Tube Collapse and Valve Closure in Ambulatory Venous Pressure Regulation: Studies with a Mechanical Model

1998 ◽  
Vol 5 (1) ◽  
pp. 42-51 ◽  
Author(s):  
Seshadri Raju ◽  
Austin B. Green ◽  
Ruth K. Fredericks ◽  
Peter N. Neglen ◽  
C. Alexander Hudson ◽  
...  
Keyword(s):  
Mechanical Model ◽  
Regulatory Mechanism ◽  
Venous Pressure ◽  
Valve Closure ◽  
Pressure Regulation ◽  
Collapsible Tube ◽  
Adjustable Valve ◽  
Wide Range ◽  
Wall Property ◽  
Property Changes

Purpose: To determine the role of valve closure and column segmentation in ambulatory venous pressure regulation. Methods: Using a mechanical model consisting of a graduated adjustable valve and a collapsible tube, we studied the differential effects of valve closure and tube collapse on venous pressure regulation. By utilizing materials with differing wall properties for the infravalvular tube, the influence of wall property changes on tube function and pressure regulation was explored. Results: Valve closure, per se, does not cause venous pressure reduction. Collapse of the tube below the valve is the primary pressure regulatory mechanism. The nonlinear volume-pressure relationship that exists in infravalvular tubes confers significant buffering properties to the collapsible tube, which tends to retain a near-constant pressure for a wide range of ejection fractions, residual tube volumes, and valve leaks. Changes in tube wall property affect this buffering action, at both the low and high ends of the physiological venous pressure range. Conclusions: The valve and the infravalvular venous segment should be considered together in venous pressure regulation. Tube collapse of the segment below the valve is the primary pressure regulatory mechanism. An understanding of the hydrodynamic principles involved in pressure regulation derived from this model will provide the basis for construction of more complex models to explore clinical physiology and dysfunction.

Tube Collapse and Valve Closure in Ambulatory Venous Pressure Regulation: Studies With a Mechanical Model

1998 ◽  
Vol 5 (1) ◽  
pp. 42-51 ◽  
Author(s):  
Seshadri Raju ◽  
Austin B. Green ◽  
Ruth K. Fredericks ◽  
Peter N. Neglen ◽  
C. Alexander Hudson ◽  
...  
Keyword(s):  
Mechanical Model ◽  
Venous Pressure ◽  
Valve Closure ◽  
Pressure Regulation

scholarly journals On the influence of delamination on laminated paperboard creasing and folding

2012 ◽  
Vol 370 (1965) ◽  
pp. 1912-1924 ◽  
Author(s):  
Lars A. A. Beex ◽  
Ron H. J. Peerlings
Keyword(s):  
Cohesive Zone ◽  
Mechanical Model ◽  
Cohesive Zone Model ◽  
Packaging Material ◽  
Friction Model ◽  
Zone Model ◽  
General Mechanics ◽  
Single Fold ◽  
Wide Range

Laminated paperboard is used as a packaging material for a wide range of products. During production of the packaging, the fold lines are first defined in a so-called creasing (or scoring) operation in order to obtain uncracked folds. During creasing as well as folding, cracking of the board is to be avoided. A mechanical model for a single fold line has been proposed in a previous study (Beex & Peerlings 2009 Int. J. Solids Struct. 46 , 4192–4207) to investigate the general mechanics of creasing and folding, as well as which precise mechanisms trigger the breaking of the top layer. In the present study, we employ this modelling to study the influence of delamination on creasing and folding. The results reveal the separate role of the cohesive zone model and the friction model in the description of delamination. They also show how the amount of delamination behaviour should be controlled to obtain the desired high folding stiffness without breaking of the top layer.

Blood flow, volume, and transit time in the pulmonary microvasculature using laser-Doppler

1994 ◽  
Vol 76 (6) ◽  
pp. 2643-2650 ◽  
Author(s):  
T. S. Hakim ◽  
E. Gilbert ◽  
E. M. Camporesi
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Transit Time ◽  
Flow Rate ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Flow Volume ◽  
Doppler Flowmetry ◽  
Blood Flow Volume ◽  
Wide Range

