中文摘要：

目的探讨小鼠胚胎心发育过程中前肠呼吸内胚层与第一生心区和第二生心区及胚胎心流出道的形态发生关系。方法胚龄7．5～13d小鼠胚胎心各3个，连续石蜡切片，用抗胰岛素增强子结合蛋白1（ISL-1）、抗心肌肌球蛋白重链（MHC）、抗“一平滑肌肌动蛋白（α—SMA）、抗Nkx2．5和抗增殖细胞核抗原（PCNA）抗体进行免疫组织化学或免疫荧光染色。结果胚胎发育7．5d，ISL-1在生心板心肌前体细胞表达并与发育中的第二生心区ISL-1阳性细胞连续。胚胎发育第10—13天，可见ISL-1强阳性的前肠腹侧呼吸内胚层细胞增生，排列不规则，失去极性，细胞间间隙明显，变为间充质样细胞，与周围ISL-1阳性间充质细胞无明确界限。紧邻动脉囊背侧壁，局部增生的内胚层向动脉囊方向生长，形成实心细胞索，ISL-1阳性间充质细胞围绕前肠腹侧呼吸内胚层及细胞索形成特征性锥体样结构。结论第一和第二生心区是连续结构，ISL-1同时是两个生心区心肌前体细胞的标记蛋白。呼吸内胚层和内胚层细胞索可能诱导第二生心区的扩展，并通过上皮-间充质转化，保持第二生心区细胞数量稳定。

英文摘要：

Objective To explore the morphological relationship of the pulmonary endoderm with the primary heart field （ PHF）, the second heart field （SHF） and the heart outflow tract during early development of mouse embryonic heart. Methods Serial sections of three mouse embryos each day from embryonic day（ED） 7.5 to embryonic day（ED） 13 were stained immunohistochemically or immunofluorescently with antibodies against insulin gene enhancer binding protein （ Islet- 1, ISL-1 ） , myosin heavy chain （MHC） , a-smooth muscle actin （ α-SMA）, Nkx2.5 and proliferating cell nuclear antigen （PCNA）. Results At ED7.5, ISL-1 positive cells in the cardiogenic plate were continuous with that of the developing SHF. From ED10 to ED13, ISL-1 positive pulmonary endoderm cells showed strong proliferation, irregular arrangement, loss the polarity with apparent intercellular space and changed to mesenchyme-like cells without obvious border with surrounding ISL-1 positive mesenchyme. Local proliferation of endoderm cells adjacent closely to the dorsal wall of aortic sac resulted in the formation of solid endoderm cord that extended towards aortic sac. Ventral to the foregut, ISL-1 positive mesenchyme cells surrounding the pulmonary endoderm and endoderm cord formed a distinctive cone-shaped structure. Conclusion PHF and SHF is a continuum and ISL-1 is an early marker for cardiac precursor cells in both structures. Pulmonary endoderm cells and the endoderm cord might play roles in inducing proliferation of ISL-1 positive cells or might transform to mescnchymal cells via epithelium-mesenchyme transition to maintain certain cell density of SHF.