Background. Volume overload of the heart, either due to cardiovascular shunts or valve dysfunction may lead to LV dysfunction and heart failure over time.
Establishment of the disease model in small animals is required in order to study cellular and molecular mechanisms underlying cardiac volume overload.
Methods: We herein describe a volume overload rat model created in our laboratory by intoducing a fistula between exposed abdominal aorta and vena cava. The aorta and vena cava between the levels of renal arteries and iliac bifurcation were exposed. A needle (18 gauge) held on a plastic syringe was inserted into the exposed abdominal aorta and advanced through the medial wall into the vena cava to create the shunt. The ventral aortic puncture site was immediately sealed with a drop of cyanoacrylate after withdrawal of the needle. Creation of a successful fistula was verified by the pulsatile flow of oxygenated blood into the vena cava from the abdominal aorta. Sham-operated animals serving as controls were subjected to the same surgical procedure except for shunt creation.
Validation of the model: Rats subjected to aortocaval fistula (ACF) showed an increase in heart-to body weight ratio compared to control animals as early as two weeks after shunt introduction (4.3±0.0002 vs 3.4±0.005). Echocardiographic imaging studies demonstrated an increase in left ventricular end-diastolic diameter in ACF animals (0.535±0.035 cm vs. 0.37±0.01 cm, p=0.003). No significant change in left ventricular end-systolic diameter in ACF group was detected (0.22±0.007 cm vs. 0.21±0.04). Cardiac function estimated by left ventricular ejection fraction was normal in both groups.
Significance. Rats with aortocaval shunts have higher heart weights and left ventricle end diastolic volume indicating hypertrophy and dilatation of the left ventricle. Our newly established model may provide with an excellent platform to delineate specific mechanisms involved in LV remodelling.
