Rodríguez-Membrilla A, Martínez V, Jiménez M, Goñalons E, Vergara P
Department of Cell Biology and Physiology, Veterinary Faculty, Universidad Autónoma de Barcelona, Bellaterra, Spain.
Am J Physiol. 1995 Feb;268(2 Pt 1):G207-14. doi: 10.1152/ajpgi.1995.268.2.G207.
The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.
主要目的是研究一氧化氮（NO）在移行性肌电复合波（MMC）转变为餐后状态特征性的不规则电活动过程中的作用。大鼠和鸡均在小肠植入电极用于肌电图检查。静脉输注NO合酶抑制剂NG-硝基-L-精氨酸（L-NNA）可在喂食的大鼠中诱导出有组织的MMC样模式。输注NO供体硝普钠可破坏MMC，在禁食的大鼠中诱导出餐后样运动模式。同样，在鸡中，L-NNA模拟禁食模式，包括II期缩短、III期延长、MMC起始部向口腔移位以及III期传播速度增加。NO合成的抑制似乎参与了禁食运动模式的诱导，而NO的增加介导了喂食模式的出现。提示NO可能是小肠运动模式控制中的最终介质。
