1型糖尿病对主动脉缩窄大鼠结构和功能的影响

Effect of type 1diabetes mellitus on structure and function of rats with aortic coarctation

目的探讨糖尿病是否能加重左心室超负荷引起的心力衰竭。方法 3周龄雄性Wistar大鼠54只,随机分为4组:假手术组14只,胸主动脉缩窄(TAC)组12只,假手术+链脲佐菌素(STZ)组15只(STZ组),TAC+STZ组(联合组)13只。记录大鼠的体质量演变,并分别于TAC术后15、50d对所有大鼠行超声心动图检查。在TAC术后66d处死大鼠,分离左心房、右心房、心室等,进行称重,天狼星红染色分析心肌纤维化。结果与假手术组比较,STZ组50d舒张末室间隔厚度(IVST)、左心室后壁舒张末厚度(PWT)、左心室质量、心率明显降低(P<0.01);TAC组15dIVST、PWT、LVM明显升高(P<0.01)。与15d比较,TAC组和联合组50d左心室肥厚百分比明显增高(P<0.01)。与假手术组比较,STZ组大鼠体质量、左心室质量、左心房质量、肺脏质量、左心室质量/胫骨长度明显降低,左心室质量/体质量明显升高;而TAC组大鼠左心室质量、左心房质量、肺脏质量、左心室质量/胫骨长度、左心室质量/体质量明显升高(P<0.05,P<0.01)。结论糖尿病明显增加了TAC诱导的左心室肥厚,但并没有加重TAC大鼠模型的心力衰竭指征,可能是因为糖基化终产物的聚集所致。

Objective To study whether diabetes mellitus （DM） can aggravate left ventricular overload-induced heart failure.Methods Fifty-four male Wistar rats aged 3 weeks were randomly divided into sham operation group （n=14）,transverse aortic coarctation （TAC） group （n=12）,sham operation ＋ streptozocin （STZ） treatment group （n =15）,TAC ＋ STZ treatment group （n =13）.Their BMI and survival rate were recorded.The animals underwent echocardiography on days 15 and 50 after TAC surgery and were sacrificed on day 66 after TAC surgery.Their left atrium,right atrium and ventricle were isolated and weighed.Myocardial fibrosis was analyzed with Sirius red staining.Results The interventricular septal thickness （IVST）,posterior wall thickness （PWT）,left ventricular mass （LVM） and heart rate were significantly lower in STZ treatment group than in sham operation group on day 50.The IVST,PWT and LVM were significantly higher in TAC group than in sham operation group on day 15 （P＜0.01）.The incidence of LVH was significantly higher in TAC group and TAC＋STZ treatment group on day 50 than on day 15 （P＜0.01）.The BMI,LVM,LAM,lung M,LVM/tibia length were significantly lower while the LVM/BMI was significantly higher in STZ treatment group than in sham operation group but the BMI,LVM,LAM,lung M,LVM/tibia length were significantly higher in TAC group than in sham operation group （P＜0.05,P＜0.01）.Conclusion DM can significantly aggravate TACinduced LVH but not heart failure due to the accumulation of glycosylated end products.