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作 者:张建福[1] 郑芳[1] 詹茂程[1] 孙东[1] 阎长栋[1]
出 处:《生理学报》1992年第6期583-590,共8页Acta Physiologica Sinica
摘 要:电刺激室旁核(PVN)有加重大鼠应激性胃粘膜损伤的作用;PVN内微量注射神经元胞体兴奋剂L-谷氨酸钠和电刺激PVN的效应相同;电解损毁双侧PVN或对其电刺激后,使应激性胃粘膜损伤明显减轻,切断膈下迷走神经或皮下注射阿托品后,可显著减轻电刺激PVN加重大鼠应激性胃粘膜损伤的效应;电刺激PVN使胃粘膜血流量减少,但对胃液量、胃酸排出量、胃蛋白酶活性及胃壁结合粘液量均无显著影响。从而表明,PVN是影响应激性胃粘膜损伤的特异性中枢部位之一,当其兴奋时,可加重应激性胃粘膜损伤,并可能是通过迷走神经胆碱能纤维起作用的,且与胃粘膜血流量的减少有关;电刺激PVN加重胃粘膜损伤似不是由胃液量、胃酸、胃蛋白酶活性及胃壁结合粘液量等因素的改变引起的。The effect of electrical stimulation of hypothalamic paraventricular nucleus(PVN) on gastric mucosal lesion induced by RWIS (restraint + water-immersionstress) in rats was investigated. The main results were as follows: (1) Electricalstimulation of the PVN could obviously increase the stress gastric mucosal lesion.(2) Microinjection of L-glutamate into PVN could produce similar effect to that ofPVN stimulation. (3) PVN lesion could significantly decrease the stress gastricmucosal lesion. (4) The above mentioned effects were attenuated by vagotomyor atropine injected subcutaneusly. (5) A further study indicated that the gastricmucosal blood flow was reduced upon PVN stimulation, but no obvious changesof gastric juice volume, total acid output, pepsin activity and gastric barrier mucuswere observed. The results mentioned above indicate that the PVN is one of the specific CNSareas capable of increasing the stress-induced gastric mucosal lesion mediatedthrough the cholinergic fibers of the vagal nerve and related to decreased gastricmucosal blood flow, while gastric acid output, pepsin activity and gastric barriermucus do not seem to play any important role.
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