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      Application of intermittent negative pressure on the lower extremity and its effect on macro‐ and microcirculation in the foot of healthy volunteers

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          Intermittent negative pressure ( INP) applied to the lower leg and foot may increase peripheral circulation. However, it is not clear how different patterns of INP affect macro‐ and microcirculation in the foot. The aim of this study was therefore to determine the effect of different patterns of negative pressure on foot perfusion in healthy volunteers. We hypothesized that short periods with INP would elicit an increase in foot perfusion compared to no negative pressure. In 23 healthy volunteers, we continuously recorded blood flow velocity in a distal foot artery, skin blood flow, heart rate, and blood pressure during application of different patterns of negative pressure (−40 mmHg) to the lower leg. Each participant had their right leg inside an airtight chamber connected to an INP generator. After a baseline period at atmospheric pressure, we applied four different 120 sec sequences with either constant negative pressure or different INP patterns, in a randomized order. The results showed corresponding fluctuations in blood flow velocity and skin blood flow throughout the INP sequences. Blood flow velocity reached a maximum at 4 sec after the onset of negative pressure (average 44% increase above baseline, < 0.001). Skin blood flow and skin temperature increased during all INP sequences ( < 0.001). During constant negative pressure, average blood flow velocity, skin blood flow, and skin temperature decreased ( < 0.001). In conclusion, we observed increased foot perfusion in healthy volunteers after the application of INP on the lower limb.

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          Most cited references 23

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          Flow stimulates endothelial cells to release a nitrovasodilator that is potentiated by reduced thiol.

          We designed a novel system to study flow-mediated endothelium-dependent vasodilation. Vascular rings of rabbit thoracic aorta were mounted for isometric tension recording in a flow chamber filled with physiological saline solution. The flow chamber contained a stir bar and was mounted on a magnetic stirrer to induce vortical flow. Norepinephrine (NE, 10(-6) M) induced contraction of the vascular rings. Bovine endothelial cells on microcarrier beads added to the chamber had little effect on contraction to NE in the absence of flow. Flow induced endothelium-dependent relaxation of the vascular rings that was dependent on the flow rate. Relaxations were annulled or reversed to a contraction with methylene blue, bovine hemoglobin, or N-monomethyl-L-arginine. Conversely, N-acetyl-L-cysteine augmented the flow-mediated relaxation. Furthermore, in the presence of N-acetyl-L-cysteine, the half-life of the endothelium-dependent relaxing factor was increased. In conclusion, the stimulus of flow induces the release by endothelial cells of a diffusible, short-lived factor with the attributes of a nitrovasodilator. The action of this endogenous vasodilator is augmented by the reduced thiol N-acetyl-L-cysteine.
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            An association between vasomotion and oxygen extraction.

            Vasomotion is defined as a spontaneous local oscillation in vascular tone whose function is unclear but may have a beneficial effect on tissue oxygenation. Optical reflectance spectroscopy and laser Doppler fluximetry provide unique insights into the possible mechanisms of vasomotion in the cutaneous microcirculation through the simultaneous measurement of changes in concentration of oxyhemoglobin ([HbO(2)]), deoxyhemoglobin ([Hb]), and mean blood saturation (S(mb)O(2)) along with blood volume and flux. The effect of vasomotion at frequencies 29.3°C (X(2) = 6.19, P 29.5 kg/m(2)) of 18.8 s was statistically significant (Mann Whitney, P < 0.004). The S(mb)O(2) fluctuated spontaneously in this saw tooth manner by an average of 9.0% (range 4.0-16.2%) from mean S(mb)O(2) values ranging from 30 to 52%. These observations support the hypothesis that red blood cells may act as sensors of local tissue hypoxia, through the oxygenation status of the hemoglobin, and initiate improved local perfusion to the tissue through hypoxic vasodilation.
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              Hydrodynamic shear stress and mass transport modulation of endothelial cell metabolism.

              Mammalian cells responds to physical forces by altering their growth rate, morphology, metabolism, and genetic expression. We have studied the mechanism by which these cells detect the presence of mechanical stress and convert this force into intracellular signals. As our model systems, we have studied cultured human endothelial cells, which line the blood vessels and forms the interface between the blood and the vessel wall. These cell responds within minutes to the initiation of flow by increasing their arachidonic acid metabolism and increasing the level of the intracellular second messengers inositol trisphosphate and calcium ion concentration. With continued exposure to arterial levels of wall shear stress for up to 24 h, endothelial cells increase the expression of tissue plasminogen activator (tPA) and tPA messenger RNA (mRNA) and decrease the expression of endothelin peptide and endothelin mRNA. Since the initiation of flow also causes enhanced convective mass transfer to the endothelial cell monolayer, we have investigated the role of enhanced convection of adenosine trisphosphate (ATP) to the cell surface in eliciting a cellular response by monitoring cytosolic calcium concentrations on the single cell level and by computing the concentration profile of ATP in a parallel-plate flow geometry. Our result demonstrate that endothelial cells respond in very specific ways to the initiation of flow and that mass transfer and fluid shear stress can both play a role in the modulation of intracellular signal transduction and metabolism.

                Author and article information

                Physiol Rep
                Physiol Rep
                Physiological Reports
                John Wiley and Sons Inc. (Hoboken )
                14 September 2016
                September 2016
                : 4
                : 17 ( doiID: 10.1111/phy2.2016.4.issue-17 )
                [ 1 ] Section of Vascular Investigations Division of Cardiovascular and Pulmonary Diseases Department of Vascular SurgeryOslo University Hospital OsloNorway
                [ 2 ] Faculty of Medicine Institute of Clinical MedicineUniversity of Oslo OsloNorway
                [ 3 ]Otivio AS Gaustadalléen 21 Oslo 0349Norway
                [ 4 ] Department of AnesthesiologyOslo University Hospital OsloNorway
                [ 5 ] Department of Vascular SurgeryOslo University Hospital OsloNorway
                [ 6 ] Oslo Center for Biostatistics and EpidemiologyResearch Support Services Oslo University Hospital OsloNorway
                Author notes
                [* ] Correspondence

                Øyvind H. Sundby, Section of Vascular Investigations, Division of Cardiovascular and Pulmonary Diseases, Department of Vascular Surgery, Oslo University Hospital Oslo University Hospital, Aker Pb 4959 Nydalen 0424 Oslo, Norway.

                Tel: + 47 22 89 48 90

                Fax: + 47 22 89 42 90

                Email: o.h.sundby@

                © 2016 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 5, Tables: 1, Pages: 11, Words: 6132
                Funded by: Norwegian Research Council
                Award ID: 241589
                Funded by: University of Oslo
                Blood Pressure
                Original Research
                Original Research
                Custom metadata
                September 2016
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:19.09.2016


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