Response of Pulmonary Artery Endothelial Cells to Altered Stress Conditions

Healthy human hearts function with two ventricles; however, single ventricle defects (SVD), a type of congenital heart defect, results in one of these ventricles not functioning properly. A series of surgeries, culminating in the Fontan procedure, are used to correct these defects, which can vary widely. The resulting Fontan physiology of the heart can cause comorbidities as the patients grow, such as pulmonary hypertension and dysrhythmias. Because this subject is understudied, it is important to determine the connection between Fontan physiology, the comorbidities, and the potential cause of the complications. It is expected that the Fontan population is to double within the next 20 years. We hypothesize that wall shear stress plays a role in pulmonary hypertension, which may be a potential cause of Fontan failure. This work aims to determine a connection between wall shear stress and expression of various molecular markers by exposing cells to various stress conditions using an orbital shaker. We found that vascular endothelial growth factor, nitric oxide, and lipids may be a potential molecular marker in clinical settings for the detection of Fontan failure.