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以大鼠浸水应激性胃溃疡为模型 ,从胃酸分泌、胃运动、胃粘膜一氧化氮合成酶 (NOS)和一氧化氮(NO)几方面观察 ip川芎嗪 (TMP)对大鼠应激性胃溃疡的影响 ,探讨 TMP的作用机制。结果 :TMP10～ 40m g/ kg可明显抑制大鼠浸水应激性胃溃疡的发生 ;TMP2 0 m g/ kg可促进胃液分泌量的增高 ,但对胃酸分泌无影响 ;并可明显抑制胃的运动 ;浸水应激后大鼠胃粘膜 NOS活力和 NO含量均明显降低 ,TMP可抑制应激导致的 NOS活力和 NO含量的降低。结论 :TMP通过抑制应激引起的胃粘膜 NOS活力的降低 ,提高胃粘膜NO含量 ,进而抑制胃运动途径来抗溃疡 ,而与胃酸分泌无关
The rat model of gastric ulcer induced by water infiltration was used to observe the effects of TMP on rat’s stress from gastric acid secretion, gastric movement, gastric nitric oxide synthase (NOS) and nitric oxide (NO). The effect of gastric ulcer, to explore the mechanism of action of TMP. RESULTS: TMP10 ~ 40mg/kg could significantly inhibit the occurrence of water-immersed gastric ulcer in rats; TMP20mg/kg could increase the secretion of gastric juice, but had no effect on gastric acid secretion, and could obviously inhibit the movement of stomach. After immersion in water, the NOS activity and NO content in gastric mucosa were significantly decreased. TMP could inhibit the decrease of NOS activity and NO content caused by stress. Conclusion : TMP can reduce the activity of NOS in the gastric mucosa induced by stress, increase the content of NO in gastric mucosa, and then inhibit the gastric motility pathway to resist ulcers, but not gastric acid secretion.