Objective To investigate the pathological manifestations of acute⁃stage radioactive myocardial damage and related mechanisms using an experimental animal model. Methods A total of 12 adult male Sprague⁃Dawley rats were randomly divided into control group and radiation group. In the radiation group, the model of radiation⁃induced myocardial damage was established by the irradiation of the anterior myocardial territory with 6⁃MV X⁃ray at a single dose of 20 Gy, and at 14 days after irradiation, HE staining was used to observe the morphological changes of cardiomyocytes and intercellular matrix, and Masson staining was used to observe the distribution of collagen fibers. The collagen volume fraction ( CVF) was used for semi⁃quantitative analysis. ELISA was used to measure the activity of total superoxide dismutase ( T⁃SOD) and the concentration of malondialdehyde ( MDA ) , and Western blot was used to measure the expression of the fibrosis marker protein collagen type I ( COL⁃1 ) and the endoplasmic reticulum stress⁃related proteins GRP78 and CHOP. The t⁃test, t ’⁃test, or nonparametric rank sum test was used for comparison between groups. Results At 14 days after local irradiation of the heart, the radiation group had disordered arrangement of cardiomyocytes, marked edema, rupture of some cardiomyocytes, mild karyopyknosis in cardiomyocytes, and infiltration of inflammatory cells in the myocardial interstitium, compared with the control group. Collagen fibers in the myocardial tissue were mainly distributed in the perivascular area and cardiomyocyte interstitium. The radiation group had a significantly higher CVF than the control group ( 11�35% vs. 5�23%, P=0�000 ) and a significant increase in the expression of COL⁃1 compared with the control group ( P=0�000) . The radiation group had significant increases in the activity of T⁃SOD and the concentration of MDA in the myocardial tissue compared with the control group ( T⁃SOD:156�61 U/mgprot vs. 137�06 U/mgprot, P= 0�042;MDA:2�36 nmol/mgprot vs. 1�31 U/mgprot, P=0�007) . Compared with the control group, the radiation group showed significant increases in the expression of endoplasmic reticulum stress⁃related proteins GRP 7 8 and CHOP ( P= 0�037 and 0�009 ) . Conclusions The pathological manifestations of acute⁃stage myocardial damage include degeneration of cardiomyocytes, inflammatory exudation in the interstitium, and deposition of collagen in the perivascular area and myocardial interstitium. Myocardial fibrosis can be observed in the acute stage of radiation⁃induced myocardial damage, and the mechanism may be related to oxidative stress and endoplasmic reticulum stress induced by radioactive rays.%目的：建立实验动物模型观察急性期放射性心肌损伤的病理学表现，探索损伤机制。方法12只成年雄性SD大鼠按完全随机法均分为对照组和照射组。照射组采用6 MV X线单次20 Gy经心前区照射构建放射性心脏损伤模型，照后第14天HE染色观察心肌细胞及细胞间质形态学改变，Masson染色观察胶原纤维分布情况。以心肌胶原容积分数（ CVF）半定量分析。 ELISA法检测总超氧化物歧化酶（ T⁃SOD）活力和丙二醛（ MDA）浓度。蛋白印迹法检测纤维化标志性蛋白Ⅰ型胶原（ COL⁃1）和内质网应激相关蛋白GRP78和CHOP的表达水平。组间比较采用t、t’或非参数秩和检验。结果大鼠心脏局部照射后第14天，照射组较对照组心肌细胞排列紊乱，明显水肿，部分心肌细胞断裂，心肌细胞核轻度固缩，心肌间质炎性细胞渗出。心肌组织胶原纤维主要分布于小血管周围及心肌细胞间质。照射组CVF明显高于对照组（11�35％、5�23％，P＝0�000），COL⁃1表达水平升高（ P＝0�000）。放射线引起心肌组织T⁃SOD活力增高（156�61、137�06 U／mgprot，P＝0�042），同时伴MDA浓度上升（2�36、1�31 nmol／mgprot，P＝0�007）。放射线引起心肌组织内质网应激蛋白 GRP78和CHOP表达水平均升高（GRP78，P＝0�037，CHOP，P＝0�009）。结论急性期放射性心肌损伤的病理学表现主要为心肌细胞变性，间质炎性渗出，小血管周围和心肌间质胶原沉积。放射性心脏损伤急性期内即可发生心肌组织纤维化，机制可能与放射线引起的氧化应激、内质网应激有关。
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