Shafik A, El-Sibai O, Ahmed I
Department of Surgery and Experimental Research, Faculty of Medicine, Cairo University, Cairo.
Front Biosci. 2001 Oct 1;6:B25-9. doi: 10.2741/shafik2.
In spite of voluminous literature that has been written on defecation, the exact mechanism has not yet been fully cleared up. The current study investigated the effect of sigmoid colon (SC) distension on anal motile activity and of anal distension on SC motility. Sixteen healthy volunteers (age 36.2 +/- 11.6 SD years, 10 men) were studied. The SC was distended by a balloon in 10 ml increments of CO2, and the anal, rectal and SC pressure response was recorded before and after their individual anesthetization. The anal, rectal and SC pressure response to anal distension in increments of 2 ml of CO2 was also registered. SC distension with big volumes (mean 86.2 +/- 1.9 ml) effected a SC pressure increase (p<0.05) and no rectal pressure response (p>0.05); the balloon was expelled to the exterior. Distension of the anesthetized SC caused no SC, rectal or anal pressure response (p>0.05, p>0.05, p>0.05, respectively); the response returned after the anesthetic effect had waned. SC distension while the rectum had been anesthetized, affected a significant SC pressure rise as well as an anal pressure decrease and balloon expulsion to the exterior. Anal balloon distension produced a significant pressure rise of the SC (p<0.001) and rectum (p<0.01). Distension of the anesthetized rectal neck (anal canal) caused no SC or rectal pressure response (p>0.05, p>0.05, respectively); response returned after the anesthetic effect had disappeared. SC distension appears to effect anal dilatation while anal distension causes SC contraction. This reciprocal action is suggested to be reflex and mediated through the "sigmoido-anal inhibitory reflex" and the "ano-sigmoid excitatory reflex". These 2 reflexes are believed to keep the SC contracting and the rectal neck dilated until complete SC evacuation occurs. The study seemingly negates the role of rectal distension as a prerequisite for balloon expulsion.
尽管已有大量关于排便的文献,但确切机制尚未完全阐明。本研究调查了乙状结肠扩张对肛门运动活性的影响以及肛门扩张对乙状结肠运动的影响。研究了16名健康志愿者(年龄36.2±11.6标准差岁,10名男性)。用二氧化碳以10毫升递增的方式给乙状结肠充气,记录个体麻醉前后肛门、直肠和乙状结肠的压力反应。还记录了以2毫升二氧化碳递增的方式进行肛门扩张时肛门、直肠和乙状结肠的压力反应。大量(平均86.2±1.9毫升)的乙状结肠扩张导致乙状结肠压力升高(p<0.05),而直肠压力无反应(p>0.05);球囊被排出体外。麻醉状态下的乙状结肠扩张未引起乙状结肠、直肠或肛门压力反应(分别为p>0.05、p>0.05、p>0.05);麻醉效果消退后反应恢复。直肠麻醉时乙状结肠扩张会导致乙状结肠压力显著升高以及肛门压力降低,球囊被排出体外。肛门球囊扩张导致乙状结肠(p<0.001)和直肠(p<0.01)压力显著升高。麻醉状态下直肠颈部(肛管)扩张未引起乙状结肠或直肠压力反应(分别为p>0.05、p>0.05);麻醉效果消失后反应恢复。乙状结肠扩张似乎会导致肛门扩张,而肛门扩张会导致乙状结肠收缩。这种相互作用被认为是反射性的,通过“乙状结肠 - 肛门抑制反射”和“肛门 - 乙状结肠兴奋反射”介导。这两种反射被认为可使乙状结肠保持收缩状态,直肠颈部保持扩张状态,直至乙状结肠完全排空。该研究似乎否定了直肠扩张作为球囊排出前提条件的作用。