Implantable cardiovascular devices are commonly used in clinical treatment for end stage cardiovascular devices. However, they may cause device-induced blood damage which can cause serious complications such as hemolysis and thrombosis. Blood damage often occurs within small passages or journals of the flow path. These regions may be associated with hot-spots in which shear stress is excessive and cells may be irreversibly strained. The successful design of these devices relies on efficiently minimizing supra-physiologic shear fields through computational modeling. However the fundamental blood mechanics under these conditions are not yet fully characterized.
This study was therefore conducted to elucidate the microscopic mechanics of cellular deformation that underlie shear-induced hemolysis. A micro fluid system was developed to emulate flow environments at hot-spots and provide optical access for microscopic visualization. The flow of red blood cells (RBCs) within micro channels was illuminated by a pair of stroboscopes resulting in a rapid succession of images -- recorded by double-exposure digital CCD camera. Red blood cell motion and deformation dynamics, as well as the surrounding fluid velocity field under various conditions of hematocrit, flow rate were quantitatively measured using particle image velocimetry (PIV) technique.
The results show that cells deform rapidly as they approach the inlet, bear the largest deformation at inlet, keep large deformation inside channel and recover as soon as flowing out of exit. Inside channel, cell deformation will reach to a threshold that the cells will not be elongated as shear stress increases. We concluded that the largest possibility for blood damage occurs at the inlet of gaps or clearance in cardiovascular devices, due to the combined effect of extensional stress and shear stress. The combined effect is great on blood mechanical damage in that it can deform the cell to a maximal value in a transient time. The sublethal damage is more likely to happen than the visible rupture of red cells in our experimental situation.
Our findings show basic mechanism underlining device-induced blood damage. The methods are proved to be effective and ready to be applied in further design and investigations.
| Identifer | oai:union.ndltd.org:PITT/oai:PITTETD:etd-12082004-112132 |
| Date | 28 January 2005 |
| Creators | Zhao, Rui |
| Contributors | Marina V. Kameneva, James F. Antaki, Zhongjun Wu, Anne M. Robertson |
| Publisher | University of Pittsburgh |
| Source Sets | University of Pittsburgh |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.library.pitt.edu/ETD/available/etd-12082004-112132/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Pittsburgh or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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