Journal
CARDIOVASCULAR DRUGS AND THERAPY
Volume 28, Issue 6, Pages 493-500Publisher
SPRINGER
DOI: 10.1007/s10557-014-6559-0
Keywords
Infarct size; Apoptosis; LV function; Cardiomyopathy; Phosphodiesterase-5 inhibitors
Funding
- American Heart Association [10SDG3770011, 14GRNT20010003]
- Virginia Commonwealth University Presidential Research Quest Fund
- National Institutes of Health [HL-51045, HL-79424, HL-93685]
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Phosphodiesterase-5 (PDE5) inhibitors were shown to exert powerful protection in various animal models of cardiomyopathy. Tadalafil is a long-acting and highly specific PDE5 inhibitor, which makes it the most attractive in its class for long-term management of patients with heart failure. We studied the effects of tadalafil in attenuating ischemic cardiomyopathy in mice. Adult male mice underwent myocardial infarction (MI) by permanent left coronary artery ligation and were treated daily with tadalafil (1 mg/kg; ip) or volume-matched 10 % DMSO for 4 weeks. Twenty four hours after coronary ligation, infarct size, measured by TTC staining, was reduced from 70.1 +/- 3.1 % in DMSO-treated group to 49.3 +/- 2.6 % with tadalafil (P < 0.05). Similarly, tadalafil treatment yielded a smaller fibrotic area (8.8 +/- 2.8 % of LV), assessed by Masson's trichrome staining, as compared to DMSO group (21.9 +/- 3.9 %, P < 0.05). Apoptosis, measured by TUNEL assay, also declined with tadalafil (2.1 +/- 0.2 %) as compared to DMSO (6.7 +/- 0.4 %, P < 0.05) at 28 days post MI. Tadalafil also attenuated the increase in cardiac hypertrophy and pulmonary edema following infarction. These parameters reflect diminished left ventricular (LV) adverse remodeling and preserved fractional shortening with tadalafil at 7 and 28 days post infarction. Tadalafil attenuates ischemic cardiomyopathy in mice and preserves LV function.
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