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| An in vitro cell culture system to study the influence of external pneumatic compression on endothelial function |
| Source: Dai G, Tsukurov O, Orkin RW, et al: Journal of Vascular Surgery 977-987, 2000 |
| Summary: A simple three-dimensional in vitro system was designed to simulate the vessels and blood flow in the leg. This system models hemodynamic shear stress and vessel wall strain associated with blood flow. Human endothelial cells were used to line the system’s “vessels” and the vessels were subjected to intermittent pulsatile flow (rapid acceleration of flow for 4 seconds followed by 56 seconds of “rest” by air pump), vessel collapse, or a combination of the two. Both t-PA and eNOS mRNA expression are up-regulated by pulsatile flow, “increased levels of t-PA can decrease the baseline level of fibrin formation, which might contribute to the decreased incidence of DVT. Upregulation of eNOS suggests increased nitric oxide production, causing vasodilation and inhibiting platelet adhesion and aggregation.” Compression only group (50% vessel collapse with steady flow rate) caused little or no change in any of the genes considered, suggesting that it is “pulsatile shear stress, not vessel compression that is responsible for these changes. This has important implications for the design of EPC systems; the objective should be to increase shear stress above a certain level rather than to achieve vessel collapse.” In previous studies (Dai 1999), both asymmetric and circumferential pressure at 50 mmHg generated the same degree of vessel collapse and vessel wall strain; however, the difference in shear stress level was considerably higher with asymmetric compression. |