Knudsen A, Frøbert O, Tøttrup A
Dept. of Surgical Gastroenterology L, Aarhus Kommunehospital, Denmark.
Scand J Gastroenterol. 1994 Dec;29(12):1083-7. doi: 10.3109/00365529409094892.
The aim of the study was to determine the effect of NG-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthesis, on primary peristalsis in the oesophageal body.
Peristalsis was induced by pharyngeal stroking in 14 lightly anaesthetized opossums. Oesophageal pressures were monitored with a four-channel, perfused catheter assembly and registered with external transducers 1, 4, 7, and 10 cm proximal to the oesophagogastric junction. Propagation time was the time taken for a contraction to travel between two recording sites and was determined in the proximal, middle, and distal parts of the oesophagus (propagation time between 10 and 7 cm, 7 and 4 cm, and 4 and 1 cm recording sites, respectively).
L-NNA (10(-7)-10(-5) mol/kg) dose-dependently reduced propagation time of the contraction in the distal oesophagus from 1.13 +/- 0.24 sec to 0.27 +/- 0.19 sec, whereas propagation in the proximal and middle parts of the oesophagus was unaffected. NG-nitro-D-arginine (D-NNA; 10(-5) mol/kg) had no influence on propagation time. In animals treated with L-NNA (10(-5) mol/kg) atropine (50 micrograms/kg) had no influence on propagation time in any part of the oesophagus. L-Arginine (10(-4) mol/kg) had no influence on the propagation time in animals treated with L-NNA (10(-5) mol/kg) and atropine (50 micrograms/kg). Neither D-NNA (10(-5) mol/kg) nor L-NNA (10(-7)-10(-5) mol/kg) influenced the amplitude of the contractions at any of the recording sites. In animals given L-NNA (10(-5) mol/kg) atropine (50 micrograms/kg) reduced the amplitude of the contraction significantly only at the distal recording site (1-cm recording site) from 62.0 +/- 4.9 mmHg to 34.5 +/- 5.3 mmHg. L-Arginine (10(-4) mol/kg) had no effect on the amplitude of contractions.
The L-arginine-NO pathway plays a role in the control of primary peristalsic contractions of the oesophagus.
本研究旨在确定一氧化氮（NO）合成抑制剂NG-硝基-L-精氨酸（L-NNA）对食管体部原发性蠕动的影响。
对14只轻度麻醉的负鼠进行咽部刺激以诱发蠕动。使用四通道灌注导管组件监测食管压力，并通过食管胃交界处近端1、4、7和10 cm处的外部换能器进行记录。传播时间是收缩在两个记录点之间传播所需的时间，在食管的近端、中部和远端进行测定（分别为10至7 cm、7至4 cm和4至1 cm记录点之间的传播时间）。
L-NNA（10⁻⁷ - 10⁻⁵ mol/kg）剂量依赖性地将远端食管收缩的传播时间从1.13 ± 0.24秒缩短至0.27 ± 0.19秒，而食管近端和中部的传播不受影响。NG-硝基-D-精氨酸（D-NNA；10⁻⁵ mol/kg）对传播时间无影响。在用L-NNA（10⁻⁵ mol/kg）治疗的动物中，阿托品（50微克/千克）对食管任何部位的传播时间均无影响。L-精氨酸（10⁻⁴ mol/kg）对用L-NNA（10⁻⁵ mol/kg）和阿托品（50微克/千克）治疗的动物的传播时间无影响。D-NNA（10⁻⁵ mol/kg）和L-NNA（10⁻⁷ - 10⁻⁵ mol/kg）均未影响任何记录点的收缩幅度。在用L-NNA（10⁻⁵ mol/kg）治疗的动物中，阿托品（50微克/千克）仅在远端记录点（1 cm记录点）显著降低收缩幅度，从62.0 ± 4.9 mmHg降至34.5 ± 5.3 mmHg。L-精氨酸（10⁻⁴ mol/kg）对收缩幅度无影响。
L-精氨酸-NO途径在食管原发性蠕动收缩的控制中起作用。
