| Autor: |
McCarthy JC; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts., Aronovitz M; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts., DuPont JJ; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts., Calamaras TD; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts., Jaffe IZ; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts., Blanton RM; Molecular Cardiology Research Institute, Tufts Medical Center, Boston, Massachusetts. |
| Abstrakt: |
In patients hospitalized with acute heart failure, temporary serelaxin infusion reduced 6-month mortality through unknown mechanisms. This study therefore explored the cardiovascular effects of temporary serelaxin administration in mice subjected to the angiotensin II (AngII)/L-NG-nitroarginine methyl ester (L-NAME) heart failure model, both during serelaxin infusion and 19 days post-serelaxin infusion. Serelaxin administration did not alter AngII/L-NAME-induced cardiac hypertrophy, geometry, or dysfunction. However, serelaxin-treated mice had reduced perivascular left ventricular fibrosis and preserved left ventricular capillary density at both time points. Furthermore, resistance vessels from serelaxin-treated mice displayed decreased potassium chloride-induced constriction and reduced aortic fibrosis. These findings suggest that serelaxin improves outcomes in patients through vascular-protective effects. |
