The acute decrease of myocardial stiffness induced by beta-adrenergic stimulation is independent of the endocardial endothelium and prostaglandins release.

• Type: Summary of Presentation in an International Conference
• Date: 2007

Authors

Falcão-Pires I (Author) FMUP; Fontes-Sousa AP (Author) Other; Brás-Silva C (Author) FMUP; Leite-Moreira AF (Author) FMUP

Conference proceedings International

Title: European Journal of Heart Failure

Initial page: 38

Heart Failure 2007

Hamburgo, Alemanha, 09 a 12 de Junho de 2007

Scientific classification

FOS: Medical and Health sciences > Other medical sciences

Other information

Resumo (PT): Recent studies have shown that neurohumoral agents such as angiotensin II (Ang II), endothelin-1 (ET-1) and β-adrenergic stimulation acutely decrease myocardial stiffness. Concerning the latter, its effect is dependent on PKA, PKC and NA+/H+ exchanger. It was also demonstrated that the effect promoted by Ang II and ET-1 is, among others, dependent on the integrity of the endocardial endothelium (EE) and the release of nitric oxide and prostaglandins. The present study investigated the role of EE and prostaglandins on β-adrenergic induced diastolic distensibility. Effects of increasing concentrations of isoproterenol (ISO; 10-10 to 10-5M) were evaluated in isolated right papillary muscles from male New Zealand White rabbits (Krebs-Ringer: 1.8mM CaCl2, 35°C) in the presence of: (i) intact EE (n=11); (ii) damaged EE (Triton X-100, 0.5%, 1s, n=7) and (iii) Indomethacin (INDO; cyclooxigenase inhibitor, 10-5M; n=7). Reported parameters include: active tension (AT; mN/mm2), maximum velocities of tension rise and decline (dT/dtmax and dT/dtmin, respectively; mN/mm2/s), passive tension (PT; mN/mm2) and muscle length (L; L/Lmax). Only significant results (mean±SEM, p<0.05) are given, expressed as%change frombaseline.ISO induced concentration-dependent positive inotropic and lusitropic effects maximal at 10-5M, which increased 93.1±15.7% AT, 286.6±32.9% dT/dtmax, and 166.1±23% dT/dtmin. The same concentration of ISO induced a significant increase of the muscular length from Lmax to 1.018±0.005 L/Lmax, which corresponds to a 37.5±7.6% decrease of PT and represents a significant decrease of myocardial stiffness. The diastolic myocardial effects of ISO were maintained after removing EE and in the presence of INDO. This study demonstrated that β-adrenergic stimulation acutely increases myocardial distensibility even after EE removal and is independent of prostaglandin release in contrast to what happened with other neurohumoral agents. This might have important pathophysiologic implications in heart failure as well as several other pathological conditions where EE dysfunction occurs.

Language: English

Type (Professor's evaluation): Scientific

Notes: Heart Failure 2007, published in journal, European Journal of Heart Failure Supplements. 2007; 6(Suppl. 1):38.