High Shear Stress Behavior of Some Representative Lubricants

1975 ◽  
Vol 97 (3) ◽  
pp. 479-485 ◽  
Author(s):  
J. Jakobsen ◽  
W. O. Winer

Shear stress independent behavior was observed for representative, synthetic, nonblended lubricants to about 4.8 × 106 N/m2 (700 psi) shear stress in high pressure viscometric measurements. This shear stress is of the same magnitude as the shear stress in sliding elastohydrodynamic contacts. It is shown that dissipation heating is the only mechanism of importance in the generation of the deviations from constant viscosity as measured with capillary tube viscometric methods. The Newtonian end corrections for the capillary tubes were found to be constant for the nonblended, liquid lubricants. Newtonian behavior will be expected of the fluids in a high shear lubrication situation. Shear induced, nonliquid behavior was found for the silicone lubricant at about 106 N/m2 and for the polymer-blended mineral oil at about 104 N/m2 at a relatively low pressure level. The observations might provide a key to an understanding of the generation of the anomalous low elastohydrodynamic film thickness as found with these lubricants. The polymer-blended oil showed shear thinning effects. The apparent viscosity was found to increase (∼30 percent) with increasing shear stress in the range of the second Newtonian viscosity level.

1975 ◽  
Vol 97 (3) ◽  
pp. 472-478 ◽  
Author(s):  
J. Jakobson ◽  
W. O. Winer

The effect of dissipation heating on the apparent viscosity measured in capillary tube viscometry is described in this paper. Conditions of low Reynolds number and high shear are assumed. End corrections to the tube flow, found to be 3π/16 times the diameter of the tube, are incorporated. The flow curves show decreasing apparent viscosity when the shear stress increases. The configuration of the flow curves plotted in logarithmic presentation are found to be identical for fluids with Newtonian behavior. Convection is the predominant mechanism in removal of the heat in short capillary tube. The estimated upper bound for the shear stress obtainable in short length capillary tubes appears to be of the order of magnitude of 10 MPa limited primarily by the pressure drop associated with the constant end correction from the flat ended inlet and exit of the tube.


2015 ◽  
Vol 112 (22) ◽  
pp. 6991-6996 ◽  
Author(s):  
Takashi Suzuki ◽  
Miho Suzuki ◽  
Shinji Ogino ◽  
Ryo Umemoto ◽  
Noritaka Nishida ◽  
...  

CD44 is the receptor for hyaluronan (HA) and mediates cell rolling under fluid shear stress. The HA-binding domain (HABD) of CD44 interconverts between a low-affinity, ordered (O) state and a high-affinity, partially disordered (PD) state, by the conformational change of the C-terminal region, which is connected to the plasma membrane. To examine the role of tensile force on CD44-mediated rolling, we used a cell-free rolling system, in which recombinant HABDs were attached to beads through a C-terminal or N-terminal tag. We found that the rolling behavior was stabilized only at high shear stress, when the HABD was attached through the C-terminal tag. In contrast, no difference was observed for the beads coated with HABD mutants that constitutively adopt either the O state or the PD state. Steered molecular dynamics simulations suggested that the force from the C terminus disrupts the interaction between the C-terminal region and the core of the domain, thus providing structural insights into how the mechanical force triggers the allosteric O-to-PD transition. Based on these results, we propose that the force applied from the C terminus enhances the HABD–HA interactions by inducing the conformational change to the high-affinity PD transition more rapidly, thereby enabling CD44 to mediate lymphocyte trafficking and hematopoietic progenitor cell homing under high-shear conditions.


2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Stefania Simeone ◽  
Talin Ebrahimian ◽  
Veronique Michaud ◽  
Stephanie Lehoux

Atherosclerotic plaques form in regions of low blood flow, whereas vessels exposed to high shear stress remain lesion-free. We hypothesized that exposing established atherosclerotic plaques to elevated shear stress leads to lesion regression by facilitating inflammatory cell movement within the plaque. We developed a model of arteriovenous fistula (AVF) in mice, where the right carotid artery is anastomosed into the jugular vein. LDLR-/- mice were placed on a high-fat diet. Control mice were sacrificed at week 12, which coincided with sham and AVF surgery. Sham and AVF mice were kept on a high-fat diet for a further 4 weeks. This procedure increases the shear stress in the brachiocephalic artery (BCA) and leads to a 51% plaque regression in AVF. All groups had comparable lipid levels. However, BCA plaque macrophage, smooth muscle cell and collagen content was halved in AVF. We observed greater gelatinase activity in plaques of AVF mice, suggesting a role for matrix metalloproteinases (MMPs) in plaque regression. MMP-9 and MMP-3 expression was increased in AVF plaques whereas MMP-2 and MMP-14 expression was decreased (p<0.05). A separate group of mice was therefore treated post-surgery with an MMP inhibitor, doxycycline, or with a TIMP-1 over-expressing plasmid. Both prevented the reduction in plaque size in the AVF group. To better define the mechanism of plaque regression in the AVF, we devised an endothelial cell (EC)-macrophage co-culture system where the ECs were exposed to high, low or no shear stress, and macrophages exposed to the EC effluent. There was a 2.5 fold increase in the migration of macrophages exposed to high shear effluent vs. low shear (p<0.05). This coincided with a 3-fold increase in the number of macrophages expressing activated β1 integrin in the high shear conditions. Uptake of apoptotic cells by macrophages was also 25% higher in the high shear vs. static (p<0.05). When repeated using the MMP inhibitor, GM6001, the high shear increase in migration was blocked in the presence of MMP inhibition; however, it had no effect on cell phagocytosis. Our findings suggest that shear stress acting on ECs may influence the cells within the plaque by increasing MMP activity allowing for better macrophage motility, an important feature of regressing plaques.


2018 ◽  
Vol 39 (suppl_1) ◽  
Author(s):  
H Spillemaeker ◽  
A Dupont ◽  
A Kauskot ◽  
A Rauch ◽  
F Vincent ◽  
...  

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1354-1361 ◽  
Author(s):  
JR O'Brien ◽  
GP Salmon

The article explores the finding that high shear alone applied to normal, native blood results in platelet aggregation. A filter with tortuous capillary-sized channels permits a study of the effect of shearing forces at different pressures. Native, heparinized, citrated and EDTA blood and platelet-rich plasma (PRP) were forced through the filter. Normal and von Willebrand's blood were studied, as were the effects of antibodies to platelet glycoproteins (GPr) and to von Willebrand's factor (vWf) and of “membrane-active” drugs. Normally, the filter blocked at 40 mmHg but not at 5 mmHg. Transmission electronmicroscopy of the filter at 40 mmHg showed blockage by platelet aggregates. Initially, the mean transit time through the filter was 8 milliseconds. Platelet retention in the filter occurred in two phases. From 0 to 3 seconds, only high-shear, vWf, and GPrIIb/IIIa were required. From 10 to 20 seconds, retention presumably involved these three attributes, but divalent cations were also essential. Only this phase was inhibited by some membrane-active drugs. ADP- and thrombin- induced aggregation requires GPrIIb/IIIaand fibrinogen. Shear-induced blocking of the filter by blood with a normal concentration of fibrinogen requires GPrIIb/IIIa and vWf. This indicates a different type of exposure of GPrIIb/IIIa. The long bleeding time in vW disease highlights the absolute requirement for vWf and emphasizes the difference in exposure of GPrIIb/IIIa induced by shear stress. Evidently, a process similar to that occurring in the filter is required in normal capillary hemostasis.


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