Dai G, Tsukurov O, Chen M, Gertler JP, Kamm RD.
Endothelial nitric oxide production during in vitro simulation of external limb
compression.
Am J Physiol Heart Circ Physiol 2002 Jun;282(6):H2066-75

Division of Biological Engineering, Massachusetts Institute of Technology,
Cambridge, Massachusetts 02139, USA.

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.