Net Pressure Gradient Research Articles

Cerebral perfusion pressure and behavior monitoring in freely moving rats.

Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP). As CPP is a calculated value, MAP and ICP must be measured simultaneously. In research models, anesthetized and acute monitoring is incapable of providing a realistic picture of the relationship between ICP and MAP under physiological and/or pathophysiological conditions. For long-term monitoring of both pressures, the principle of telemetry can be used. The aim of this study was to map changes in CPP and spontaneous behavior using continuous pressure monitoring and video recording for 7 days under physiological conditions (group C - 8 intact rats) and under altered brain microenvironment induced by brain edema (group WI - 8 rats after water intoxication) and neuroprotection with methylprednisolone - MP (group WI+MP - 8 rats with MP 100 mg/kg b.w. applicated intraperitoneally during WI). The mean CPP values in all three groups were in the range of 40-60 mm Hg. For each group of rats, the percentage of time that the rats spent during the 7 days in movement pattern A (standard movement stereotype) or B (atypical movement) was defined. Even at very low CPP values, the standard movement stereotype (A) clearly dominated over the atypical movement (B) in all rats. There was no significant difference between control and experimental groups. Chronic CPP values with correlated behavioral type may possibly answer the question of whether there is a specific, universal, optimal CPP at all.

Formation of the Layered Circulation in South China Sea With the Mixing Stimulated Exchanging Current Through Luzon Strait

AbstractUsing the layered circulation in the South China Sea (SCS) as an example, a process‐oriented simulation was conducted to explore how the lateral exchanging current and basin circulation responded to the contrasting mixing in the marginal sea‐open ocean system and to the internal modulation over basin slope. Under conditions of intensified turbulent mixing () in the SCS, a crossing Luzon Strait density difference was generated and the net ageostrophic pressure gradient force drove the layered exchanging current with intensified westward deep intrusion into the SCS and an eastward middle outflow. The lateral exchanging current in turn developed a layered basin circulation in the semi‐enclosed middle and deep layers through directly providing external planetary vorticity flux, and releasing the internal potential energy indirectly. The vertical migration of the layered circulation structure over bottom slope owing to flow‐topography interaction is the major intrinsic response to the external exchanging current particularly in the semi‐enclosed deep basin. Although a small was adequate to maintain the basic layered circulation pattern, an intensified was required to extend the deep cyclonic circulation to the bottom. The intrusion of the western boundary current from open ocean not only maintained the strong upper cyclonic circulation but also intensified deep intrusion and modulated the deep layer circulation through vertical coupling. Both the deep density difference between the SCS and open ocean as well as associated vertical coupling should be considered to well understand the intensity of water exchange and the consequent layered circulation in the SCS.

Tantangan dalam Menjaga Cerebral Perfusion Pressure (CPP) yang Aman pada Cedera Otak Traumatik

Cerebral perfusion pressure (CPP) is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the intracranial pressure (ICP), CPP = MAP-CVP or CPP =MAP – ICP if ICP>CVP. Cerebral perfusion pressure must be maintained within narrow limits because too litle pressure could cause brain tissue become ischemic, and too much could raise intracranial pressure. The normal range lies between 60 and 80 mmHg, but these values can shift to the left or right depending on individual patient physiology. As CPP is a calculated measure, MAP and ICP must be measured simultaneously, most commonly by invasive means. When brain injury occurs, cerebral capillaries can become “leaky” or more permeable to water. In addition, cerebral blood vessels may dilate in respons to brain tissue injury, hypoxemia, hypercarbia, acidosis, or hypotension. If blood pressure becomes elevated, the increased CPP can lead to increased cerebral blood flow. The recommended goal of CPP per the Brain Trauma Foundation (BTF) guideline is 50-70 mmHg. Targeting high CPP >70 mmHg has not been shown to be beneficial in patient with traumatic brain injury and is associated with an increased risk of acute respiratory distress syndrome (ARDS).

