山莨菪碱对利血平大鼠胃粘膜损伤的影响

目的:研究山食若碱对利血平大鼠胃粘膜损伤的影响及其作用机制。方法:利用利血平大鼠胃粘膜损伤模型，观察腹注山食若碱对利血平大鼠胃粘膜损伤、胃酸分泌、胃粘液分泌、胃运动、胃粘膜血流量及胃粘膜一氧化氮含量和一氧化氮合成酶活性变化的影响结果:山蓑若碱能抑制利血平大鼠胃粘膜损伤灶的形成;山食若碱能抑制利血平大鼠胃酸分泌，但对胃液分泌的量无影响;山食若碱能促进利血平大鼠胃粘液分泌和胃粘膜血流量，抑制胃的运动;山莫若碱能抑制利血平导致的大鼠胃粘膜一氧化氮含量的降低和一氧化氮合成酶活性的降低。结论:山食若碱抑制利血平大鼠胃粘膜损伤的形成与其抑制胃酸分泌、胃的运动，促进胃粘液分泌、增加胃粘膜血流量有关;NO可能在介导山莫若碱抑制利血平大鼠胃粘膜损伤形成中有重要作用。

Effect of anisodamine on the reserpine-induced gastric mucosal lesion in rats

AIM: To determine the effects of anisodamine (Ani) administered intraperitoneally on the gastric mucosal lesion induced by reserpine.METHODS:In reserpine-treated rats, gastric mucosal lesion, gastric acid secretion, gastric barrier mucus secretion, gastric contraction, gastric mucosal blood flow (GMBF), gastric mucosal nitric oxide synthase (NOS) activity and nitric oxide (NO) content were examined.RESULTS:Ani in doses of 1,5 and 10 mg/kg significantly inhibited the formation of gastric lesions induced by reserpine, with the suppressive rate of 60.0%, 66.7% and 76.6%, respectively. Ani (10 mg/kg) significantly inhibited the secretion of gastric acid, but had no effect on the volume of gastric juice. Ani (10 mg/kg) significantly prompted the secretion of gastric barrier mucus. Our findings also showed that Ani (10 mg/kg) significantly suppressed the frequency and amplitude of gastric contraction. Ani (10 mg/kg) significantly prompted GMBF. In reserpine treated rats, gastric mucosal NOS activity and NO content were decreased and Ani (10 mg/kg) could inhibit the decrease in NOS activity and NO content.CONCLUSIONS:The protective effect of Ani may results in part from inhibiting gastric acid secretion, prompting gastric barrier mucus secretion, suppressing gastric contraction and improving GMBF. NO seems to play an important mediator role in the Ani protective mechanisms.