TY - JOUR
T1 - The cumulative and sublethal effects of turbulence on erythrocytes in a stirred-tank model
AU - Aziz, Abdulhameed
AU - Werner, Brian C.
AU - Epting, Kevin L.
AU - Agosti, Christopher D.
AU - Curtis, Wayne R.
N1 - Funding Information:
The first author is indebted to multiple colleagues at The Pennsylvania State University at University Park, particularly advisors Dr. Wayne Curtis and Dr. Lance Collins for constant encouragement in this project and for me to continue a career in research. We are also indebted to Benjamin Holcombe, Sara E. Leister and Amy Hsiao for significant contributions in the synthesis of the Curtis/Collins turbulence project. We also thank Brandon Curtis for engineering creativity in constructing our mixing control device. I also thank The Howard Hughes Medical Institute Summer Research program and Pennsylvania State University’s Schreyer Honors College for making this research possible. Lastly, I dedicate this paper to my parents, who consistently supported me in achieving all of my educational endeavors. The execution of this work was made possible with equipment obtained through support of the National Science Foundation (grant BES-9522033) as well as industrial matching funds for an NSF Young Investigator Award (BCS-9358452).
PY - 2007/12
Y1 - 2007/12
N2 - Mechanical forces generated by prosthetic heart devices (artificial valves, artificial hearts, ventricular assist devices) have been known to cause damage and destruction of erythrocytes. Turbulent flow within such devices generates shear stresses and can induce cell damage. Current models of cell damage rate utilize only the power input per unit mass as a modeling parameter. A stirred-tank reactor provides for a more extensive characterization of turbulence through eddy scale calculations. Through a simplified model, turbulence can be characterized by evaluating the Kolmogorov microscale. Our analysis of erythrocyte rupture in a stirred tank reactor suggests that parameters such as eddy wavelength and eddy velocity may better characterize and model the turbulent damage. Further, hemolysis of red blood cells by turbulent effects has been shown to have a fixed rate for constant levels of power input. Damage inflicted on the remaining, intact erythrocytes (sublethal damage) was evaluated by exposure to turbulence followed by osmotic fragility (OF) testing. Logistic models were fit to the OF data indicating a significant osmotic sensitivity in the sublethal damaged population between control and turbulence-exposed cells (χ 2 test; p < 0.001). This susceptibility indicates a significant cell population more susceptible to destruction as a result of turbulent exposure. This work has therefore helped identify optimization parameters for evaluating cell damage potential when engineering cardiovascular prosthetic devices.
AB - Mechanical forces generated by prosthetic heart devices (artificial valves, artificial hearts, ventricular assist devices) have been known to cause damage and destruction of erythrocytes. Turbulent flow within such devices generates shear stresses and can induce cell damage. Current models of cell damage rate utilize only the power input per unit mass as a modeling parameter. A stirred-tank reactor provides for a more extensive characterization of turbulence through eddy scale calculations. Through a simplified model, turbulence can be characterized by evaluating the Kolmogorov microscale. Our analysis of erythrocyte rupture in a stirred tank reactor suggests that parameters such as eddy wavelength and eddy velocity may better characterize and model the turbulent damage. Further, hemolysis of red blood cells by turbulent effects has been shown to have a fixed rate for constant levels of power input. Damage inflicted on the remaining, intact erythrocytes (sublethal damage) was evaluated by exposure to turbulence followed by osmotic fragility (OF) testing. Logistic models were fit to the OF data indicating a significant osmotic sensitivity in the sublethal damaged population between control and turbulence-exposed cells (χ 2 test; p < 0.001). This susceptibility indicates a significant cell population more susceptible to destruction as a result of turbulent exposure. This work has therefore helped identify optimization parameters for evaluating cell damage potential when engineering cardiovascular prosthetic devices.
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U2 - 10.1007/s10439-007-9387-6
DO - 10.1007/s10439-007-9387-6
M3 - Article
C2 - 17909969
AN - SCOPUS:36448953486
SN - 0090-6964
VL - 35
SP - 2108
EP - 2120
JO - Annals of Biomedical Engineering
JF - Annals of Biomedical Engineering
IS - 12
ER -