|Abstract: ||人工器官如心室輔助器、人工心瓣、氧合裝置等，會在心血管中造成非生理性的流況，這些流況所產生的血流應力會引發血液的破壞，特別是紅血球的損傷，稱為溶血。一般以溶血指數(Index of Hemolysis, IH(%))來表示，此溶血指數是切應力大小及暴露時間的函數。Giersiepen et al.(1990)依據Wurzinger et al.(1986)的實驗導出的溶血指數模式，IH(%) 。此模式廣被應用在計算流體力學(CFD)對新設計人工器官的評估上。新型人工器官經由此模式CFD所計算的溶血指數和實際原形的實驗值有相當大的差異。式中的應力是由簡單Couette黏度儀所產生之剪應力，而實際流場應包含有剪應力和拉伸應力。單由剪應力無法準確預估其溶血指數。因此本研究分別利用層流場與紊流場進行真實的紅血球破壞實驗，以了解其中的破壞機制。在層流實驗中，分別利用不同幾何形狀入口的短毛細管與微流道，其在進口端會產生一強烈的拉伸應力場，此流場先經由CFD的計算，求出其應力值，然後採用豬的新鮮紅血球，進行溶血的測試，以了解拉伸應力對溶血的影響。結果顯示和先前的研究結果是一致的，拉伸應力為紅血球破壞的主要機械力，且其閥值約為800-1000 Pa。在紊流實驗中，以軸對稱自由噴射流場所產生的紊流剪力場，進行溶血實驗。首先利用雷射都普勒流速儀(LDV)及質點影像流速儀(PIV)，進行流場的量測，再將清洗過的紅血球置入已知紊流應力的流場中，進行溶血實驗。先前的溶血被認為是紊流場中的雷諾應力所造成。近年來提出的假說認為和血球大小相當尺度的小渦流所形成的黏滯消散應力才是破壞血球的真正機械力。但由於受限於目前儀器的解析度，而無法量測到消散應力的最小渦流尺度，經由紊流場中可解析及次格點間的動力平衡假設下，由可解析所得的應變率張量中，利用Smagonrinsky的模式，則可估算紊流消散率，進而推求其黏滯消散應力。結果得到紅血球破壞的主軸切應力閥值為500 Pa，而黏滯消散應力為40 Pa，至少小於雷諾應力一個量級。此黏滯消散應力和層流的實驗結果比較也是除了差ㄧ個量級之外，其時間尺度小於三個量級。由此得知紅血球在紊流與層流中有不同的破壞機制，所以一個可靠的溶血指數模式必須完全了解紅血球在不同剪力場下的破壞機制。|
Artificial prostheses such as left ventricular assist devices, artificial heart valves, and oxygenators can create non-physiologic flow conditions within the cardiovascular system. The stress forces generated in these flow fields can induce blood cell damage, particularly red blood cell damage or hemolysis. The Index of Hemolysis (IH; %) is affected by the magnitude of shear stress and exposure time. Giersiepen et al. (1990), based on experiments by Wurzinger et al. (1986), determined that the Index of Hemolysis can be calculated by IH(%) . This model has been widely used in computational fluid dynamics (CFD) for the evaluation of new artificial prosthesis designs. However, the IH calculated via CFD are often inconsistent with actual measured values from experiments done on prototypes. The stress value in the equation is based on the shear stress generated from a simple Couette viscometer; however, actual flow field forces include both shear stress and extensional stress. As such, the shear stress alone cannot accurately determine IH. We applied laminar and turbulent flow that was utilized to hemolysis porcine RBCs, in order to compare the IH derived. In laminar flow, we created a strong extensional stress flow field with the sharp contraction of short capillary and small channels. The flow field generated at the entrance of the capillary was calculated with CFD to determine the stress values, which was followed by hemolysis experiments with porcine red blood cells to determine the effects of extensional stress on hemolysis. Our results were consistent with prior studies in that the extensional stress was the primary mechanical force involved in hemolysis with a threshold value of 800-1000 Pa. In turbulent flow, We applied two-dimensional laser Doppler velocimetry (LDV) and particle image velocimetry (PIV) to measure the flow field of a free submerged axi-symmetric jet that was utilized to hemolysis the porcine red blood cells in selected locations. However, the resolution of current instrumentation is insufficient to measure the smallest eddy sizes. Assuming a dynamic equilibrium between the resolved and sub-grid scale (SGS) energy flux, the SGS energy flux was calculated from the strain rate tensor computed from the resolved velocity fields and the SGS stress was determined by the Smagorinsky model, from which the turbulence dissipation rate and then the viscous dissipative stresses were estimated. Our results showed that the hemolytic threshold of major principal Reynolds stresses is up to 500 Pa and the viscous dissipative stresses is 40-60 Pa, it’s at least an order of magnitude less than the Reynolds stresses. The viscous dissipative stresses for hemolysis also tend to be an order of magnitude lower than the laminar shear thresholds. In addition, the time scales are three orders of magnitude smaller than the laminar shear. Because of these differences, a reliable damage quantification model needs to fully understand about the varying mechanisms of blood cell damage by different shear stress conditions.