Gradient and pressure recovery of a self-expandable transcatheter aortic valve depends on ascending aorta size: In vitro study

ObjectiveIn this study we aimed to understand the role of interaction of the Medtronic Evolut R transcatheter aortic valve with the ascending aorta (AA) by evaluating the performance of the valve and the pressure recovery in different AA diameters with the same aortic annulus size. MethodsA 26-mm Medtronic Evolut R valve was tested using a left heart simulator in aortic root models of different AA diameter (D): small (D = 23 mm), medium (D = 28 mm), and large (D = 34 mm) under physiological conditions. Measurements of pressure from upstream to downstream of the valve were performed using a catheter at small intervals to comprehensively assess pressure gradient and pressure recovery. ResultsIn the small AA, the measured peak and mean pressure gradient at vena contracta were 11.5 ± 0.5 mm Hg and 7.8 ± 0.4 mm Hg, respectively, which was higher (P < .01) compared with the medium (8.1 ± 0.4 mm Hg and 5.2 ± 0.4 mm Hg) and large AAs (7.4 ± 1.0 mm Hg and 5.4 ± 0.6 mm Hg). The net pressure gradient was lower for the case with the medium AA (4.1 ± 1.2 mm Hg) compared with the small AA (4.7 ± 0.8 mm Hg) and large AA (6.1 ± 1.4 mm Hg; P < .01). ConclusionsWe have shown that small and large AAs can increase net pressure gradient, because of the direct interaction of the Medtronic Evolut R stent with the AA (in small AA) and introducing higher level of turbulence (in large AA). AA size might need to be considered in the selection of an appropriate device for transcatheter aortic valve replacement.

Porcine and bovine aortic valve comparison for surgical optimization: A fluid-structure interaction modeling study

BackgroundPorcine aortic valve (PAV) and bovine aortic valve (BAV) are commonly used in aortic valve replacement (AVR) surgeries. A detailed comparison for their hemodynamic and structural stress/strain performances would help to better understand valve cardiac function and select valve type and size for AVR outcome optimizations. MethodsEight fluid-structure interaction models were constructed to compare hemodynamic and stress/strain behaviors of PAV and BAV with 4 sizes (19, 21, 23, and 25 mm). Blood flow velocity, systolic cross-valve pressure gradient (SCVPG), geometric orifice area (GOA), flow shear stresses (FSS), and stress/strain were obtained for comparison. ResultsCompared with PAV, BAV has better hemodynamic performance, with lower maximum flow velocity (7.17%) and pressure (9.82%), smaller pressure gradient (mean and peak SCVPG: 8.92% and 9.28%), larger GOA (9.56%) and lower FSS (6.61%). The averages of the mean and peak net pressure gradient values from 4 BAV models were 8.10% and 8.35% lower than that from PAV models. Larger valve sizes for both PAV and BAV had improved hemodynamic performance. Maximum flow velocity, pressure, mean SCVPG and maximum FSS from 25 mm BAV were 36.80%, 15.81%, 39.05% and 38.83% lower than those from 19 mm BAV. The GOA of PAV and BAV 25 mm Valve were 43.75% and 33.07% larger than 19 mm valves, respectively. BAV has lower stress on the leaflets than PAV. ConclusionsBAV had better hemodynamic performance and lower leaflets stress than PAV. More patient studies are needed to validate our findings.

Genesis of Antibiotic Resistance (AR) LII: Laminar to Turbulent flow transition triggered by “Physiological Shunt” Induce Hypoxia (Anoxia?) Augmenting AR Clinical Persister (S) (ARCP)

