title: [Influence of metabolism modifiers of cyclic nucleotides on contractility of right ventricle of rat heart with intact and removed endocardial endothelium].
abstract: BACKGROUND
  Endocardial endothelium, a natural biological barrier between circulating blood in heart ventricle and cells, creates a complex yet finely tuned balance of interactions with the immediate environment.
  
  
  OBJECTIVE
  We investigated the roles of theophylline, nonspecific phosphodiesterase inhibitor, and imidazole, an activator of phosphodiesterase on contractility of the right ventricle of rat heart, with intact and removed endocardial endothelium.
  
  
  METHODS
  Adult rats, of both sexes, type Wistar albino, were used in this experiment. All experiments were conducted on the preparations of the right ventricle using two experimental models. In the first experimental model, an endocardial endothelium (EE) was preserved, and in the second model, an endocardial endothelium (-EE) was removed using 1% solution Triton X-100.
  
  
  RESULTS
  Theophylline (1 x 10(-2) mol/l) expressed the positive inotropic effect on the heart, regardless of the presence of the endocardial endothelium. Inotropic response as multiple process can be induced by inhibition of phosphodiesterase, accumulation of cyclic nucleotides and activation of Ca2+ channels. Imidazole (2 x 10(-3) mol/l) increased the contractility of the right ventricle of the heart with EE. The modulator effect of endocardial endothelium on contractility of imidazole proved to be significant. As imidazole influenced the contractility of the right ventricle only in the presence of the endocardial endothelium, it is assumed that its effect is mediated via deliverance of endothelial mediators with positive inotropic effect.
  
  
  CONCLUSIONS
  An intact endocardial endothelium is necessary for completion of contractile performance of the heart.
authors.affiliation: Institute of Physiology, School of Medicine, Kosovska Mitrovica. srna@eunet.rs
authors.forename: Sonja
authors.initials: S
authors.lastname: Smiljić
authors.forename: Dragica
authors.initials: D
authors.lastname: Radović
authors.forename: Milanka
authors.initials: M
authors.lastname: Miletić
authors.forename: Vojkan
authors.initials: V
authors.lastname: Nestorović
authors.forename: Goran
authors.initials: G
authors.lastname: Trajković
authors.forename: Sladjana
authors.initials: S
authors.lastname: Savić
mesh_terms: D000818:Animals; D004699:Endocardium / Q000187:drug effects / Q000502:physiology*; D004727:Endothelium / Q000187:drug effects / Q000502:physiology*; D004789:Enzyme Activation; D007093:Imidazoles / Q000494:pharmacology*; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D009712:Nucleotides, Cyclic / Q000378:metabolism*; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D010727:Phosphoric Diester Hydrolases / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013806:Theophylline / Q000494:pharmacology*; D016278:Ventricular Function, Right / Q000187:drug effects* / Q000502:physiology
chemical_list: D007093:Imidazoles; D009712:Nucleotides, Cyclic; D010726:Phosphodiesterase Inhibitors; C029899:imidazole; D013806:Theophylline; D010727:Phosphoric Diester Hydrolases