THEORETICAL SOLUTIONS FOR A STEADY LAMINAR FLOW OF A COMPRESSIBLE FLUID IN THE ENTRANCE REGION OF A TUBE

1956 ◽  
Author(s):  
TAU-YI TOONG ◽  
JOSEPH KAYE
1983 ◽  
Vol 105 (3) ◽  
pp. 290-296 ◽  
Author(s):  
M. S. Bhatti

A closed-form analytical solution is developed to hitherto unsolved problem of steady laminar flow of a Newtonian fluid in the entrance region of elliptical ducts. The analysis is based on the Karman-Pohlhausen integral method and entails solution of the integrated forms of the mass and the momentum balance equations. According to this analysis, the hydrodynamic entrance length based on 99 percent approach to the fully developed flow is equal to 0.5132λ/(1+λ2) where λ is the aspect ratio. Also, the fully developed incremental pressure defect is found to be 7/6 which is independent of the aspect ratio. In the limit when the flow becomes fully developed, the solution converges to the known exact asymptotic solution. Available, wide-ranging velocity measurements for a circular tube agree with the analytical predictions within 7 percent. Also, available pressure drop measurements near the inlet of a circular tube agree with the analytical predictions within 2 percent.


2018 ◽  
Vol 30 (26) ◽  
pp. 264002 ◽  
Author(s):  
F Cecconi ◽  
A Puglisi ◽  
A Sarracino ◽  
A Vulpiani

1981 ◽  
Vol 103 (4) ◽  
pp. 785-790 ◽  
Author(s):  
J. H. Masliyah ◽  
K. Nandakumar

The Navier-Stokes equation in a rotating frame of reference is solved numerically to obtain the flow field for a steady, fully developed laminar flow of a Newtonian fluid in a twisted tube having a square cross-section. The macroscopic force and energy balance equations and the viscous dissipation term are presented in terms of variables in a rotating reference frame. The computed values of friction factor are presented for dimensionless twist ratios, (i.e., length of tube over a rotation of π radians normalized with respect to half the width of tube) of 20, 10, 5 and 2.5 and for Reynolds numbers up to 2000. The qualitative nature of the axial velocity profile was observed to be unaffected by the swirling motion. The secondary motion was found to be most important near the wall.


Author(s):  
Sarah Basehore ◽  
Samantha Bohlman ◽  
Callie Weber ◽  
Swathi Swaminathan ◽  
Yuji Zhang ◽  
...  

Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production. It is unknown, however, whether varied blood flow conditions, which affect eNOS phosphorylation, modulate eNOS activity via O-GlcNAcylation-dependent mechanisms. Objective: The goal of this study was to test if steady laminar flow, but not oscillating disturbed flow, decreases eNOS O-GlcNAcylation, thereby elevating eNOS phosphorylation and NO production. Methods and Results: Human umbilical vein endothelial cells (HUVEC) were exposed to either laminar flow (20 dynes/cm2 shear stress) or oscillating disturbed flow (4{plus minus}6 dynes/cm2 shear stress) for 24 hours in a cone-and-plate device. eNOS O-GlcNAcylation was almost completely abolished in cells exposed to steady laminar but not oscillating disturbed flow. Interestingly, there was no change in protein level or activity of key O-GlcNAcylation enzymes (OGT, OGA, or GFAT). Instead, metabolomics data suggest that steady laminar flow decreases glycolysis and hexosamine biosynthetic pathway (HBP) activity, thereby reducing UDP-GlcNAc pool size and consequent O-GlcNAcylation. Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production. Finally, we detected significantly higher O-GlcNAcylated proteins in endothelium of the inner aortic arch in mice, suggesting that disturbed flow increases protein O-GlcNAcylation in vivo. Conclusions: Our data demonstrate that steady laminar but not oscillating disturbed flow decreases eNOS O-GlcNAcylation by limiting glycolysis and UDP-GlcNAc substrate availability, thus enhancing eNOS phosphorylation and NO production. This research shows for the first time that O-GlcNAcylation is regulated by mechanical stimuli, relates flow-induced glycolytic reductions to macrovascular disease, and highlights targeting HBP metabolic enzymes in endothelial cells as a novel therapeutic strategy to restore eNOS activity and prevent EC dysfunction in cardiovascular disease.


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