Sagor G R, Ghatei M A, Al-Mukhtar M Y, Wright N A, Bloom S R
Gastroenterology. 1983 May;84(5 Pt 1):902-6.
It is generally agreed that the adaptive response in the residual bowel after major intestinal resection is dependent on luminal nutrition and pancreaticobiliary secretions. Recent evidence, however, suggests that humoral mechanisms, e.g., gastrin or enteroglucagon, may also play a part in this process. A 75% proximal small bowel exclusion was performed in 16 male Wistar rats and the excluded bowel was fashioned into a Thiry-Vella fistula. Half of the animals were allowed food ad libitum, while the rest were fed intravenously. The animals were killed at 12 days, and plasma, gastrin, and enteroglucagon were measured, while cell proliferation was determined by measuring the crypt cell production rate employing a stathmokinetic method using vincristine and crypt microdissection. In addition to these animals, 16 rats had a jejunal transection only, with half of these animals nourished intravenously, while the remainder were allowed food ad libitum. In the Thiry-Vella rats, plasma enteroglucagon was greater with oral feeding (566 +/- 59 pmol/L) than with intravenous feeding (120 +/- 452 pmol/L) (p less than 0.01), but gastrin levels did not differ in the two groups. In the ileum in continuity, crypt cell production rate per hour was greater in the orally fed animals (52 +/- 8) compared with the intravenously fed group (18 +/- 5) (p less than 0.001). In the excluded fistula, crypt cell production rate per hour was reduced by 23.8 +/- 2 in orally fed rats, but this was greater than in the intravenously fed group (16 +/- 1.5) (p less than 0.01). Both orally and intravenously fed transected rats had significantly lower plasma hormone levels, and reduced crypt cell production rate compared with the respective Thiry-Vella groups. This study suggests a distinct role for a humoral agent responsible for the proliferative changes seen after small bowel resection, and in this respect enteroglucagon appears more relevant than gastrin.
人们普遍认为，大肠切除术后残余肠段的适应性反应取决于肠腔营养和胰胆分泌。然而，最近的证据表明，体液机制，如胃泌素或肠高血糖素，也可能参与这一过程。对16只雄性Wistar大鼠进行了75%近端小肠旷置术，并将旷置的肠段制成Thiry-Vella瘘管。一半动物随意进食，其余动物通过静脉喂食。在第12天处死动物，测量血浆、胃泌素和肠高血糖素，同时通过使用长春新碱和隐窝显微切割的静止动力学方法测量隐窝细胞生成率来确定细胞增殖。除了这些动物外，16只大鼠仅进行空肠横断术，其中一半动物通过静脉营养，其余动物随意进食。在Thiry-Vella大鼠中，口服喂养组的血浆肠高血糖素水平（566±59 pmol/L）高于静脉喂养组（120±452 pmol/L）（p<0.01），但两组胃泌素水平无差异。在连续的回肠中，口服喂养动物的每小时隐窝细胞生成率（52±8）高于静脉喂养组（18±5）（p<0.001）。在旷置的瘘管中，口服喂养大鼠的每小时隐窝细胞生成率降低了23.8±2，但仍高于静脉喂养组（16±1.5）（p<0.01）。与各自的Thiry-Vella组相比，口服和静脉喂养的横断大鼠血浆激素水平均显著降低，隐窝细胞生成率也降低。这项研究表明，一种体液因子在小肠切除术后的增殖变化中起独特作用，在这方面，肠高血糖素似乎比胃泌素更相关。
