酸性成纤维细胞生长因子对大鼠肠缺血-再灌注损伤影响的研究

Effects of acidic fibroblast growth factor on intestinal mucosal damage due to ischemia/reperfusion

目的 观察外源性酸性成纤维细胞生长因子 ( a FGF)对肠缺血再灌注损伤肠道保护效应及与组织损伤修复的关系。方法 采用肠系膜上动脉 ( SMA)夹闭 4 5 m in后松夹方法制备肠缺血再灌注损伤动物模型。将 Wistar大鼠随机分为假手术组、单纯肠缺血再灌注组及 a FGF治疗组。假手术组分离 SMA但不夹闭 ,4 5 min后取血并活杀动物 ;其余两组分别松夹形成血流再灌注 ,缺血再灌注组从尾静脉注射 0 .15 ml生理盐水 ,a FGF治疗组则从尾静脉给予 0 .15 m l( 4 g) a FGF。于再灌注后 0 .5、1、2、6、12和 2 4 h取血检测血浆D乳酸水平 ;活杀动物后取小肠组织行苏木素伊红 ( HE)染色 ,光镜下观察组织病理形态学改变 ;观察两组大鼠肠缺血再灌注损伤后不同时间点的存活率。结果 与肠缺血再灌注组各时间点比较 ,a FGF治疗组动物存活率均高于对照组 ,以 2 4 h最为显著 ,有统计学意义 ( P<0 .0 5 ) ;血浆 D 乳酸水平于再灌注后 1h则明显低于缺血再灌注组 ,至 2 4 h仍呈降低趋势 ( P均 <0 .0 5 ) ;小肠黏膜病理形态学改变较缺血再灌注组轻。结论 外源性 a FGF对肠缺血再灌注损伤有保护作用 。

Objective To investigate the effect of exogenous acidic fibroblast growth factor(aFGF) on ischemia/reperfusion(I/R) injury of the intestine in rat, and to explore the mechanism of its protective effect . Methods The model of rat intestinal I/R injury was replicated by clamping the superior mesenteric artery (SMA) for 45 minutes followed by reperfusion. Seventyeight Wistar rats were divided randomly into shamoperation group, intestinal I/R control group and aFGF treated group. In shamoperation group, SMA were separated but not occluded. Animals were sacrificed, samples of blood and tissue from the intestine were obtained 45 minutes after ischemia in shamoperation group and 0 5, 1, 2, 6, 12, and 24 hours after reperfusion in the other groups. Plasma Dlactate level was measured and rat survival rate was noted. Histological changes in intestinal tissue were observed under light microscope. Results The results showed that rat survival rate in aFGF treatment group was higher than that of intestinal I/R control group ( P <0 05), and plasma Dlactate levels were markedly lower in aFGF group than that of intestinal I/R control group ( P <0 05). Improvement in pathological changes was observed at 1, 2, 6, 12, and 24 hours after the reperfusion in aFGF treatment group compared with intestinal I/R control group. Conclusion These data suggest that aFGF has a protective effect on intestinal I/R damage, and it may be related to the mitogenic effects and some hormonelike activities of aFGF.