Zhao Xiaotuan, Yin Jieyun, Chen Jihong, Song Gengqing, Wang Lijie, Zhu Hongbing, Brining Doug, Chen Jiande D Z
Division of Gastroenterology, Department of Internal Medicine, University of Texas Medical Branch, Galveston, Texas 77555-0632, USA.
Am J Physiol Regul Integr Comp Physiol. 2009 Jan;296(1):R36-42. doi: 10.1152/ajpregu.90627.2008. Epub 2008 Oct 22.
The aim of this study was to investigate the effects and mechanisms of intestinal electrical stimulation (IES) on gastric tone, antral and pyloric contractions, and gastric emptying in dogs. Female hound dogs were equipped with a duodenal or gastric cannula, and one pair of serosal electrodes was implanted in the small intestine. The study consisted of five different experiments. Liquid gastric emptying was assessed by collection of chyme from the duodenal cannula in a number of sessions with and without IES and with and without N-nitro-l-arginine (l-NNA). Postprandial antral and pyloric contractions were measured with and without IES and in the absence and presence of l-NNA or phentolamine by placement of a manometric catheter into the antrum and pylorus via the duodenal cannula. Gastric tone was assessed by measurement of gastric volume at a constant pressure. Gastric emptying was substantially and significantly delayed by IES or l-NNA compared with the control session. IES-induced delay of gastric emptying became normal with addition of l-NNA. IES reduced gastric tone, which was blocked by l-NNA. IES also inhibited antral contractions (frequency and amplitude), and this inhibitory effect was not blocked by l-NNA but was blocked by phentolamine. IES alone did not affect pyloric tone or resistance, but IES + l-NNA decreased pyloric tone. In conclusion, IES reduces gastric tone via the nitrergic pathway, inhibits antral contractions via the adrenergic pathway, does not affect pyloric tone, and delays liquid gastric emptying. IES-induced delay of gastric emptying is attributed to its inhibitory effects on gastric motility.
本研究旨在探讨肠道电刺激（IES）对犬胃张力、胃窦和幽门收缩以及胃排空的影响及其机制。雌性猎犬配备十二指肠或胃插管，并在小肠植入一对浆膜电极。该研究包括五个不同的实验。通过在有和没有IES以及有和没有N-硝基-L-精氨酸（L-NNA）的多个时间段内从十二指肠插管收集食糜来评估液体胃排空。通过将测压导管经十二指肠插管插入胃窦和幽门，在有和没有IES以及在没有和存在L-NNA或酚妥拉明的情况下测量餐后胃窦和幽门收缩。通过在恒定压力下测量胃容积来评估胃张力。与对照时间段相比，IES或L-NNA使胃排空显著延迟。添加L-NNA后，IES引起的胃排空延迟恢复正常。IES降低胃张力，这被L-NNA阻断。IES还抑制胃窦收缩（频率和幅度），这种抑制作用不被L-NNA阻断，但被酚妥拉明阻断。单独的IES不影响幽门张力或阻力，但IES + L-NNA降低幽门张力。总之，IES通过一氧化氮能途径降低胃张力，通过肾上腺素能途径抑制胃窦收缩，不影响幽门张力，并延迟液体胃排空。IES引起的胃排空延迟归因于其对胃动力的抑制作用。
