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目的 探讨胰岛Ａ细胞参与溃疡自愈调节的可能途径。 方法 应用形态计量、放射免疫测定及透射电镜方法，研究大鼠实验性胃溃疡自愈期间胰岛Ａ细胞的面数密度、超微结构及血清胰高血糖素的变化。 结果 与正常组及盐水组比较，Ａ细胞面数密度于溃疡后６ｄ、１０ｄ 明显增加（Ｐ＜ ０．０１）。溃疡后１４ｄ 开始呈减小趋势，２８ｄ 基本恢复正常。Ａ细胞超微结构变化在溃疡后第６～１４ｄ 较明显，主要表现为：（１）细胞核增大，异染色质减少，核周隙扩张；（２）部分Ａ 细胞粗面内质网增多，有的呈板层状排列，有的扩张成囊泡；（３）部分Ａ 细胞内分泌颗粒增多，大小不等，密度不一。血浆胰高血糖素水平从溃疡后１４ｄ 到２１ｄ 呈增高趋势（Ｐ＜ ０．０１），２８ｄ 时接近正常。 结论 胰岛Ａ细胞的形态和功能变化表明，它通过增加其细胞数目及增强其合成与分泌胰高血糖素的功能，积极参与了胃溃疡自愈的调节过程。
Objective To investigate the possible ways of islet A cells involved in the regulation of ulcer healing. Methods Morphometry, radioimmunoassay and transmission electron microscopy were used to study the number density, ultrastructure and serum levels of glucagon in islet A cells during experimental healing of gastric ulcer in rats. Results Compared with the normal group and the saline group, the number density of A cell surface increased significantly on the 6th day and the 10th day after ulcer (P <0.01). 14d after ulcer began to reduce the trend, 28d returned to normal. The ultrastructural changes of A cells in the sixth ~ 14d after ulcer were more obvious, mainly as follows: (1) The nucleus was enlarged, the heterochromatin was reduced and the perivascular space was expanded; (2) Some were lamellar arrangement, and some expansion into vesicles; (3) Part A cells increased endocrine particles, ranging in size and density. Plasma glucagon levels increased from 14d to 21d after ulcer (P <0.01), and nearly normal at 28d. Conclusion The morphological and functional changes of islet A cells suggest that it actively participates in the regulation of gastric ulcer healing by increasing the number of cells and enhancing the function of glucagon synthesis and secretion.