Autonomic pathways in development of neural stimulation-induced gastric mucosal damage.

Autonomic pathways in development of neural stimulation-induced gastric mucosal damage.
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DOI:
10.1152/ajpgi.1994.266.2.g179
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发表时间:
1994-02
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
L. Hierlihy;J. Wallace;A. Ferguson
L. Hierlihy;J. Wallace;A. Ferguson
中科院分区:
其他
文献类型:
--
作者:
L. Hierlihy;J. Wallace;A. Ferguson

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电刺激迷走神经(5 Hz,5 V,1 ms)或下丘脑室旁核(PVN)(200 microA,60 Hz,100微秒脉冲宽度)可诱发胃粘膜糜烂。我们已经利用各种药理学和手术干预,以确定自主神经系统的不同组成部分的发展,这种神经诱导的胃损伤在腰麻Sprague-Dawley大鼠的贡献。在所有实验中,对损伤进行肉眼评估,并以0(正常)至3(严重)等级进行盲法评分,将样品切片,用于随后在光学显微镜水平上对损伤进行组织学评估。与未处理的对照动物相比,经六甲铵(30 mg/kg iv)或阿托品(2 mg/kg iv)预处理的动物在迷走神经刺激后表现出胃损伤评分降低(P 0.05)。在研究的时间段内,这种脊髓横断本身并没有引起胃粘膜的任何显著变化。这些数据强调了自主神经系统的重要性,特别是迷走神经刺激引起的胃损伤的发展中的副交感神经成分。此外,目前的研究表明,迷走神经或PVN刺激诱导的胃损伤是依赖于神经投射到交感神经节前神经元的脊髓的中间外侧细胞柱。
Gastric mucosal erosions can be induced by electrical stimulation of either vagus nerves (5 Hz, 5 V, 1 ms) or the paraventricular nucleus (PVN) of the hypothalamus (200 microA, 60 Hz, 100-microseconds pulse width). We have utilized various pharmacological and surgical interventions to determine the contributions of different components of the autonomic nervous system to the development of this neurally induced gastric damage in urethan-anesthetized Sprague-Dawley rats. In all experiments damage was assessed macroscopically and scored blindly on a 0 (normal) to 3 (severe) scale with samples sectioned for subsequent histological assessment of damage at the light microscopic level. Animals pretreated with either hexamethonium (30 mg/kg iv) or atropine (2 mg/kg iv) demonstrated reduced gastric damage scores after vagal stimulation compared with untreated control animals (P 0.05). Such cord transection itself did not cause any significant change to the gastric mucosa in the time period studied. These data emphasize the importance of the autonomic nervous system, in particular the parasympathetic component in the development of vagal stimulation-induced gastric damage. In addition, the present studies suggest that neither vagal nor PVN stimulation-induced gastric damage is dependent on neural projections to sympathetic preganglionic neurons of the intermediolateral cell column of the spinal cord.