Treatment with a novel NHE-1 inhibitor at 3 mg/kg increased ejection fraction from 23% to 33% and prevented maladaptive left ventricle remodeling in a rat model of chronic heart failure.
Does a novel NHE-1 inhibitor improve hemodynamics, LV function, and remodeling in a rat model of chronic heart failure?
Absolute Event Rate: 33% vs 23%
p-value: p=<0.05
This study was designed to determine the potential therapeutic effects of a new sodium-hydrogen exchanger (NHE-1) inhibitor in the rat coronary artery ligation model of chronic heart failure. After the induction of acute myocardial infarction, rats were entered into a randomly designed pilot dose study from 0.3 mg/kg, 1.0 mg/kg, and 3.0 mg/kg. Solid state micrometer hemodynamics, echocardiographic, and pressure-volume relationships were measured after 6 weeks of treatment. Treatment with this NHE-1 inhibitor at 3 mg/kg increased (P<0.05) ejection fraction from 233% (N=6) to 332% (N=13), while the 1 mg/kg dose decreased (P<0.05) the infarct size in CHF rats from 21.71.4% (N=7) to 15.90.7% (N=3) and prevented (P<0.05) dilatation of the left ventricle in CHF rats in diastole (1.00.1 cm, N=6) to 0.90.1 cm, N=10) and in systole (0.90.1 cm, N=6) to 0.80.1, N=10). These study results suggest that this new NHE-1 inhibitor may be potentially useful in treating CHF with an improvement in maladaptive left ventricle remodeling. Because the mechanism of action of this agent is entirely different than the currently applied approach in treating CHF that focuses on aggressive neuro-hormonal blockade and because this agent does not adversely affect important hemodynamic variables, further investigations with this agent may be warranted.
Elizabeth Juneman (Mon,) conducted a other in Chronic Heart Failure (Myocardial Infarction Model) (n=71). Sodium-Hydrogen Exchanger (NHE-1) Inhibitor (BIX) vs. Control (standard rat chow) was evaluated on Ejection fraction (p=<0.05). Treatment with a novel NHE-1 inhibitor at 3 mg/kg increased ejection fraction from 23% to 33% and prevented maladaptive left ventricle remodeling in a rat model of chronic heart failure.