Capillary transit time is determined by the ratio of capillary volume to flow rate. Exercise-induced hypoxemia is thought to occur because of the short transit time of erythrocytes in capillaries. The effect of flow rate on capillary volume (recruitment vs. distension) is controversial. In a perfused left lower lobe preparation in canine lungs, we used laser-Doppler flowmetry (model ALF21R) to monitor changes in blood flow, volume, and transit time in the microvasculature near the subpleural surface. Changes in total flow, blood volume, and total transit time (tt) were also measured. The results showed that microvascular volume approached maximum when flow rate was at resting value (0.4 l/min) and pressure in the pulmonary artery was > 6 mmHg relative to the level of the capillaries. In contrast, the total blood volume increased gradually over a wide range of flow rates. When flow increased 4.2 times (from 155 to 650 ml/min), tt decreased from 7.32 to 3.53 s; meanwhile, microvascular flow increased from 6.0 to 12.7 units and microvascular transit time decreased from 3.14 to 1.81 units. The changes in microvascular volume and transit time were essentially independent of whether the venous pressure was higher or lower than alveolar pressure. At very high flow (6–10 times resting value), tt fell gradually to approximately 1 s. Direct monitoring of transit time with the laser-Doppler also revealed a gradual decline in microvascular transit time as flow rate increased from 2 to 10 times the normal flow. (ABSTRACT TRUNCATED AT 250 WORDS)

Filtration coefficient in cat hindlimb using protein concentration changes

1989 ◽  
Vol 256 (1) ◽  
pp. H186-H194 ◽  
Author(s):  
P. D. Watson ◽  
M. B. Wolf
Keyword(s):  
Protein Concentration ◽  
Venous Pressure ◽  
Filtration Coefficient ◽  
Volume Changes ◽  
Vascular Volume ◽  
Perfusate Flow ◽  
Wide Range ◽  
Concentration Changes ◽  
The Difference ◽  
Pentobarbital Sodium Anesthesia

The maximum value of capillary filtration coefficient (CFC) in maximally vasodilated cat skeletal muscle is disputed. It was hypothesized that the wide range of reported values was caused by the inability of gravimetric and volumetric measurements of tissue volume to separate transcapillary filtration from vascular volume changes. Consequently, we developed a method of measuring filtration rates from changes in venous protein concentration using Evan's blue-labeled albumin in the isolated hindlimb (pentobarbital sodium anesthesia). The filtration coefficient (PFFC) calculated from these filtration rates after a step in venous pressure should not be influenced by vascular volume changes. When the perfusate flow rate through the hindlimb was greater than 15 ml.min-1.100 g muscle-1, PFFC was 0.0085 +/- 0.0015 (SD, n = 8) ml.min-1.mmHg-1.100 g muscle-1. PFFC was observed to be unvarying from 1 to 12 min after the venous pressure elevation, in contrast to CFC values, which fall during the same period. It is argued that the difference between CFC and PFFC values is caused by vascular volume changes.

Autoregulation of cochlear blood flow in guinea pigs

1994 ◽  
Vol 266 (2) ◽  
pp. H458-H467 ◽  
Author(s):  
J. N. Brown ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Guinea Pigs ◽  
Venous Pressure ◽  
Vena Cava ◽  
Systemic Blood Pressure ◽  
Vascular Effects ◽  
Cochlear Blood Flow ◽  
Pharmacological Agents ◽  
Posterior Portion ◽  
Wide Range

Autoregulation of blood flow in the inner ear following uncontrolled changes in systemic blood pressure (BP), which was induced by the application of pharmacological agents that cause local and/or systemic vascular effects, has been reported in previous studies. In the current study, carotid BP was systematically manipulated without drugs, while the resulting cochlear blood flow (CBF) changes were measured using a laser Doppler flowmeter (LDF). Anesthesized guinea pigs were used, and the probe of a LDF was held against the ventral-posterior portion of the surgically exposed cochlea. A mechanical occluder was placed around the descending aorta or the inferior vena cava. BP could be elevated or lowered over a wide range and was held stable during 2-min occlusions. The mean level (+/- SD) of regulation (% delta CBF/% delta BP) for BP changes less than +/- 35% of preocclusion baseline was 0.24 +/- 0.2 (or 0.18 +/- 0.2 if BP is corrected by subtracting central venous pressure). Significant regulation occurred for BP between 20 and 70 mmHg. A demonstration of the cochlear origin of the regulatory response was obtained by “pharmacological blockade” following topical application of the vasodilator, sodium nitroprusside, to the cochlea. In this condition, CBF changed in nearly direct proportion to BP.

Effect of temperature and baroreceptor stimulation on reflex venomotor responses

1984 ◽  
Vol 57 (5) ◽  
pp. 1384-1392 ◽  
Author(s):  
A. Tripathi ◽  
X. Shi ◽  
C. B. Wenger ◽  
E. R. Nadel
Keyword(s):  
Heart Rate ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Effect Of Temperature ◽  
Lower Body ◽  
Venous Capacitance ◽  
Ambient Temperatures ◽  
Wide Range ◽  
Baroreceptor Stimulation ◽  
Venous Volume

To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.

