title: Enhancement of myocardial and vascular function after phosphodiesterase-5 inhibition in a rat model.
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.
  
  
  CONCLUSIONS
  Our data supports the hypothesis that the usage of vardenafil as "inodilators" could have beneficial effects in heart failure patients.
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 326, Heidelberg, Germany. sivakkanan.loganathan@googlemail.com
authors.forename: Sivakkanan
authors.initials: S
authors.lastname: Loganathan
authors.forename: Tamás
authors.initials: T
authors.lastname: Radovits
authors.forename: Sevil
authors.initials: S
authors.lastname: Korkmaz
authors.forename: Kristóf
authors.initials: K
authors.lastname: Hirschberg
authors.forename: Enikö
authors.initials: E
authors.lastname: Barnucz
authors.forename: Alexander
authors.initials: A
authors.lastname: Weymann
authors.forename: Timo
authors.initials: T
authors.lastname: Bömicke
authors.forename: Rawa
authors.initials: R
authors.lastname: Arif
authors.forename: Matthias
authors.initials: M
authors.lastname: Karck
authors.forename: Gábor
authors.initials: G
authors.lastname: Szabó
mesh_terms: D000818:Animals; D001011:Aorta / Q000187:drug effects*; D006328:Cardiac Catheterization; D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006339:Heart Rate / Q000187:drug effects; D007093:Imidazoles / Q000008:administration & dosage / Q000494:pharmacology*; D066298:In Vitro Techniques; D007275:Injections, Intravenous; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D009213:Myography; D058986:Phosphodiesterase 5 Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D010879:Piperazines / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013318:Stroke Volume / Q000187:drug effects; D013450:Sulfones / Q000008:administration & dosage / Q000494:pharmacology; D013997:Time Factors; D014227:Triazines / Q000008:administration & dosage / Q000494:pharmacology; D000069058:Vardenafil Dihydrochloride; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*; D016277:Ventricular Function, Left / Q000187:drug effects*; D017725:Ventricular Pressure / Q000187:drug effects
chemical_list: D002316:Cardiotonic Agents; D007093:Imidazoles; D058986:Phosphodiesterase 5 Inhibitors; D010879:Piperazines; D013450:Sulfones; D014227:Triazines; D014665:Vasodilator Agents; D000069058:Vardenafil Dihydrochloride