目前，一则刊登在最新一期Circulation杂志上的一项研究"Sildenafil and B-Type Natriuretic Peptide Acutely Phosphorylate Titin and Improve Diastolic Distensibility In Vivo"发现壮阳药或可治疗舒张性心力衰竭。

　　德国科学家经研究发现，壮阳药能够以一种令人吃惊的方式帮助心脏恢复——降低心肌的僵硬度，从而治疗舒张性心力衰竭。这种药物研制之初的目的就是用于治疗心脏病，但更著名的功效却是提高性能力这种堪称意外之喜的“副作用”。

　　研究发现壮阳药能够为心脏患者带去福音。这种药物能够让过于僵硬的心室壁变得更具弹性。研究中，科学家揭示出壮阳药如何让舒张性心力衰竭患者受益。这种心脏病患者的主心室出现异常僵硬，无法充分泵血，导致血液进入肺部，引发呼吸困难。

　　科学家发现壮阳药能够激活一种促使心肌细胞中一种蛋白“放松”的酶。在服用壮阳药几分钟后，科学家在患有舒张性心力衰竭的狗身上发现这种效用。研究领导人、德国波鸿鲁尔大学的沃尔夫冈-林克教授表示：“我们第一次找到可用于治疗动物的疗法，我们希望能够在人类患者身上复制这种成功。”

　　壮阳药对血管产生类似影响，这也就是为什么这种药物研制之初的目的用于治疗高血压和心脏病。壮阳药中的有效成分西地那非能够抑制与血流控制机制有关的酶。然而，这种酶在身体不同部位存在微小差异。研制壮阳药的英国科学家最初陷入失望之中，因为这种药物无法有效治疗高血压患者。但令他们感到吃惊的是，壮阳药却对阳痿患者产生神奇疗效。

　　壮阳药能够有效抑制阴茎中的磷酸二酯酶，增加流入阴茎的血量。林克教授的研究小组发现，壮阳药能够对心脏细胞中同样的酶产生抑制作用，让心肌中的肌联蛋白变得更具弹性。林克说：“肌联蛋白分子与橡皮筋类似，对心壁的硬度产生决定性作用。”据统计，有近一半心力衰竭急诊患者存在心脏舒张问题。舒张性心力衰竭影响半个心动周期的心脏舒张，此时心室完成收缩，重新充满血。

原文阅读：

Sildenafil and B-Type Natriuretic Peptide Acutely Phosphorylate Titin and Improve Diastolic Distensibility In Vivo

Kalkidan Bishu， MD; Nazha Hamdani, PhD; Selma F. Mohammed, MBBS; Martina Kruger, PhD; Tomohito Ohtani, MD, PhD; Ozgur Ogut, PhD; Frank V. Brozovich, MD, PhD; John C. Burnett Jr, MD; Wolfgang A. Linke, PhD; Margaret M. Redfield, MD

　　Background—In vitro studies suggest that phosphorylation of titin reduces myocyte/myofiber stiffness. Titin can be phosphorylated by cGMP-activated protein kinase. Intracellular cGMP production is stimulated by B-type natriuretic peptide (BNP) and degraded by phosphodiesterases, including phosphodiesterase-5A. We hypothesized that a phosphodiesterase-5A inhibitor (sildenafil) alone or in combination with BNP would increase left ventricular diastolic distensibility by phosphorylating titin.Methods and Results—Eight elderly dogs with experimental hypertension and 4 young normal dogs underwent measurement of the end-diastolic pressure-volume relationship during caval occlusion at baseline, after sildenafil, and BNP infusion. To assess diastolic distensibility independently of load/extrinsic forces, the end-diastolic volume at a common end-diastolic pressure on the sequential end-diastolic pressure-volume relationships was measured (left ventricular capacitance). In a separate group of dogs (n=7 old hypertensive and 7 young normal), serial full-thickness left ventricular biopsies were harvested from the beating heart during identical infusions to measure myofilament protein phosphorylation. Plasma cGMP increased with sildenafil and further with BNP (7.31±2.37 to 26.9±10.3 to 70.3±8.1 pmol/mL; P<0.001). Left ventricular diastolic capacitance increased with sildenafil and further with BNP (51.4±16.9 to 53.7±16.8 to 60.0±19.4 mL; P<0.001). Changes were similar in old hypertensive and young normal dogs. There were no effects on phosphorylation of troponin I, troponin T, phospholamban, or myosin light chain-1 or -2. Titin phosphorylation increased with sildenafil and BNP, whereas titin-based cardiomyocyte stiffness decreased.Conclusion—Short-term cGMP-enhancing treatment with sildenafil and BNP improves left ventricular diastolic distensibility in vivo, in part by phosphorylating titin..

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