Epicardial coronary venous pressures: autonomic responses

1982 ◽  
Vol 60 (5) ◽  
pp. 698-706 ◽  
Author(s):  
G. A. Klassen ◽  
J. A. Armour
Keyword(s):  
Coronary Artery ◽  
Vagal Stimulation ◽  
Venous Pressure ◽  
Outflow Tract ◽  
The Other ◽  
Sympathetic Stimulation ◽  
Pressure Regulation ◽  
Autonomic Responses ◽  
Intramyocardial Pressure

Intramyocardial, ventricular, aortic, and central and peripheral coronary artery as well as peripheral and central coronary venous pressures were measured simultaneously in dog hearts. A gradient of coronary vascular pressures was detected and quantitated. Stellate stimulation increased all pressures. Isoproterenol induced outflow tract obstructions so that aortic and central coronary artery pressures were unchanged while the other pressures increased. Vagal stimulation dissociated the intramyocardial venous pressure relationship in as much as arterial pressures decreased while epicardial coronary venous pressure was increased. These data suggest that coronary venous pressure in response to sympathetic stimulation increases as intramyocardial pressure increases. However, vagal stimulation permits a dissociation of these effects suggesting that coronary venous pressure regulation is complex.

A Simple Model for Predicting Heat Aging of EPDM Rubber

2004 ◽  
Vol 77 (2) ◽  
pp. 242-256 ◽  
Author(s):  
Arnis U. Paeglis
Keyword(s):  
Physical Properties ◽  
Strain Energy ◽  
Physical Property ◽  
Elongation At Break ◽  
Epdm Rubber ◽  
Wide Range ◽  
Rate Relationship ◽  
Property Changes ◽  
Simple Empirical Model

Abstract Heat aging stability is a hallmark of EPDM rubber and a requirement for use in automotive, roofing and other applications. Retention of physical properties after accelerated heat aging is a typical specification for such long-term uses. This paper examines the utility of such tests in predicting results over a range of temperatures, 116 °C, 125 °C, 135 °C and 150 °C, in some cases for as long as 365 days. A simple empirical model was developed to predict the retention of physical properties using fractional strain energy, that is, the ratio of the aged to unaged products of tensile strength and elongation at break. Characteristic rates, an Arrhenius rate relationship and activation energies were determined. This model provides a basis to predict physical property changes over a wide range of temperatures and times, as well as for considerations of equivalent heat aging tests and use in different applications.

scholarly journals O-acetylation controls the glycosylation of bacterial serine-rich repeat glycoproteins.

2020 ◽  
pp. jbc.RA120.016116
Author(s):  
Ravin Seepersaud ◽  
Alexander C. Anderson ◽  
Barbara A. Bensing ◽  
Biswa P Choudhury ◽  
Anthony J. Clarke ◽  
...  
Keyword(s):  
Linkage Analysis ◽  
Regulatory Mechanism ◽  
Human Platelets ◽  
Bacterial Virulence ◽  
Wild Type ◽  
Post Translational Modification ◽  
Gram Positive Bacteria ◽  
Wide Range ◽  
Platelet Binding

The serine-rich repeat (SRR) glycoproteins of Gram-positive bacteria are a family of adhesins that bind to a wide range of host ligands, and expression of SRR glycoproteins is linked with enhanced bacterial virulence. The biogenesis of these surface glycoproteins involves their intracellular glycosylation and export via the accessory Sec (aSec) system. While all aSec components are required for SRR glycoprotein export, Asp2 of Streptococcus gordonii also functions as an O-acetyltransferase that modifies GlcNAc residues on the SRR adhesin GspB. Since these GlcNAc residues can also be modified by the glycosyltransferases Nss and Gly, it has been unclear whether the post-translational modification of GspB is coordinated. We now report that acetylation modulates the glycosylation of exported GspB. Loss of O-acetylation due to aps2 mutagenesis led to the export of GspB glycoforms with increased glucosylation of the GlcNAc moieties. Linkage analysis of the GspB glycan revealed that both O-acetylation and glucosylation occurred at the same C6 position on GlcNAc residues, and that O-acetylation prevented Glc deposition. Whereas streptococci expressing non-acetylated GspB with increased glucosylation were significantly reduced in their ability to bind human platelets in vitro, deletion of the glycosyltransferases nss and gly in the asp2 mutant restored platelet binding to wild-type levels. These findings demonstrate that GlcNAc O-acetylation controls GspB glycosylation, such that binding via this adhesin is optimized. Moreover, since O-acetylation has comparable effects on the glycosylation of other SRR adhesins, acetylation may represent a conserved regulatory mechanism for the post-translational modification of the SRR glycoprotein family.

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