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目的：观察缺血再灌注导致肠道组织细胞凋亡发生的特征与规律，并探讨碱性成纤维细胞生长因子（ｂＦＧＦ）对细胞凋亡发生的影响和作用机制。方法：将７２只Ｗｉｓｔａｒ大鼠分成ｂＦＧＦ治疗组，生理盐水对照治疗组及假手术组３组。利用大鼠肠系膜上动脉夹闭４５分钟与再灌注４８小时模型，病理学与末端脱氧核糖转移酶介导的生物素化脱氧尿嘧啶缺刻标记技术（ＴＵＮＥＬ）方法，定量评价缺血再灌注导致大鼠肠道组织细胞凋亡与坏死的特征和ｂＦＧＦ的治疗作用。结果：肠系膜上动脉夹闭可导致肠道组织明显的缺血性损伤和细胞凋亡发生，凋亡细胞出现在肠粘膜上皮与粘膜下交界处，表现为肠粘膜上皮细胞核固缩或边缘化，部分可见凋亡小体。经ｂＦＧＦ治疗后，细胞凋亡现象可明显减轻。结论：缺血再灌注导致的肠道损伤主要来源于组织坏死与激活凋亡机制两方面，而这两方面作用均与细胞内钙离子超载密切相关；ｂＦＧＦ减轻肠道缺血性损伤可能与它能调控凋亡机制有关
OBJECTIVE: To observe the characteristics and regularity of apoptosis induced by ischemia-reperfusion in intestine tissue and to investigate the effect and mechanism of basic fibroblast growth factor (bFGF) on apoptosis. Methods: Seventy two Wistar rats were divided into three groups: bFGF treatment group, saline control treatment group and sham operation group. The model of rat superior mesenteric artery occlusion for 45 minutes and reperfusion for 48 hours was used to evaluate the effect of ischemia-reperfusion on the pathological and terminal deoxyribo-transferase-mediated biotinylated deoxyuridine nick labeling (TUNEL) Apoptosis and necrosis of rat intestinal tissue and the therapeutic effect of bFGF. Results: The superior mesenteric artery occlusion could lead to obvious ischemic injury and apoptosis in intestinal tissue. Apoptotic cells appeared at the junction of intestinal mucosa epithelium and submucosa, manifested as nuclear condensation or marginalization of intestinal epithelial cells, Part of the apoptotic body can be seen. The bFGF treatment, the phenomenon of apoptosis can be significantly reduced. CONCLUSIONS: Intestinal damage caused by ischemia-reperfusion mainly comes from two aspects: tissue necrosis and activation of apoptosis, both of which are closely related to intracellular calcium overload; bFGF may reduce intestinal ischemic injury may be associated with it Can regulate the mechanism of apoptosis