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Thorac Cardiovasc Surg 2012; 60(04): 247-254
DOI: 10.1055/s-0031-1298059
Original Basic Science
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Enhancement of Myocardial and Vascular Function after Phosphodiesterase-5 Inhibition in a Rat Model

Sivakkanan Loganathan
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Tamás Radovits
2   Heart Center, Semmelweis University, Budapest, Hungary
,
Sevil Korkmaz
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Kristóf Hirschberg
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Enikö Barnucz
2   Heart Center, Semmelweis University, Budapest, Hungary
,
Alexander Weymann
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Timo Bömicke
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Rawa Arif
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Matthias Karck
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
,
Gábor Szabó
1   Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany
› Author Affiliations
Further Information

Publication History

09 May 2011

16 August 2011

Publication Date:
17 January 2012 (online)

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Abstract

Background Recent studies have shown the potential of PDE-5 inhibition on acute and chronic heart failure. Nevertheless it remained unclear, how far load-reducing properties and direct effects on myocardial contractility are responsible for these observations. In the present study, we investigated the effects of vardenafil on myocardial contractility and vascular function in a dose–response study.

Methods We performed left ventricular pressure-volume analysis in young adult rats by using a Millar microtip conductance catheter. Pressure-volume loops were recorded before and after intravenous injection of vardenafil (3, 10, 30, 100, 300 μg/kg, n = 6/group).

Results Treatment with vardenafil resulted in a significant (p < 0.05) increase in the load-independent cardiac contractility parameters reaching its maximum at the dose of 100μg/kg (ESPVR: 2.15 ± 0.15 vs. 3.29 ± 0.26 mm Hg/μL; PRSW: 93.28 ± 4.04 vs. 134.90 ± 6.27 mm Hg; peak positive dP/dt/EDV: 38.73 ± 7.97 vs. 53.02 ± 3.74 mm Hg·s−1·µL−1; before versus after 100 μg/kg vardenafil). Results of the in vitro organ-bath experiments showed an augmented vasorelaxation of precontracted aortic rings after vardenafil treatment.

Conclusion Our data supports the hypothesis that the usage of vardenafil as “inodilators” could have beneficial effects in heart failure patients.

Keywords

contractility - heart failure - cardiac function - PDE-5 inhibition
 

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