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观察失血再灌注胃体部粘膜损伤及丹参提取物Ｆ与甲氰咪胍抗胃粘膜损伤的作用。方法：复制大鼠失血性休克再灌注损伤模型。实验分生理盐水（ＮＳ）组、丹参提取物Ｆ（ＤＳＥＦ）组及甲氰咪胍（ＣＩ）组。结果：（１）ＤＳＥＦ组及 ＣＩ组的胃体部粘膜损伤指数及重度损伤均明显低于 ＮＳ组（ Ｐ＜ ０． ０１），但ＤＳＥＦ组与 ＣＩ组间无显著性差鼻（ Ｐ＞０．０５）。（２） ＤＳＥＦ组的前列腺素 Ｅ２（ＰＧＥ２）、 ６－酮－前列腺素Ｆ１α／ （６－ｋｅＦ－ｔｏ－ＰＧＦ１α）及 ６－ｋｅｔｏ－ＰＧＦ１α／血栓素Ｂ２（ＴＸＢ２）比值明显高于ＮＳ及ＣＩ组（Ｐ＜０．０１， Ｐ＜０．０５）；而 ＴＸＢ２含量明显低于ＮＳ组及ＣＩ组（Ｐ＜０．０５）。但ＣＩ组与ＮＳ组间无显著性差异（Ｐ＞０．０５）。（３）ＤＳＥＦ组及ＣＩ组的细胞内钙含量明显低于 ＮＳ组（Ｐ＜ ０．０１），而 ＤＳＥＦ组与 ＣＩ组间无显著性差异（Ｐ＞ ０． ０５）。结论：在失血性休克再灌注诱导的大鼠胃体部粘膜损伤中，ＤＳＥＦ与 ＣＩ均具有防治作用，但机制不同。 ＤＳＥＦ既具有增强胃粘膜保护因子的作用又具有削弱攻击因子的作用，甲氰咪胍只有抵抗攻击因子的作用。
To observe the damage of gastric mucosa after hemorrhagic reperfusion and the effect of salvia miltiorrhiza extract F and cimetidine on gastric mucosal lesion. Method: To duplicate the model of hemorrhagic shock and reperfusion injury in rats. The rats in experiment group were divided into NS group, DSEF group and Cimetidine group. Results: (1) Mucosa injury index and severe injury of gastric mucosa in DSEF group and CI group were significantly lower than those in NS group (P <0.01), but there was no significant difference between DSEF group and CI group (P> 0.05). 05). (2) The ratios of prostaglandin E2 (PGE2), 6-keto-PGF1α / (6-keF-to-PGF1α) and 6-keto- PGF1α / TXB2 in DSEF group were significantly higher than those in NS and CI Group (P <0.01, P <0.05), while TXB2 content was significantly lower than NS group and CI group (P <0.05). However, there was no significant difference between CI group and NS group (P> 0.05). (3) The intracellular calcium content of DSEF group and CI group was significantly lower than that of NS group (P <0.01), while there was no significant difference between DSEF group and CI group (P> 0.05). Conclusion: Both DSEF and CI can prevent and treat gastric mucosal lesion induced by hemorrhagic shock and reperfusion in rats, but the mechanisms are different. DSEF not only enhances the function of gastric mucosal protective factor but also weakens the attack factor, and only cimetidine can resist the attack factor.