Aim: To observe the gastric mucosal injury caused by hemorrhagic shock and reperfusion and to compare the effect between Salvia miltiorrhizae extract F (SEF) and cimetidine (CI) on it.
Methods: A model of hemorrhage/reperfusion injury was produced by Itoh method. Wistar rats were randomly divided into three groups: 0.9% sodium chloride treatment group (NS group), SEF treatment group (SEF group), and CI treatment group (CI group). Saline, SEF and CI were injected respectively. The index of gastric mucosal lesions (IGML) was expressed as the percentage of lesion area in the gastric mucosa. The degree of gastric mucosal lesions was categorized into grades 0, 1, 2, 3. Atom absorption method was used to measure the intracellular calcium content. Radioimmunoassay was used to measure the concentrations of prostaglandins.
Results: IGML (%) and grade 3 (%) were 23.18+/-6.82, 58.44+/-9.07 in NS group, 4.42+/-1.39, 20.32+/-6.95 in SEF group and 3.74+/-1.56, 23.12+/-5.09 in CI group, and the above parameters in SEF group and CI group decreased significantly (IGML: SEF vs NS, t = 6.712, P = 0.000<0.01; CI vs NS, t = 6.943, P = 0.000<0.01; grade 3: SEF vs NS, t = 8.386, P = 0.000; CI vs NS, t = 8.411, P = 0.000), but the grade 0 and grade 1 damage in SEF group (22.05+/-5.96, 34.12+/-8.12) and CI group (18.54+/-4.82, 30.15+/-7.12) were markedly higher than those in NS group (3.01+/-1.01, 8.35+/-1.95; grade 0: SEF vs NS, t = 8.434, P = 0.000<0.01; CI vs NS, t = 7.950, P = 0.000<0.01; grade 1: SEF vs NS, t = 8.422, P = 0.000<0.01; CI vs NS, t = 8.448, P = 0.000<0.01). The intracellular calcium content (microg/mg) in SEF group (0.104+/-0.015) and CI group (0.102+/-0.010) was markedly lower than that in NS group (0.131+/-0.019, SEF vs NS, t = 2.463, P = 0.038<0.05; CI vs NS, t = 3.056, P = 0.017<0.05). The levels (pg/mg) of PGE(2), 6-keto-PGF(1alpha) and 6-keto-PGF(1alpha)/TXB(2) were 540+/-183, 714+/-124, 17.38+/-5.93 in NS group and 581+/-168, 737+/-102, 19.04+/-8.03 in CI group, 760+/-192, 1 248+/-158, 33.42+/-9.24 in SEF group, and the above parameters in SEF group markedly raised (PGE(2): SEF vs NS, t = 2.282, P = 0.046<0.05; SEF vs CI, t = 2.265, P = 0.047<0.05; 6-keto-PGF(1alpha): SEF vs NS, t = 6.583, P = 0.000<0.000; SEF vs CI, t = 6.708, P = 0.000<0.01; 6-keto-PGF(1alpha)/TXB(2): SEF vs NS, t = 3.963, P = 0.003<0.001; SEF vs CI, t = 3.243, P = 0.009<0.01), whereas TXB(2) level in SEF group (45.37+/-7.54) was obviously lower than that in NS group (58.28+/-6.74, t = 3.086, P = 0.014<0.05) and CI group (54.32+/-6.89, t = 2.265, P = 0.047<0.05). No significant difference was shown between NS group and CI group (PGE(2): t = 0.414, P = 0.688>0.05; 6-keto-PGF(1alpha): t = 0.310, P = 0.763>0.05; TXB(2): t = 1.099, P = 0.298>0.05; 6-keto-PGF(1alpha)/TXB(2): t = 0.372, P = 0.718>0.05).
Conclusion: Both SEF and CI could inhibit reperfusion-induced injury in gastric mucosa, but with different mechanisms. SEF could not only enhance the protective effect of gastric mucosa, but also abate the injury factors, while CI can only abate the injury factors.