目的：探讨大鼠糖尿病程进展中，心肌舒张功能和心肌纤维化程度进行性改变的情况。方法腹腔注射链脲佐菌素（ STZ）制备1型糖尿病大鼠模型。试验动物共分成4组：对照组，糖尿病4周组，8周组，12周组。测定各组大鼠心脏血流动力学参数，评价大鼠心肌舒张功能的变化；以Western blot测定各组大鼠心肌Ⅰ、ⅠⅠⅠ型胶原蛋白的表达，及心肌Masson染色的方法，评价心肌纤维化进展程度。结果糖尿病模型成功后，大鼠体重和心脏重量出现逐步下降；第8周开始出现左室舒张末压（ LVEDP）的显著增加，持续至第12周；左室峰值收缩压（ LVPSP）在第12周发生显示下降；同时，MASSON染色的结果显示，大鼠心肌间质纤维化程度逐步增加。Western blot结果显示，Ⅰ、ⅠⅠⅠ型胶原蛋白表达也于第8周同步出现显著增加。结论糖尿病可导致进展性心肌纤维化，是糖尿病程中心肌舒张功能减退的重要原因之一。%Objective To investigate the progressive alterations in myocardial fibrosis and cardiac diastolic dysfunction of rats with the progress of diabetes. Methods Rats were divided into 4 groups(n=12,each):a control group,and streptozotocin-induced rat models of dia-betes groups,examined after 4,8,or 12 weeks. The cardiac diastolic dysfunction of the diabetic rats were evaluated by the hemodynamic measure-ment. The myocardial fibrosis was assessed by the expressions of collagenⅠandⅠⅠⅠ,and MASSON staining. Results With the progression of dia-betes,the body weight and heart weight decreased step by step. Cardiac diastolic dysfunction was detected in the rats at the eighth week,The car-diac diastolic showed the significant increase in LVEDP. Ⅰn the meanwhile,the expressions collagenⅠandⅠⅠⅠwere increased significantly. The sig-nificant alteration in cardiac systolic function occurred at the twelfth week,which showed the marked decline in LVPSP. Conclusion Diabetes can result in progressive myocardial fibrosis,which is one of the important reasons for cardiac diastolic dysfunction in diabetes.
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