Zarroug Abdalla E, Libsch Karen D, Houghton Scott G, Duenes Judith A, Sarr Michael G
Gastroenterology Research Unit, Mayo Clinic College of Medicine and Department of Surgery, Mayo Clinic, Rochester, Minnesota 55905, USA.
J Gastrointest Surg. 2006 Apr;10(4):586-92. doi: 10.1016/j.gassur.2005.07.033.
Postprandial augmentation of absorption of water and electrolytes is believed to occur in the jejunum. Neural mechanisms of control, however, have not been studied in the in situ jejunum or in the transplanted bowel. The aim of this study was to determine if postprandial augmentation of absorption occurs in the in situ jejunum and to evaluate neural mechanisms controlling postprandial jejunal absorption. Based on our previous work, we hypothesized that postprandial augmentation of absorption does not occur in the jejunum in situ and that extrinsic denervation of the jejunum is associated with decreased postprandial absorption. Absorption was studied in an 80 cm, in situ jejunal segment in six dogs by using an isosmolar electrolyte solution alone, or with 80 mmol/L glucose before and after jejunal transection to disrupt intrinsic neural continuity of the study segment with the remaining gut. Net absorptive fluxes of water and electrolytes were measured in the fasted state and after a 400-kcal meal. Another six dogs were studied 3 weeks after our validated model of extrinsic denervation of jejunoileum; identical fasting and postprandial absorptive states were evaluated. Postprandial augmentation of absorption of water and electrolytes did occur in the jejunum (P < 0.03) both in the absence and in the presence of intraluminal glucose. After intrinsic neural transection or extrinsic denervation, no postprandial augmentation of absorption occurred, with or without glucose. Postprandial augmentation of absorption of water and electrolytes occurs in the in situ jejunum. Disrupting intrinsic neural continuity or extrinsic denervation (as after intestinal transplantation) abolishes postprandial augmentation.
餐后空肠对水和电解质的吸收增强被认为会发生。然而，控制的神经机制尚未在原位空肠或移植肠中进行研究。本研究的目的是确定原位空肠是否会出现餐后吸收增强，并评估控制餐后空肠吸收的神经机制。基于我们之前的工作，我们假设原位空肠不会出现餐后吸收增强，并且空肠的外在去神经支配与餐后吸收减少有关。通过单独使用等渗电解质溶液或在空肠横断前后使用80 mmol/L葡萄糖，对6只狗的80 cm原位空肠段进行吸收研究，以破坏研究段与其余肠道的内在神经连续性。在禁食状态和摄入400千卡餐后测量水和电解质的净吸收通量。在我们验证的空肠回肠外在去神经支配模型建立3周后，对另外6只狗进行了研究；评估了相同的禁食和餐后吸收状态。无论管腔内是否存在葡萄糖，空肠均出现了餐后水和电解质吸收增强（P < 0.03）。在进行内在神经横断或外在去神经支配后，无论有无葡萄糖，均未出现餐后吸收增强。原位空肠会出现餐后水和电解质吸收增强。破坏内在神经连续性或外在去神经支配（如肠道移植后）会消除餐后吸收增强。
