These results suggest that selection of device type and flow rate can influence vascular pulsatility and input impedance, which might affect clinical outcomes.

A need exists for a mock circulation that behaves in a physiologic manner for testing cardiac devices in normal and pathologic states. To address this need, an integrated mock cardiovascular system consisting of an atrium, ventricle, and systemic and coronary vasculature was developed specifically for testing ventricular assist devices (VADs). This test configuration enables atrial or ventricular apex inflow and aortic outflow cannulation connections. The objective of this study was to assess the ability of the mock ventricle to mimic the Frank-Starling response of normal, heart failure, and cardiac recovery conditions. The pressure-volume relationship of the mock ventricle was evaluated by varying ventricular volume over a wide range via atrial (preload) and aortic (afterload) occlusions. The input impedance of the mock vasculature was calculated using aortic pressure and flow measurements and also was used to estimate resistance, compliance, and inertial mechanical properties of the circulatory system. Results demonstrated that the mock ventricle pressure-volume loops and the end diastolic and end systolic pressure-volume relationships are representative of the Starling characteristics of the natural heart for each of the test conditions. The mock vasculature can be configured to mimic the input impedance and mechanical properties of native vasculature in the normal state. Although mock circulation testing systems cannot replace in vivo models, this configuration should be well suited for developing experimental protocols, testing device feedback control algorithms, investigating flow profiles, and training surgical staff on the operational procedures of cardiovascular devices.

The phenotype and function of vascular cells in vivo are influenced by complex mechanical signals generated by pulsatile hemodynamic loading. Physiologically relevant in vitro studies of vascular cells therefore require realistic environments where in vivo mechanical loading conditions can be accurately reproduced. To accomplish a realistic in vivo-like loading environment, we designed and fabricated an Endothelial Cell Culture Model (ECCM) to generate physiological pressure, stretch, and shear stress profiles associated with normal and pathological cardiac flow states. Cells within this system were cultured on a stretchable, thin (∼500 μm) planar membrane within a rectangular flow channel and subject to constant fluid flow. Under pressure, the thin planar membrane assumed a concave shape, representing a segment of the blood vessel wall. Pulsatility was introduced using a programmable pneumatically controlled collapsible chamber. Human aortic endothelial cells (HAECs) were cultured within this system under normal conditions and compared to HAECs cultured under static and "flow only" (13 dyn/cm(2)) control conditions using microscopy. Cells cultured within the ECCM were larger than both controls and assumed an ellipsoidal shape. In contrast to static control control cells, ECCM-cultured cells exhibited alignment of cytoskeletal actin filaments and high and continuous expression levels of β-catenin indicating an in vivo-like phenotype. In conclusion, design, fabrication, testing, and validation of the ECCM for culture of ECs under realistic pressure, flow, strain, and shear loading seen in normal and pathological conditions was accomplished. The ECCM therefore is an enabling technology that allows for study of ECs under physiologically relevant biomechanical loading conditions in vitro.

Objectives In a univentricular Fontan circulation, modest augmentation of existing cavopulmonary pressure head (2–5 mmHg) would reduce systemic venous pressure, increase ventricular filling, and thus, substantially improve circulatory status. An ideal means of providing mechanical cavopulmonary support does not exist. We hypothesized that a viscous impeller pump, based on the von Kármán viscous pump principle, is optimal for this role. Methods A 3-dimensional computational model of the total cavopulmonary connection was created. The impeller was represented as a smooth 2-sided conical actuator disk with rotation in the vena caval axis. Flow was modeled under 3 conditions: 1) passive flow with no disc; 2) passive flow with a non-rotating disk, and 3) induced flow with disc rotation (0–5K rpm). Flow patterns and hydraulic performance were examined for each case. Hydraulic performance for a vaned impeller was assessed by measuring pressure rise and induced flow over 0–7K rpm in a laboratory mock loop. Results A nonrotating actuator disc stabilizes cavopulmonary flow, reducing power loss by 88%. Disk rotation (from baseline dynamic flow of 4.4 L/min) resulted in a pressure rise of 0.03 mmHg. A further increase of pressure of 5–20 mmHg and 0–5 L/min flow were obtained with a vaned impeller at 0–7K rpm in a laboratory mock loop. Conclusions A single viscous impeller pump stabilizes and augments cavopulmonary flow in 4 directions, in the desired pressure range, without venous pathway obstruction. It applies to the existing staged protocol as a temporary bridge-to-recovery or –transplant in established univentricular Fontan circulations. It may also enable compressed palliation of single ventricle without need for intermediary surgical staging or use of a systemic-to-pulmonary arterial shunt.