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采用大鼠肠系膜上动脉夹闭致肠缺血模型，观察酸性成纤维细胞生长因子（ａＦＧＦ）对肠缺血－再注流诱发肝损伤的防治效应。２４只大鼠随机分成ａＦＧＦ治疗组与肝素ＰＢＳ对照治疗组，分别于肠系膜上动脉夹闭４５ｍｉｎ后放松血管夹即刻从颈外静脉注入ａＦＧＦ２．６μｇ或相同剂量的肝素ＰＢＳ。用血浆酶学与肝形态学指标评价治疗效果。结果表明，经ａＦＧＦ治疗大鼠伤后第１天血浆中ＳＧＰＴ与ｓＧＯＴ较对照组明显减少（ＳＧＰＴ分别为１０００．２±３６７Ａｎｍｏｌ·ｓ￣（－１）／Ｌ与２６４５．５±１０５６．９ｎｍｏｌ·ｓ￣（－１）／Ｌ；ＳＧＯＴ分别为４２８０．９±１２４７．７ｎｍｏｌ·ｓ￣（－１）／Ｌ与６１２３．４±２０１９．２ｍｍｏｌ·ｓ￣（－１）／Ｌ，Ｐ＜０．０５）。组织学检查发现，经ａＦＧＦ治疗后大鼠肝嗜酸细胞浸润、脂肪降解、肝细胞空泡变等较对照组明显减轻，而糖原含量增多。ａＦＧＦ对肠缺血致肝损伤显著的防治效应可能来自于它在体内诱导的促分裂效应与非促分裂激素样活性等方面。提示：采用ａＦＧＦ治疗，有可能为内脏损伤修复开辟一条新的途径。
The rat model of intestinal ischemia induced by intestinal mesenteric artery occlusion was used to observe the preventive and therapeutic effects of aFGF on intestinal ischemia-reperfusion-induced liver injury. Twenty-four rats were randomly divided into aFGF treatment group and heparin PBS control treatment group, respectively, after clamping the superior mesenteric artery for 45 min, the vessel clips were relaxed and immediately injected with aFGF2.6 μg or the same dose of heparin PBS from the external jugular vein. Evaluation of therapeutic effect by plasma enzymology and liver morphology. The results showed that the SGPT and sGOT in plasma decreased significantly at 1 day after injury (SGPT were 1000.2 ± 367Anmol · s -1 / L and 2645.5 ± 1056.9nmol · s-1 / L; SGOT were 4280.9 ± 1247.7 nmol · s -1 / L and 6123.4 ± 2019.2 mmol · s -1 / L, P <0. 05). Histological examination found that aFGF treatment of rat liver eosinophil infiltration, fat degradation, hepatocyte vacuolization compared with the control group was significantly reduced, while the glycogen content increased. A significant protective effect of aFGF on intestinal ischemia-induced liver injury may come from its in vivo-induced mitogenic effects and non-mitogenic hormone-like activity. Tip: With aFGF treatment, it is possible to open up a new way for the repair of visceral injuries.