一项研究说，万艾可能帮助减缓和逆转杜兴氏肌营养不良小鼠模型的心脏损伤。

尽管有一些药物能够帮助维持一些杜兴氏肌营养不良患者的心脏功能，许多患者因为心脏功能不全而产生充血性心衰竭。杜兴氏肌营养不良是一种常常致命的肌肉消耗性遗传病，它是由缺乏肌肉蛋白质——抗肌萎缩蛋白导致的。

由于抗肌萎缩蛋白很可能帮助在几种组织中维持称为环磷酸鸟苷的信号传导分子的正常水平，Joseph A. Beavo、Stanley C. Froehner及其同事测试了万艾可对肌营养不良小鼠模型的心功能的作用，万艾可能阻断一种分解环磷酸鸟苷的酶。这组作者报告说，在短时间内，用万艾可治疗不仅减缓了心功能不全的发作，而且还恢复了患肌营养不良的小鼠左心室的功能。万艾可有助于维持和恢复患肌营养不良的小鼠左心室的心室舒张和压缩功能。

此外，这组作者发现，万艾可对没有肌营养不良的小鼠的心功能没有作用。这组作者说，万艾可在影响心功能方面的准确作用模式尚不清楚，但是他们的发现提示这种药物可能有助于预防和逆转杜兴氏肌营养不良患者的心脏损伤。

英文摘要：

PNAS doi: 10.1073/pnas.1013077107

Sildenafil reverses cardiac dysfunction in the mdx mouse model of Duchenne muscular dystrophy
Candace M. Adamoa, Dao-Fu Daib,1, Justin M. Percivalc,1, Elina Minamid, Monte S. Willise, Enrico Patruccoa, Stanley C. Froehnerc,2, and Joseph A. Beavoa,2

Duchenne muscular dystrophy (DMD) is a progressive and fatal genetic disorder of muscle degeneration. Patients with DMD lack expression of the protein dystrophin as a result of mutations in the X-linked dystrophin gene. The loss of dystrophin leads to severe skeletal muscle pathologies as well as cardiomyopathy, which manifests as congestive heart failure and arrhythmias. Like humans, dystrophin-deficient mice (mdx mice) show cardiac dysfunction as evidenced by a decrease in diastolic function followed by systolic dysfunction later in life. We have investigated whether sildenafil citrate (Viagra), a phosphodiesterase 5 (PDE5) inhibitor, can be used to ameliorate the age-related cardiac dysfunction present in the mdx mice. By using echocardiography, we show that chronic sildenafil treatment reduces functional deficits in the cardiac performance of aged mdx mice, with no effect on normal cardiac function in WT controls. More importantly, when sildenafil treatment was started after cardiomyopathy had developed, the established symptoms were rapidly reversed within a few days. It is recognized that PDE5 inhibitors can have cardioprotective effects in other models of cardiac damage, but the present study reports a prevention and reversal of pathological cardiac dysfunction as measured by functional analysis in a mouse model of DMD. Overall, the data suggest that PDE5 inhibitors may be a useful treatment for the cardiomyopathy affecting patients with DMD at early and late stages of the disease.