The mechanism(s) of biosimilar induced adverse clinical events in inflammatory disorders and its impact on the evolution of ARCP inherent on the incidence of morbidity and the mortality rate remains to be substantiated. A biosimilar to Neulasta (Pegfilgrastim) administered for myelosuppressive chemotherapy has been reported to have a clinically significant incidence of febrile neutropenia. Similar modalities with other biosimilars have also been presented (Int J Hematol.2010 Dec;92(5):765–8; Case Rep Nephrol Urol. 2012 Jul–Dec; 2(2): 165–171); The contraindication for the original formulation is reported to be acute respiratory distress syndrome (ARDS), Glomerulonephritis (GN), Leukocytosis, and Capillary Leak Syndrome (CLS). As per the differential diagnosis for the febrile neutropenia could be of acute respiratory distress syndrome (ARDS) with or without pulmonary edema. Under such clinical presentation tissue hypoxia (Stagnant anoxia (Hypoxicischemic injury), Anoxic anoxia?) with or without “Sweet Syndrome” with an unknown etiology waning the ventilation‐perfusion coupling in patients undergoing chemo/radiation therapy for clinical oncology modalities (J. Clin. Med. 2019, 8(2), 143). CLS has been ascribed with reversible plasma extravasation and loss of net filtration pressure gradient (NFP) in the microcirculation which is analogous to sepsis, septic shock, septicemia impelled hypotension possibly (hypovolemic shock?) with the end result of multiple organ failure (Kidney International, 2017: 92:1, 37). It is hypothesized that such clinical presentation of ensuing hypoxia (plausibly systemic anoxia?) causing VA/Q (VA = alveolar ventilation; Q= blood flow) is below normal which is about 2% of cardiac output (CO) referred to as “shunted blood” (deoxygenated). The total amount of “shunted blood” in the capillary bed – microcirculation per minute is “Physiological shunt” with dysregulated net filtration pressure (NFP) potentially a state of critical closing pressure (CCP) ebb the capillary exchange. Under such physiological sate declining perfusion pressure / perfusion index (PI) and tissue pO2 causing progressive hypoxia and/or anoxia. It is suggested that hypoxia serve as a trigger for generating an adverse pressure gradient impacting the expression pattern of antibiotic resistance gene(s) repertoire (ARCP). Altered ARGR expression profile is known to cause selection pressure on ARCP. In particular, ensuing anaerobic milieu in vivo, engender selection pressure on anaerobic AR pathogens including Gram negative rods, Gram‐positive cocci, Gram‐positive spore‐ and non‐spore‐forming bacilli and Gram‐negative cocci resulting in an aberrant expression pattern of ARGR. Taken together, such the clinical presentation would likely to lead to patients treated with biosimilar(s) become unresponsive to antibiotic therapy leading to an emergence of ARCP impairing the ability for clinical stratification and a defined point of clinical intervention preempting an instant CCP subsequent emergence Antibiotic Resistance Pandemic (ARP).Support or Funding InformationSupported by professional development funds by SWTJC to Subburaj Kannan

Genesis of Antibiotic Resistance LV: Validity Contexture of Mixing Length Hypothesis Turbulence Modelling (MLH ‐ TM) in an exacerbated mortality rate of Early Resuscitation Protocol ‐ Early Goal‐Directed Therapy (ERP‐EGDT) for sepsis.

To decipher the validity of Prantel’s Mixing Length Theory (MLH‐TM) in ERP‐EGDT for sepsis with comorbidity (CC) Capillary Leakage Syndrome ( CLS), also called as Vascular Leak Syndrome ( VLS); Systemic Capillary Leak Syndrome ( SCLS); Sepsis Induced Coagulopathy ( SIC); Sepsis‐induced Disseminated Intravascular Coagulation syndrome ( DIC)) a hypothesis that MLH could be of the valid diagnostic tool in clinical stratification of symptoms pertaining to sepsis with comorbidity, in real‐time scale to determine the onset of “Critical Closing Pressure” (CCP), and consequent collapse of vasculature is presented. Per contexture of the aforementioned objectives, NCT01663701 was chosen because of the case selection criteria and clinical case presentation, to the point data analysis, accessibility of data sets in the public domain and follow‐up care of both primary outcome of in‐hospital mortality and secondary efficacy outcome including 28‐day mortality and time to death. As per MLH, that a lump of fluid particles in one layer of the fluid flow, retains its original momentum at a specific location prior to the transition. During the transition from laminar viscous sublayer to buffer layer to turbulent zone, the turbulent velocity component and viscosity of the lump is dependent on a turbulent fluctuation. The universal velocity distribution law for smooth pipes: laminar viscous sublayer, buffer zone, and the turbulent zone is correlated with intact capillary bed. As indicated, this profile and eq:10.45 to 10.47, for rough pipe where protrusion extending outside of the laminar viscous sublayer, is correlated with dysfunctional vascular endothelium scramming the turbulent zone, escalating an adverse pressure gradient (ISBN: 9780070667624; 2008). It is known that such an adverse pressure gradient can plausibly induce an alteration in antibiotic resistance gene repertoire (ARGR) expression profile augmenting a selection pressure on AR persisters. Diagnostic index such as platelet aggregation, activation of the coagulation cascade and endothelial cell damage in sepsis‐induced coagulopathy originating from comorbidities are known to promote DIC and subsequent loss of capillary bed by glycocalyx shedding (J.Clin.Med.2019, 8,728; Crit.Care (2019) 23:259). Taken together, loss of vascular autoregulation and loss of the intravascular net filtration pressure (~25mmHg) gradient in the capillary bed revives MLH as imperative. It is our interpretation that subsequent to ERP‐EGDT, within the four hour period of admitting to ER/ICU/medical ward, a decrease in arterial pressure leading to increase the resistance with a gradual collapse of capillary bed, due to reduced distending pressure below a critical level (≤ 20mmHg) referred to as Critical closing pressure exacerbating the mortality rate in ERP‐EGDT for sepsis. With the turbulence modeling, in particular, the time scale, knowledge on its viscosity profile of fluid bolus along the damaged endotheliam (rough wall boundary layer), would benefit patient care by mitigating the mortality rate.Support or Funding InformationSupported by the professional development funds by SWTJC to Subburaj Kannan

