传输型便秘发病机制的研究

慢传输型便秘(STC)的发病机制主要与肠神经系统(ENS)、Cajal间质细胞(ICC)、平滑肌、神经递质等有关。研究发现STC结肠组织中ENS出现退行性变化,肌间神经丛空泡变性,ICC数量减少,形态改变,平滑肌退行性变,多种神经递质发生改变。本文就STC发病机制的研究作一综述。     

慢传输型便秘发病机制的研究

慢传输型便秘（STC）是指由于结肠动力障碍,使内容物滞留在结肠及结肠运输缓慢所致的便秘。STC的病因复杂,确切的发病机制尚不完全清楚,症状顽固,治疗困难,主要与精神心理因素、肠神经系统（ENS）病理变化、Cajal间质细胞（ICC）的病理改变、平滑肌及肠神经递质变化等因素有关。此文就STC发病机制方面的研究进展作一综述,以期对临床治疗提供指导。     

慢传输型便秘发病机制的研究进展

慢传输型便秘(STC)病因未明,多种因素如肠神经系统、肠神经递质、胃肠激素、Cajal间质细胞等与其发病相关。此文就此予以阐述,为STC临床治疗提供依据。     

慢传输型便秘动物模型研究进展

慢传输型便秘（slowtransitconstipationSTC）是一种以结肠通过时间延长和结肠动力下降为特征的顽固性便秘，是功能性便秘中常见的类型。随着人们饮食结构、生活习惯以及精神心理等因素的影响，其发病率呈逐年上升趋势。美国一项回顾性研究发现STC占慢性便秘患者的42．0%，是慢性便秘常见的病理类型。国内流行病学调查显示，     

慢传输型便秘发病机理研究进展

慢传输型便秘(slow transit constipation，STC)主要表现为结肠传输减慢，病因不明，治疗困难。文章对近年来sTC发病机理方面的研究进展，肠神经系统神经递质如NO、VIP、阿片肽；胃肠激素如SS、CCK等的变化及Cajal间质细胞、肠神经元病变、精神心理等因素与STC的关系作一综述。     

Decreased interstitial cells of Cajal in the sigmoid colon of patients with slow transit constipation

Background and aims Slow transit constipation (STC) is a colonic motor disorder that is characterized by measurably delayed movement of materials through the colon. Although abnormalities in the neuronal networks of the colon have been demonstrated in patients with STC, the etiology of STC remains unclear. Interstitial cells of Cajal (ICC) have been shown to be the pacemaker cells of the intestine and have been implied in the pathogenesis of a number of gastrointestinal motility dysfunctions, including idiopathic STC. This study aimed to determine the normal distribution of ICC within the colon of the Chinese and also to determine if ICC are decreased in Chinese STC patients.Patients and methods Twelve patients with STC and eight age-matched normal controls were studied. Specimens of sigmoid colon were obtained immediately after resection. ICC were identified with a monoclonal antibody to c-kit by an indirect immunofluorescence method. Immunostained tissues were examined with a laser scanning confocal microscope and the area occupied by ICC was calculated with an image analysis system.Results ICC were located in the external muscle layers including myenteric plexus (MP) and submucosal border (SMB). Two types of Kit-positive ICC were observed: bipolar cells characterized by one or two long processes and multipolar cells characterized by long stellate processes extending in various directions. A higher percentage of ICC was present in the MP regions and circular muscle (CM) layers compared with the SMB and longitudinal muscle (LM) layers. Tissues from STC patients showed a considerable decrease in the number of ICC located in the four regions (ICC-LM, ICC-MP, ICC-CM, ICC-SMB), especially the ICC-SMB, in which ICC almost completely disappeared.Conclusions Similar distribution of ICC was observed in the normal sigmoid colon of the Chinese. Decreased area of c-kit+ ICC may play an important role in the pathophysiology of STC. It remains to be determined whether the loss of ICC is primary or secondary to another lesion.     

