High-precision aortic banding with O-rings: a versatile model for studying heart failure mechanisms in rats.

Animal models play a critical role in cardiovascular research, and reliable and reproducible phenotypes are essential. Aortic banding is a well-established technique for inducing pressure overload/heart failure in rats; however, conventional methods often lead to variability in outcomes. This study aims to use rubber O-rings to achieve reliable pressure overload in rats and to investigate how varying ring sizes result in distinct cardiac phenotypes 6 wk postsurgery. Male Sprague-Dawley rats (∼100 g, ∼4 wk old) underwent surgical aortic banding using nitrile O-rings of three different sizes (1.5, 1.3, and 1.07 mm) plus a sham-operated group. The rats were then monitored for 6 wk, after which cardiac function and structure were evaluated using echocardiography and magnetic resonance imaging (n = 70 rats). Expression of molecular markers of cardiac remodeling was also quantified. We found that all banded rats developed significant left ventricular hypertrophy, with ∼42%-58% higher ventricular weights than controls. The 1.07 mm group showed a decline in stroke volume and ejection fraction, indicative of reduced systolic function, while also exhibiting signs of diastolic dysfunction. Congestion indices were also severely impacted in the 1.07 mm group, and tissue fibrosis gene expression was higher in the 1.5 mm and 1.07 mm groups. The O-ring method successfully creates distinct cardiac phenotypes that reflect various degrees of heart failure, from hypertrophy to congestion with reduced ejection fraction. The associated increase in cardiac fibrosis gene expression and impaired diastolic function with tighter constriction underscores the utility of this model for studying heart failure mechanisms.NEW & NOTEWORTHY This study shows that the high-precision O-ring aortic banding method in rats reliably produces graded and reproducible cardiac phenotypes, ranging from compensated hypertrophy to congestive heart failure with reduced ejection fraction. By linking fixed degrees of pressure overload to distinct systolic, diastolic, and fibrotic adaptations quantified by echocardiography, MRI, and molecular analyses, the model provides a robust and translational platform for mechanistic studies of pressure overload-induced heart failure.