Simulating high ebb currents in the North Passage of the Yangtze estuary using a vertical 1-D model

A strong maximum ebb current (>3 m/s) in the upper water column was observed at Station CS3 in the middle of the North Passage of the Yangtze River Estuary during the wet season, which was higher than either its upstream or downstream counterparts. To better understand the mechanisms and factors causing the strong ebb current, a vertical one-dimensional (1-D) model was used to conduct a diagnostic study. The model used time series of observed tidal amplitudes, vertical salinity, and suspended sediment concentration (SSC) profiles to compute the density and turbulence. Two tunable parameters, the tidal amplitude attenuation coefficient (i.e., the phase lag) and the background surface pressure gradient that represents the net pressure gradient induced by the freshwater discharge and baroclinic effect, were used to determine the best match with the observed high velocity amplitudes in addition to the bottom roughness height. Three hypotheses of possible causes are tested: (1) the large freshwater discharge, (2) the bottom stratification effects (which were caused by a possible high near-bed suspended sediment gradient), and (3) the unique location of the CS3 station that was influenced by local geometry. The findings show that neither of the first two factors has much influence on the pronounced ebb velocities. Instead, the energy loss caused by the change of channel geometry and a maximum convex bathymetry in the North Passage of the Yangtze River Estuary are the main reasons behind the extremely high observed ebb current velocity profiles. The high near-bottom SSC and gradient located within 0.5 m above the bed only slightly alters the velocity profiles. This 1-D model is convenient for testing a different hypothesis and for coupling with other selected variables to account for the floc size distributions in future studies.

Eddy Generation and Jet Formation via Dense Water Outflows across the Antarctic Continental Slope

AbstractAlong various stretches of the Antarctic margins, dense Antarctic Bottom Water (AABW) escapes its formation sites and descends the continental slope. This export necessarily raises the isopycnals associated with lighter density classes over the continental slope, resulting in density surfaces that connect the near-freezing waters of the continental shelf to the much warmer circumpolar deep water (CDW) at middepth offshore. In this article, an eddy-resolving process model is used to explore the possibility that AABW export enhances shoreward heat transport by creating a pathway for CDW to access the continental shelf without doing any work against buoyancy forces. In the absence of a net alongshore pressure gradient, the shoreward CDW transport is effected entirely by mesoscale and submesoscale eddy transfer. Eddies are generated partly by instabilities at the pycnocline, sourcing their energy from the alongshore wind stress, but primarily by instabilities at the CDW–AABW interface, sourcing their energy from buoyancy loss on the continental shelf. This combination of processes induces a vertical convergence of eddy kinetic energy and alongshore momentum into the middepth CDW layer, sustaining a local maximum in the eddy kinetic energy over the slope and balancing the Coriolis force associated with the shoreward CDW transport. The resulting slope turbulence self-organizes into a series of alternating along-slope jets with strongly asymmetrical contributions to the slope energy and momentum budgets. Cross-shore variations in the potential vorticity gradient cause the jets to drift continuously offshore, suggesting that fronts observed in regions of AABW down-slope flow may in fact be transient features.