胶质细胞源性神经生长因子与慢传输性便秘

慢传输型便秘(STC)至今病因未明。肠神经系统(ENS)可独立调节肠道功能,其在慢传输型便秘中的改变具有重要意义。胶质细胞源性神经营养因子(GDNF)不仅可促进多种神经元的存活与分化,而且对多种原因造成的神经损伤具有明显的保护作用。此文主要从肠神经系统的功能变化和胶质细胞源性神经营养因子的营养作用这两方面来阐述与功能性便秘之间的相关性。     

慢传输性便秘结肠阿片受体的病理生理改变

目的 为了更加深入地了解慢传输性便秘的发病机理和病理生理改变。方法 应用放射配体结合分析检测了患结肠mu、Kappa阿片受体含量变化。结果 与正常对照组比较,STC患结肠壁肌层ma、Kappa阿片受体含量增加。结论 STC患内源性阿片肽活性增加,肠道运动受抑制,提示阿片受体拮抗剂可能是治疗STC的一个新途径。     

Normal aspects of colorectal motility and abnormalities in slow transit constipation

Human colonic motility is a relatively difficult topic to investigate. However, the refinement of manometric techniques in recent years enabled us to study both the proximal and distal segments of the viscus. The present paper reviews our knowledge about normal aspects of colorectal motility in man and the abnormalities found in slow transit constipation (STC), one of the most frequent and difficult to treat subtypes of constipation. An internetbased search strategy of the Medline and Science Citation Index was performed using the keywords colon, colonic, colorectal, constipation, slow transit, motility, rectal, rectum in various combinations with the Boolean operators AND, OR and NOT. Only articles related to human studies were used, and manual cross-referencing was also performed. Most of colonic motor activity is represented by single nonpropagated contractions, rarely organized in bursts; this activity is maximal during the day, especially after waking and following meals. In addition, a specialized propagated activity with propulsive features is detectable, represented by high-and low-amplitude propagated contractions. In the severe form of constipation represented by the slow transit type, the above motor activity is completely deranged. In fact, both basal segmental activity (especially in response to meals) and propagated activity (especially that of high amplitude) are usually decreased, and this may represent a physiologic marker of this disorder. Human colonic motor activity is quite a complex issue, still only partly understood and investigated, due to anatomic and physiological difficulties. In recent years, however, some more data have been obtained, even in proximal segments. These data have helped in elucidating, although only in part, some pathophysiological mechanisms of chronic constipation, and especially of the STC subtype.     

针刺治疗老年慢传输型便秘60例临床观察

目的 观察针刺治疗老年慢传输型便秘的疗效及对肠动力的影响.方法 随机将60例老年慢传输型便秘患者分为两组,其中,实验组：30例老年患者运用针刺治疗,每日1次,每次30分钟.对照组：30例给予口服莫沙必利治疗,每次5mg,每日三次.两组均共治疗2周.结果 实验组30例,痊愈14例（46.67％）,有效15例（50％）,无效1例（3.33％）,总有效率96.67％;对照组30例,痊愈8例（26.67％）,有效16例（53.33％）,无效6例（20％）,总有效率80％,实验组疗效优于对照组,两组差异有统计学意义（P＜0.05）.结论 针刺治疗老年慢传输型便秘具有较好的临床疗效,并能有效促进肠蠕动.     

糖尿病慢传输运动结肠Cajal间质细胞和干细胞因子的变化

目的:了解Cajal间质细胞(ICC)、干细胞因子(SCF)在糖尿病大鼠结肠慢传输运动模型中的变化,探讨其作用及可能的调控机制.方法:54只♂ SD大鼠分为糖尿病和正常对照组,经腹腔注射链脲佐菌素建立糖尿病大鼠模型,于造模后6,8,10 wk各组分别处死9只大鼠,以免疫组化、透射电镜研究近端结肠组织中ICC的变化,以Western blot方法检测近端结肠组织中膜结合型干细胞因子的表达,以ELISA测定血清中可溶型SCF的浓度,分析他们之间的相关性.结果:糖尿病大鼠血糖随时间增加而升高,而胃肠推进率却降低(P＞0.05).免疫组化结果显示,6,8,10 wk时的糖尿病大鼠肌间ICC表达较对照组明显减少(P＜0.05),且糖尿病大鼠近端结肠ICC数量随时间推移有逐渐降少的趋势.透射电镜显示糖尿病大鼠结肠ICC线粒体肿胀、空泡样变,细胞器数量明显减少.与对照组相比,糖尿病大鼠血清中可溶型SCF显著降低(6 wk:0.93±0.53 μg/L vs 1.87±0.92 μg/L,P＜0.05;8 wk: 0.78±0.21 μg/L vs 1.76±0.94 μg/L,P＜0.05;10 wk:0.73±0.20 μg/L vs1.82±0.96 μg/L,P＜0.05),而结肠组织中的膜结合型SCF无明显差异(P＞0.05),且可溶型干细胞因子与ICC具有相同的变化趋势.结论:糖尿病胃肠动力障碍大鼠存在血清中可溶性干细胞因子浓度下降以及结肠组织中ICC数量减少和结构破坏,这些变化及其可能存在的序贯性调控作用可能是糖尿病出现结肠慢传输变化的基础.