Cho C H, Qui B S, Bruce I C
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
J Gastroenterol Hepatol. 1996 Feb;11(2):125-8. doi: 10.1111/j.1440-1746.1996.tb00048.x.
Indirect evidence suggests that stress ulceration is provoked by vagal hyperactivity. However, direct evidence of hypervagal activity during stress conditions is lacking. Experiments were designed to directly measure vagal activity under different stress conditions in rats. Starvation stress for 48 h did not change the mean amplitude of action potentials, but their frequency was significantly decreased. Restraint stress at 22 degrees C increased vagal activity, both amplitude and frequency, in the first 60 min; these responses were markedly enhanced by cold (4 degrees C) and persisted for at least 2 h. Starvation for 48 h did not induce any gastric mucosal lesions. Restraint alone produced petechiae in the gastric mucosa, but cold restraint induced severe haemorrhagic ulcers. It is concluded that cold restraint stress provokes a prolonged vagal hyperactivity, which is one of the causative factors for gastric ulceration.
间接证据表明，应激性溃疡是由迷走神经活动亢进引起的。然而，缺乏应激状态下迷走神经活动亢进的直接证据。设计实验直接测量大鼠在不同应激条件下的迷走神经活动。48小时的饥饿应激并未改变动作电位的平均幅度，但其频率显著降低。在22摄氏度下的束缚应激在最初60分钟内增加了迷走神经活动，包括幅度和频率；寒冷（4摄氏度）显著增强了这些反应，并持续至少2小时。48小时的饥饿并未诱发任何胃黏膜损伤。单独束缚会在胃黏膜产生瘀点，但冷束缚会诱发严重的出血性溃疡。结论是，冷束缚应激会引发长时间的迷走神经活动亢进，这是胃溃疡形成的致病因素之一。
