Okumura T, Grant A P, Taylor I L, Ohning G, Taché Y, Pappas T N
Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Regul Pept. 1995 Feb 14;55(3):311-9. doi: 10.1016/0167-0115(94)00117-g.
These studies examined the effect of 2-deoxy-D-glucose (2-DG) on gastric mucosal integrity. Intravenous administration of 2-DG in doses of 100 and 125 mg/kg dose-dependently produced multiple, hemorrhagic gastric mucosal lesions while 75 mg/kg of 2-DG failed to induce gastric lesions. Intracisternal injection of 2-DG in doses of 10 and 20 mg/kg also induced gastric mucosal damage in a dose-dependent manner whereas the injection of 5 mg/kg of 2-DG intracisternally did not induce the development of gastric lesions. Gastric mucosal damage by intravenous 2-DG was completely blocked by bilateral gastric branch vagotomy. Intracisternal but not intraperitoneal injection of anti-TRH antibody 8964 significantly reduced the severity of gastric mucosal lesions evoked by intravenous administration of 2-DG. These results suggest that 2-DG acts in the brain to induce gastric mucosal damage through vagal dependent pathways. Endogenous TRH in the central nervous system may be involved in the production of gastric mucosal damage by 2-DG.
这些研究考察了2-脱氧-D-葡萄糖(2-DG)对胃黏膜完整性的影响。静脉注射剂量为100和125mg/kg的2-DG可剂量依赖性地产生多发性出血性胃黏膜损伤,而75mg/kg的2-DG未能诱发胃损伤。脑池内注射剂量为10和20mg/kg的2-DG也可剂量依赖性地诱发胃黏膜损伤,而脑池内注射5mg/kg的2-DG未诱发胃损伤。双侧胃分支迷走神经切断术可完全阻断静脉注射2-DG所致的胃黏膜损伤。脑池内而非腹腔内注射抗促甲状腺激素释放激素(TRH)抗体8964可显著减轻静脉注射2-DG诱发的胃黏膜损伤的严重程度。这些结果表明,2-DG在脑内通过迷走神经依赖性途径诱发胃黏膜损伤。中枢神经系统内的内源性TRH可能参与了2-DG所致胃黏膜损伤的产生。