We carry out in vivo hemodynamic measurements to study right-ventricular properties, pulmonary-vasculature properties and their interaction during open chest surgeries in an animal model of pulmonary arterial hypertension (PAH). The blood pressure-volume relations in the right ventricle sheds light on the contractility of the ventricular wall and the elasticity of the arterial system. We are specifically interested in how the contractility of the right ventricle compares to the elasticity of the pulmonary arteries and how these parameters change in response to pressure overload due to PAH. Similarly, with measurements of blood pressure and flow in the pulmonary artery we investigate the changes in impedance spectrum as a function of PAH.
Right Ventricle Mechanics
Our research on right ventricular (RV) mechanics focuses on understanding the tissue-level properties of the myocardium and its’ constituents. Here, we use a planar biaxial testing protocol to obtain stress-strain measurements of intact (fully cellularized) and decellularized RV samples. Our goal is to then describe these mechanical tissue-level changes as a function of PAH.
We are interested in modeling the mechanical properties of the left and right pulmonary arteries in a normo- and hypertensive rat animal model. The harvested vessels are subjected to tubular biaxial testing in the axial and circumferential directions. The resulting dynamic stress-strain relation is analyzed and modeled to quantify vessel characteristics during the progression of PAH.
Structural Studies of the Pulmonary Vasculature
Using a multi-photon microscope, we scan transmurally the pulmonary arteries and identify the collagen and elastin fiber organization. This approach is based on the second-harmonic generation imaging. For these experimental studies, the vessels are placed in a chamber filled with saline solution and stretched to match their in vivo conditions as close as possible.
Fluid Structure Interaction Models
Our research goal is to incorporate our tissue-level findings into a fluid dynamics model to ultimately describe the interaction of the vascular wall and flow during the progression of PAH. The modeling approach includes quasi-linear viscoelasticity theory framework and Euler’s equations. Given our organ-level hemodynamic measurements, our modeling work involves optimization and parameter estimation routines, prediction, and model validations.