Kang Yu-Ming, Bielefeldt Klaus, Gebhart G F
Department of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, Iowa 52242, USA.
J Neurophysiol. 2004 May;91(5):1981-9. doi: 10.1152/jn.01097.2003.
In the present study we examined the effects of acute thermal and chemical stimuli and gastric ulceration on mechanosensitive gastric vagal afferent fibers. Single-fiber recordings were made from the cervical vagus nerve. Mechanosensitive afferent fibers were identified by response to gastric distension (GD). Intragastric pressure was maintained below 3 mmHg during intragastric instillation of saline, heated saline, HCl, or glycocholic acid. Responses to graded GD (5-60 mmHg, 20 s, 4-min interval) were determined before and after 30-min exposure to thermal or chemical stimuli. All mechanosensitive fibers studied were C-fibers (mean CV: 1.07 +/- 0.07 m/s). Saline (37 degrees C) did not affect resting activity or alter responses to GD, but exposure to heated saline (46 degrees C) significantly increased resting activity and sensitized responses to GD. The decrease in resting activity was hydrochloric acid concentration dependent (0.025-0.2 N), but responses to GD were sensitized after 30-min exposure to 0.1 N HCl (n = 7). The bile acid glycocholic acid significantly increased resting activity and desensitized responses to GD at an intragastric pH of 7, and similarly increased resting activity but sensitized responses to GD (n = 6) at an intragastric pH of 1.2. Vagal afferents recorded in rats with gastric ulcers had significantly greater resting activity and responses to GD than sham ulcer rats; intragastric instillation of glycocholic acid (pH 1.2) further increased afferent fiber excitability. These findings indicate that acute gastric thermal and chemical stimuli alter the response characteristics of mechanosensitive vagal afferents in the absence of inflammation or structural damage. Accordingly, acute sensitization of gastric afferents through different stimulus modalities may contribute to the development of dyspeptic symptoms. In the presence of gastric inflammation, mechanosensitive vagal afferents exhibit a further increase in excitability.
在本研究中，我们检测了急性热刺激、化学刺激及胃溃疡对机械敏感的胃迷走传入纤维的影响。从颈迷走神经进行单纤维记录。通过对胃扩张（GD）的反应来识别机械敏感传入纤维。在向胃内灌注生理盐水、温热生理盐水、盐酸或甘胆酸期间，胃内压维持在3 mmHg以下。在暴露于热刺激或化学刺激30分钟之前和之后，测定对分级胃扩张（5 - 60 mmHg，20秒，间隔4分钟）的反应。所有研究的机械敏感纤维均为C纤维（平均传导速度：1.07±0.07 m/s）。生理盐水（37℃）不影响静息活动，也不改变对胃扩张的反应，但暴露于温热生理盐水（46℃）会显著增加静息活动，并使对胃扩张的反应敏感化。静息活动的降低依赖于盐酸浓度（0.025 - 0.2 N），但在暴露于0.1 N盐酸30分钟后，对胃扩张的反应敏感化（n = 7）。在胃内pH为7时，胆汁酸甘胆酸显著增加静息活动，并使对胃扩张的反应脱敏，而在胃内pH为1.2时，同样增加静息活动，但使对胃扩张的反应敏感化（n = 6）。患有胃溃疡的大鼠所记录的迷走传入纤维的静息活动和对胃扩张的反应显著高于假手术溃疡大鼠；向胃内灌注甘胆酸（pH 1.2）进一步增加了传入纤维的兴奋性。这些发现表明，在没有炎症或结构损伤的情况下，急性胃热刺激和化学刺激会改变机械敏感迷走传入纤维的反应特性。因此，通过不同刺激方式对胃传入纤维进行急性致敏可能会导致消化不良症状的出现。在存在胃炎症的情况下，机械敏感迷走传入纤维的兴奋性会进一步增加。
