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The goal of this study was to design, fabricate, and characterize a biocompatible flow chamber to study the performance of artificial heart valves. The system consists of a testing fluid chamber and a water chamber (separated by a latex diaphragm), following the design of a left ventricular assist device. Two St. Jude bileaflet mechanical heart valves were placed oppositely in the testing fluid chamber to control flow direction. The flow rate of the testing fluid chamber was set at 5.6 L/min, with a stroke volume of 80 ml. The performance of the system was examined through three-dimensional numerical simulation and in vitro experiments with whole blood and washed platelets. Hemolysis was measured with whole blood using a spectrophotometer. Platelet activation was measured by platelet surface P-selectin expression using flow cytometry. The three-dimensional computational fluid dynamics model demonstrated that the flow field in the chamber was laminar and physiological. Results from in vitro experiments indicated that the flow conditions in the chamber did not induce hemolysis or platelet activation with the presence of St. Jude heart valves. Overall, the flow chamber can provide a feasible environment to study the hemodynamic performance of artificial heart valves.

Secondhand smoke (SHS) has been reported to affect endothelial cells (EC) activities, but it is unclear if this effect would be altered under flow conditions. The goal of this study was to investigate if EC from different vascular beds would respond to SHS differently under dynamic shear stress. Human coronary artery EC (HCAEC), human umbilical vein EC (HUVEC) and human pulmonary artery EC (HPAEC) were grown to confluence and treated with SHS extract overnight. Cells were then exposed to pulsatile shear stress (0.1–1 Pa) in a cone and plate shearing device for 1 hour at 37°C. EC activation was measured by cell surface ICAM‐1 expression using a solid phase ELISA approach. The results demonstrated that SHS increased cell surface ICAM‐1 expression significantly on HCAEC, but did not have much effect on HUVEC and HPAEC. After EC were exposed to dynamic shear stress, ICAM‐1 expression on HCAEC decreased to the level observed on untreated cells. No change was observed with HUVEC. For HPAEC, shear stress decreased ICAM‐1 expression significantly, compared to untreated cells. These results demonstrated that EC from different vascular beds respond to SHS differently, and SHS could be more damaging to EC located in coronary arteries. Physiological pulsatile shear stress could inhibit cell activation in HCAEC and HPAEC, suggesting its protective role for arterial EC. This work is support by OCAST HR10–027.