caa a22 4500 475833406 CHVBK 20180406123847.0 cr unu---uuuuu 170329e20001201xx s 000 0 eng 10.1023/A:1007890126061 doi (NATIONALLICENCE)springer-10.1023/A:1007890126061 Endothelin-A Receptor Antagonism during Acute Myocardial Infarction in Rats [Elektronische Daten] [Janice Pfeffer, Peter Finn, Leonardo Zornoff, Marc Pfeffer] Endothelin levels are increased in rats with experimentally induced myocardial infarction. The purpose of this study was to determine whether endothelin-A (ETA) receptor antagonism alters ventricular remodeling and the development of heart failure after myocardial infarction (MI). We administered 10 mg/kg/day of A-127722 to rats post-MI for 6 weeks. A hemodynamic study was performed and passive pressure-volume curves obtained. In rats without infarcts, ETA receptor antagonist (n=8; vehicle, n = 5) had no effect. However, in rats with infarcts ETA antagonism (n = 14, MI = 35%; vehicle: n = 19, MI = 32%) reduced systemic arterial and LV systolic (but not end-diastolic) pressures and shifted the pressure-volume relationship to the right. Because LV mass was not changed, the volume-to-mass ratio was increased and was correlated inversely with the ability of the LV to maximally develop pressure. This increase in volume at low distending pressures was also coupled with a tendency (P < 0.06) for reduced scar thickness, suggesting that early initiation of an ETA receptor antagonism increased infarct expansion. The reduction in blood pressure offset the increase in volume such that wall stresses were unchanged, as was LV mass. The early use of ETA receptor antagonism in the rat model of myocardial infarction did not beneficially alter LV remodeling. Kluwer Academic Publishers, 2000 ventricular remodeling nationallicence myocardial infarction nationallicence left ventricular pressures nationallicence pressure-volume relation nationallicence Pfeffer Janice Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut Finn Peter Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut Zornoff Leonardo Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut Pfeffer Marc Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut Cardiovascular Drugs and Therapy Kluwer Academic Publishers 14/6(2000-12-01), 579-587 0920-3206 14:6<579 2000 14 10557 https://doi.org/10.1023/A:1007890126061 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1007890126061 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Pfeffer Janice Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut NATIONALLICENCE 700 1- Finn Peter Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut NATIONALLICENCE 700 1- Zornoff Leonardo Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut NATIONALLICENCE 700 1- Pfeffer Marc Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA aut NATIONALLICENCE 773 0- Cardiovascular Drugs and Therapy Kluwer Academic Publishers 14/6(2000-12-01), 579-587 0920-3206 14:6<579 2000 14 10557 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer