Bastidas J A, Orandle M S, Zinner M J, Yeo C J
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Md.
Surgery. 1990 Aug;108(2):376-83.
A meal stimulates the absorption of water and electrolytes from the proximal jejunal lumen. Neither sham feeding nor gastric distention alters this meal-induced jejunal absorption, implying no role for the cephalic or gastric phases of digestion. This study tested the hypothesis that the small bowel is the origin of the proabsorptive signal for meal-induced jejunal absorption. Twenty-five-centimeter canine proximal jejunal Thiry-Vella fistulas were constructed, and chronic duodenal catheters were placed. Jejunal absorption studies (n = 72) were performed by luminal perfusion of the jejunal segments with an isotonic buffer containing radioactive carbon-labeled polyethylene glycol. Each study consisted of a 1-hour basal period followed by a 3-hour experimental period. Ten groups were studied: control, orally ingested mixed meal, and 600 ml duodenal infusions of either water, saline solution, protein, lipid, carbohydrate, 150 mmol/L mannitol, 300 mmol/L mannitol, or 600 mmol/L mannitol, each delivered at 10 ml/min over 60 minutes. The control, water, and saline solution groups showed no significant changes in integrated 3-hour jejunal absorption above basal. The ingested mixed meal significantly increased water and electrolyte absorption (p less than 0.0001). The isovolumetric, isocaloric duodenal nutrient infusions of protein, lipid, and carbohydrate all significantly increased jejunal water and electrolyte absorption (p less than 0.0001). The poorly absorbed solute mannitol significantly increased absorption (p less than 0.0001) in a dose-dependent fashion. These results indicate that the proabsorptive signal for meal-induced jejunal absorption originates from or distal to the duodenum. This newly defined enteroenteric response occurs independently of nutrient composition and responds to increasing osmolarity of poorly absorbed solutes such as mannitol.
一顿饭会刺激空肠近端肠腔内水和电解质的吸收。假饲或胃扩张均不会改变这种由进食引起的空肠吸收，这意味着消化的头期或胃期不起作用。本研究检验了以下假设：小肠是进食引起空肠吸收的促吸收信号的起源部位。构建了25厘米长的犬近端空肠Thiry-Vella瘘管，并放置了慢性十二指肠导管。通过向空肠段腔内灌注含有放射性碳标记聚乙二醇的等渗缓冲液进行空肠吸收研究（n = 72）。每项研究包括1小时的基础期，随后是3小时的实验期。研究了十组：对照组、口服混合餐，以及十二指肠输注600毫升水、盐溶液、蛋白质、脂质、碳水化合物、150毫摩尔/升甘露醇、300毫摩尔/升甘露醇或600毫摩尔/升甘露醇，每组均以10毫升/分钟的速度在60分钟内输注完毕。对照组、水和盐溶液组在3小时的整合空肠吸收方面，相较于基础水平无显著变化。摄入的混合餐显著增加了水和电解质的吸收（p < 0.0001）。等容、等热量的十二指肠营养输注蛋白质、脂质和碳水化合物均显著增加了空肠水和电解质的吸收（p < 0.0001）。吸收较差的溶质甘露醇以剂量依赖方式显著增加了吸收（p < 0.0001）。这些结果表明，进食引起空肠吸收的促吸收信号起源于十二指肠或十二指肠远端。这种新定义的肠-肠反应独立于营养成分发生，并对吸收较差的溶质（如甘露醇）渗透压的升高作出反应。
