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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Gatón J, Fernández de la Gándara F, Velasco A

Department of Surgery, Faculty of Medicine, University of Valladolid, Spain.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1993 Sep;106(1):125-9. doi: 10.1016/0742-8413(93)90263-k.

Adrenergic and cholinergic mechanisms seem to be involved in the pathogenesis of stress ulcers. 2. In this study, gastric ulcers were induced in rats by immobilization and cold. Prior intraperitoneal administration of both anticholinergic (atropine) as well as alpha-blocking medication (phenoxybenzamine) produced a very significant decrease in stress ulcers. 3. Additionally, using the technique of continuous intravenous perfusion in rats, acetylcholine was shown to have a gastric ulcerogenic effect, in contrast to noradrenaline. 4. It is concluded that acetylcholine is the peripheral mediator in stress ulcers, while noradrenaline intervenes at the encephalic level in stress ulcer pathogenesis.

肾上腺素能和胆碱能机制似乎参与了应激性溃疡的发病过程。2. 在本研究中，通过束缚和寒冷诱导大鼠胃溃疡。预先腹腔注射抗胆碱能药物（阿托品）以及α-受体阻滞剂（酚苄明）可使应激性溃疡显著减少。3. 此外，采用大鼠连续静脉灌注技术，结果显示乙酰胆碱与去甲肾上腺素相反，具有致胃溃疡作用。4. 得出的结论是，乙酰胆碱是应激性溃疡的外周介质，而去甲肾上腺素在应激性溃疡发病机制中作用于脑水平。

Gatón J, Fernández de la Gándara F, Velasco A

Department of Surgery, Faculty of Medicine, University of Valladolid, Spain.

Comp Biochem Physiol C Comp Pharmacol Toxicol. 1993 Sep;106(1):125-9. doi: 10.1016/0742-8413(93)90263-k.

Adrenergic and cholinergic mechanisms seem to be involved in the pathogenesis of stress ulcers. 2. In this study, gastric ulcers were induced in rats by immobilization and cold. Prior intraperitoneal administration of both anticholinergic (atropine) as well as alpha-blocking medication (phenoxybenzamine) produced a very significant decrease in stress ulcers. 3. Additionally, using the technique of continuous intravenous perfusion in rats, acetylcholine was shown to have a gastric ulcerogenic effect, in contrast to noradrenaline. 4. It is concluded that acetylcholine is the peripheral mediator in stress ulcers, while noradrenaline intervenes at the encephalic level in stress ulcer pathogenesis.

肾上腺素能和胆碱能机制似乎参与了应激性溃疡的发病过程。2. 在本研究中，通过束缚和寒冷诱导大鼠胃溃疡。预先腹腔注射抗胆碱能药物（阿托品）以及α-受体阻滞剂（酚苄明）可使应激性溃疡显著减少。3. 此外，采用大鼠连续静脉灌注技术，结果显示乙酰胆碱与去甲肾上腺素相反，具有致胃溃疡作用。4. 得出的结论是，乙酰胆碱是应激性溃疡的外周介质，而去甲肾上腺素在应激性溃疡发病机制中作用于脑水平。