Uccheddu A, Murgia C, Licheri S, Dessy E, Ghinami E, Scattone S, Cagetti M
Istituto di Chirurgia, I Clinica Chirurgica, Università degli Studi di Cagliari.
G Chir. 1991 Nov-Dec;12(11-12):572-4.
The authors studied the role of slow bowel transit in the development of colonic neoplasias in rats treated with 1,2-dimethylhydrazine (DMH). Forty Sprague-Dawley male rats, weighing 400 g, were used in the experiment and were divided into 4 groups of 10 rats each. The first and the second group were given, weekly, subcutaneous injections of DMH at a dose of 25 mg/kg for 25 and 27 weeks respectively; in these groups constipation was obtained by reducing water intake throughout the period of the experiment. The third and the fourth group (control groups) received DMH at the dose of 25 mg/kg for 25 and 27 weeks respectively and water "ad libitum". The rats were weighed once a week and stool output, weight, and number of scybala/day were recorded once every four weeks. Rats were sacrificed one week after the final injection of DMH and every intestinal lesion macroscopically identified was histologically examined. All rats showed weight loss from the 22nd week to the sacrifice. The mean stool weight/day was 21.2 g +/- 1.47 in the groups A and B; while for the groups C and D it was 23.6 g +/- 1.81 (p = 0.019). The number of scybala/day was 26 +/- 3 in the groups A and B, whereas in the groups C and D was 34 +/- 4 (p = 0.05). An increased number of cancers per rat was recorded in the groups A and B compared to control groups, respectively from 0.66 to 1.4 at 25 weeks (p = 0.02) and from 0.9 to 2.44 at 27 weeks (p = 0.07). A corresponding increase in the number of polyps after 25 weeks was demonstrated, taking into account the possible polyp-cancer sequence. Our study suggests that the slow bowel transit induced an increased number of colonic neoplasia in relation to the prolonged contact of the carcinogen with the mucosa or to its greater concentration in the colonic lumen due to the fecal output reduction.
作者研究了慢肠传输在1,2 - 二甲基肼（DMH）处理的大鼠结肠肿瘤发生过程中的作用。实验使用了40只体重400克的Sprague - Dawley雄性大鼠，分为4组，每组10只。第一组和第二组分别每周皮下注射剂量为25毫克/千克的DMH，持续25周和27周；在这些组中，通过在整个实验期间减少水摄入量来诱发便秘。第三组和第四组（对照组）分别接受剂量为25毫克/千克的DMH，持续25周和27周，并自由饮水。每周称一次大鼠体重，每四周记录一次粪便排出量、重量和粪粒数量。在最后一次注射DMH一周后处死大鼠，并对肉眼识别的每个肠道病变进行组织学检查。所有大鼠从第22周直到处死均出现体重减轻。A组和B组的平均每日粪便重量为21.2克±1.47；而C组和D组为23.6克±1.81（p = 0.019）。A组和B组的每日粪粒数量为26±3，而C组和D组为34±4（p = 0.05）。与对照组相比，A组和B组每只大鼠的癌症数量增加，在25周时分别从0.66增加到1.4（p = 0.02），在27周时从0.9增加到2.44（p = 0.07）。考虑到可能的息肉 - 癌症序列，25周后息肉数量相应增加。我们的研究表明，由于粪便排出量减少，慢肠传输导致结肠肿瘤数量增加，这与致癌物与黏膜的接触时间延长或其在结肠腔内因粪便排出减少而浓度升高有关。
