A computational model of ureteral peristalsis and an investigation into ureteral reflux.

The aim of this study is to create a computational model of the human ureteral system that accurately replicates the peristaltic movement of the ureter for a variety of physiological and pathological functions. The objectives of this research are met using our in-house fluid-structural dynamics code (CgLes-Y code). A realistic peristaltic motion of the ureter is modelled using a novel piecewise linear force model. The urodynamic responses are investigated under two conditions of a healthy and a depressed contraction force. A ureteral pressure during the contraction shows a very good agreement with corresponding clinical data. The results also show a dependency of the wall shear stresses on the contraction velocity and it confirms the presence of a high shear stress at the proximal part of the ureter. Additionally, it is shown that an inefficient lumen contraction can increase the possibility of a continuous reflux during the propagation of peristalsis.

In-vitro investigation of the hemodynamic responses of the cerebral, coronary and renal circulations with a rotary blood pump installed in the descending aorta.

This study investigates the hemodynamic responses of the cardiovascular system when a rotary blood pump is operating in the descending aorta, with a focus on the cerebral, coronary and renal autoregulation, using our in-house cardiovascular emulator. Several improvements have been made from our previous studies. A novel coronary system was developed to replicate the native coronary perfusion. Three pinch valves actuated by stepper motors were used to simulate the regional autoregulation systems of the native cerebral, coronary and renal circulations. A rotary pump was installed in the descending aorta, in series with the heart, and the hemodynamic responses of the cardiovascular system were investigated with a focus on cerebral, coronary and renal circulation over a wide range of pump rotor speeds. Experiments were performed twice, once with the autoregulation systems active and once with the autoregulation systems inactive, to reflect that there will be some impairment of autoregulatory systems in a patient with heart failure. It was shown that by increasing the rotor speed to 3000 rpm, the cardiac output was improved from 2.9 to 4.1 L/min as a result of an afterload reduction induced by the pressure drop upstream of the pump. The magnitudes of changes in perfusion in the cerebral, coronary and renal circulations were recorded with regional autoregulation systems active and inactive.