Glucose acts in the CNS to regulate gastric motility during hypoglycemia.
Glucose acts in the CNS to regulate gastric motility during hypoglycemia.
复制标题
葡萄糖在中枢神经系统中发挥作用，在低血糖期间调节胃动力。
DOI：
10.1152/ajpregu.00179.2003
复制
发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Gillis,RichardA
中科院分区：
文献类型：
--
作者：
Shi,Min;Jones,AllisonR;Niedringhaus,MarkS;Pearson,RebeccaJ;Biehl,AnnM;FerreiraJr,Manuel;Sahibzada,Niaz;Verbalis,JosephG;Gillis,RichardA
我们的目的是：1)建立静脉注射d-葡萄糖持续抑制胃窦运动的动物模型，2)利用该模型评估静脉注射葡萄糖是否抑制外周或中枢神经系统的运动，并阐明决定(S)胃运动功能是否对血糖变化敏感的因素(S)。用α-氯醛糖-氨基甲酸乙酯麻醉大鼠，用缝合在胃窦的应变力传感器测量胃窦运动。在某些情况下，通过监测胃内球囊压力来测量胃窦动力和胃张力。用25%d-葡萄糖以2ml/h的速度持续静脉滴注，引起大鼠血糖升高，低血糖(皮下注射胰岛素，2.5IU/只)引起胃收缩，胃窦运动和胃张力受到抑制。相反，当葡萄糖输注对1)自发发生的胃收缩，2)静脉注射苯儿茶酚引起的迷走神经切断动物的胃收缩，以及3)TRH类似物RX77368微量注射到迷走神经背侧运动核引起的胃收缩时，没有观察到对胃运动功能的抑制。采用胰岛素诱导低血糖增强胃运动功能的模型，我们发现切断迷走神经肝支(n=5)和辣椒素破坏迷走神经感觉传入神经(n=5)均不影响IVD-葡萄糖抑制胃运动功能的能力。我们的结果表明，决定胃运动功能是否对血糖变化敏感的一个重要因素是刺激胃收缩的方法，而静脉注射葡萄糖抑制胃运动的主要部位是中枢神经系统而不是外周。
Our purposes were to1) develop an animal model where intravenously (iv) administeredd-glucose consistently inhibited antral motility, and2) use this model to assess whether iv glucose acts to inhibit motility from a peripheral or a central nervous system site and to elucidate the factor(s) that determine(s) whether stomach motor function is sensitive to changes in blood glucose. Rats were anesthetized with α-chloralose-urethane, and antral motility was measured by a strain-gauge force transducer sutured to the antrum. In some cases, antral motility and gastric tone were measured by monitoring intragastric balloon pressure. Increases in blood glucose were produced by continuous iv infusion of 25%d-glucose at 2 ml/h. Inhibition of antral motility and gastric tone was observed when gastric contractions were induced by hypoglycemia (subcutaneously administered insulin, 2.5 IU/animal). In contrast, no inhibition of gastric motor function was observed when glucose infusion was tested on gastric contractions that were1) spontaneously occurring,2) evoked by iv administered bethanechol in vagotomized animals, and3) evoked by the TRH analog RX77368, microinjected into the dorsal motor nucleus of the vagus. Using the model of insulin-induced hypoglycemia to increase gastric motor activity, we found that neither sectioning the hepatic branch of the vagus (n= 5), nor treating animals with capsaicin to destroy sensory vagal afferent nerves (n= 5) affected the ability of ivd-glucose to inhibit gastric motor function. Our results indicate that an important factor determining whether stomach motor function will be sensitive to changes in blood glucose is the method used to stimulate gastric contractions, and that the primary site of the inhibitory action of iv glucose on gastric motility is the central nervous system rather than the periphery.