中文摘要：

目的观察低剂量睾酮（TU）对心肌梗死后慢性心力衰竭雄性大鼠心室重塑及心功能的影响。方法60只健康雄性SD大鼠随机行冠状动脉结扎45只和假手术15只（PS组）。6周后行超声学检查左心室射血分数（LVEF）≤45％确定为模型成功标准。将存活模型鼠32只随机分为两组：TU干预组16只（TU组）给予TU5mg／（kg·2周）肌肉注射；安慰剂组16只（PL组）给予安慰剂。给药12周后进行超声检查评价心功能，放射免疫分析法测定血清睾酮浓度，RT-PCR测定心肌组织肿瘤坏死因子α（TNF—α）mRNA及基质金属蛋白酶（MMP）9mRNA表达量。结果心肌梗死后雄性大鼠血清睾酮浓度、LVEF均较PS组明显下降（P均〈0．05），心肌组织TNF—α mRNA、MMP-9mRNA表达均较PS组明显增多（P均〈0．05），低剂量睾酮干预后，LVEF较PL组明显改善（P〈0．05），心肌组织TNF—α mRNA和MMP-9mRNA表达明显减少（P均〈0．05），病死率明显降低（P〈0．05）。结论低剂量睾酮可抑制心肌梗死后雄性大鼠的免疫失衡和心室重塑，从而改善其心功能并降低病死率。

英文摘要：

Objective To investigate the effects of low dose testosterone on heart function, and ventricular remodeling in male rats with postinfarction congestive heart failure （CHF）. Methods Sixty SD rats were undergone surgery,of which,45 rats were performed coronary artery ligation and other 15 were sham group （PS group）. Six weeks later, left ventricular function of survived rats was examined by echocardiography, and LVEF≤45% was defined as the standard of successful CHF model. All survived model rats were randomly divided into 2 groups：TU group （n = 16） treated with TU 5 mg/kg per 2 weeks intramuscular injection;placebo （PL） group （ n = 16） treated with PL. After treatment for 12 weeks ,left ventricular ejection fraction（LVEF） was assessed by echocardiography again. Serum testosterone level was determined by radioimmunoassay. The expression of tumor necrosis factor-α （TNF-α） mRNA and matrix metalloproteinase （MMP）-9mRNA in myocardial tissue was measured by RT-PCR. Results In male post-myocardial infarction rats, serum testosterone level and LVEF were decreased significantly than PS group（ P 〈 O. 05 ）, and the expression of TNF-α mRNA and MMP-9 mRNA in myocardial tissue was increased significantly than PS group （ P 〈 0.05 ）. After low dose TU therapy, LVEF of rats in TU group improved significantly（P 〈 0.05）, and the expression of TNF-α mRNA and MMP-9 mRNA in myocardial tissue was reduced significantly （ P 〈 0.05 ） . Meanwhile, the mortality was decreased （P 〈 0.05）. Conclusion Low dose testosterone therapy can restore the inflammatory imbalance and suppress the ventricular remodeling in male post-myocardial infarction rats and improve left ventricular function, as well as reduce mortality.