Endothelial nitric oxide production during in vitro simulation of external limb compression

1  Division of Biological Engineering, Massachusetts Institute of Technology, Cambridge 02139; and 2  Vascular Surgery Research Laboratory, Division of Vascular Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 External pneumatic compression (EPC) is eff...

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Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2002-06, Vol.282 (6), p.H2066-H2075
Hauptverfasser: Dai, Guohao, Tsukurov, Olga, Chen, Michael, Gertler, Jonathan P, Kamm, Roger D
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container_end_page H2075
container_issue 6
container_start_page H2066
container_title American journal of physiology. Heart and circulatory physiology
container_volume 282
creator Dai, Guohao
Tsukurov, Olga
Chen, Michael
Gertler, Jonathan P
Kamm, Roger D
description 1  Division of Biological Engineering, Massachusetts Institute of Technology, Cambridge 02139; and 2  Vascular Surgery Research Laboratory, Division of Vascular Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 External pneumatic compression (EPC) is effective in preventing deep vein thrombosis (DVT) and is thought to alter endothelial thromboresistant properties. We investigated the effect of EPC on changes in nitric oxide (NO), a critical mediator in the regulation of vasomotor and platelet function. An in vitro cell culture system was developed to simulate flow and vessel collapse conditions under EPC. Human umbilical vein endothelial cells were cultured and subjected to tube compression (C), pulsatile flow (F), or a combination of the two (FC). NO production and endothelial nitric oxide synthase (eNOS) mRNA expression were measured. The data demonstrate that in the F and FC groups, there is a rapid release of NO followed by a sustained increase. NO production levels in the F and FC groups were almost identical, whereas the C group produced the same low amount of NO as the control group. Conditions F and FC also upregulate eNOS mRNA expression by a factor of 2.08   ± 0.25 and 2.11 ± 0.21, respectively, at 6 h. Experiments with different modes of EPC show that NO production and eNOS mRNA expression respond to different time cycles of compression. These results implicate enhanced NO release as a potentially important factor in the prevention of DVT. deep vein thrombosis; hemodynamics; nitric oxide synthase
doi_str_mv 10.1152/ajpheart.00288.2001
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Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>1  Division of Biological Engineering, Massachusetts Institute of Technology, Cambridge 02139; and 2  Vascular Surgery Research Laboratory, Division of Vascular Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114 External pneumatic compression (EPC) is effective in preventing deep vein thrombosis (DVT) and is thought to alter endothelial thromboresistant properties. We investigated the effect of EPC on changes in nitric oxide (NO), a critical mediator in the regulation of vasomotor and platelet function. An in vitro cell culture system was developed to simulate flow and vessel collapse conditions under EPC. Human umbilical vein endothelial cells were cultured and subjected to tube compression (C), pulsatile flow (F), or a combination of the two (FC). NO production and endothelial nitric oxide synthase (eNOS) mRNA expression were measured. 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Human umbilical vein endothelial cells were cultured and subjected to tube compression (C), pulsatile flow (F), or a combination of the two (FC). NO production and endothelial nitric oxide synthase (eNOS) mRNA expression were measured. The data demonstrate that in the F and FC groups, there is a rapid release of NO followed by a sustained increase. NO production levels in the F and FC groups were almost identical, whereas the C group produced the same low amount of NO as the control group. Conditions F and FC also upregulate eNOS mRNA expression by a factor of 2.08   ± 0.25 and 2.11 ± 0.21, respectively, at 6 h. Experiments with different modes of EPC show that NO production and eNOS mRNA expression respond to different time cycles of compression. 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subjects Blotting, Northern
Cells, Cultured
Culture Media, Conditioned
Endothelium, Vascular - metabolism
Enzyme Inhibitors - pharmacology
Gravity Suits
Humans
Models, Biological
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type I
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Nitrites - metabolism
Pressure
Pulsatile Flow
Rheology
RNA, Messenger - analysis
Space life sciences
Umbilical Veins
Venous Thrombosis - prevention & control
title Endothelial nitric oxide production during in vitro simulation of external limb compression
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