Peripheral Venous Pressure as an Indicator of Preload Responsiveness During Volume Resuscitation from Hemorrhage.

Fluid resuscitation of hypovolemia presumes that peripheral venous pressure (PVP) increases more than right atrial pressure (RAP), so the net pressure gradient for venous return (PVP-RAP) rises. However, the heart and peripheral venous system function under different compliances that could affect their respective pressures during fluid infusion. In a porcine model of hemorrhage resuscitation, we examined whether RAP increases more than PVP, thereby reducing the venous return pressure gradient and blood flow. Anesthetized pigs (n = 8) were bled to a mean arterial blood pressure of 40 mm Hg and resuscitated with stored blood and albumin for pulmonary artery occlusion pressures (PAOPs) of 5, 10, 15, and 20 mm Hg. Venous pressures, inferior vena cava blood flow (ultrasonic flowprobe), and left ventricular diastolic compliance (Doppler echocardiography) were measured. Stroke volume variability was calculated. With volume resuscitation, the slope of RAP exceeded PVP (P ≤ 0.0001) when PAOP is 10 to 20 mm Hg, causing the pressure gradient for venous return to progressively decrease. Inferior vena cava blood flow did not further increase after PAOP > 10 mm Hg. The E/e' ratio increased (P = 0.001) during resuscitation indicating reduced diastolic compliance. A significant curvilinear relationship was found between PVP and stroke volume variability (R = 0.62; P < 0.001), where fluid responders had PVP < 15 mm Hg. Fluid resuscitation above a PAOP 10 mm Hg reduces myocardial compliance and reduces the venous return pressure gradient. The hemodynamic response to fluid resuscitation becomes limited by diastolic properties of the heart. PVP measurement during hemorrhage resuscitation may predict fluid responsiveness and nonresponsiveness.

4D Flow MRI-based pressure loss estimation in stenotic flows: Evaluation using numerical simulations.

To assess how 4D flow MRI-based pressure and energy loss estimates correspond to net transstenotic pressure gradients (TPGnet) and their dependence on spatial resolution. Numerical velocity data of stenotic flow were obtained from computational fluid dynamics (CFD) simulations in geometries with varying stenosis degrees, poststenotic diameters and flow rates. MRI measurements were simulated at different spatial resolutions. The simplified and extended Bernoulli equations, Pressure-Poisson equation (PPE), and integration of turbulent kinetic energy (TKE) and viscous dissipation were compared against the true TPGnet . The simplified Bernoulli equation overestimated the true TPGnet (8.74 ± 0.67 versus 6.76 ± 0.54 mmHg). The extended Bernoulli equation performed better (6.57 ± 0.53 mmHg), although errors remained at low TPGnet . TPGnet estimations using the PPE were always close to zero. Total TKE and viscous dissipation correlated strongly with TPGnet for each geometry (r(2) > 0.93) and moderately considering all geometries (r(2) = 0.756 and r(2) = 0.776, respectively). TKE estimates were accurate and minorly impacted by resolution. Viscous dissipation was overall underestimated and resolution dependent. Several parameters overestimate or are not linearly related to TPGnet and/or depend on spatial resolution. Considering idealized axisymmetric geometries and in absence of noise, TPGnet was best estimated using the extended Bernoulli equation. Magnetic Resonance in Medicine published by Wiley Periodicals, Inc. on behalf of International Society for Magnetic Resonance.

Shear Senses and Viscous Dissipation of Layered Ductile Simple Shear Zones

Velocity profiles and shear heat profiles for inclined, layered Newtonian simple shear zones are considered. Reverse fault-like simple shear of the boundaries and upward net pressure gradient act together in such shear zones. As the velocity of the boundary increases, the point of highest velocity shifts from the lower layer of less viscosity into the upper layer. The shear heat profile shows a temperature peak inside the lower layer. For a more viscous upper layer, the point of highest velocity is located inside the upper layer and shifts towards the upper boundary of the shear zone. The shear heat profile shows a maximum temperature within the upper layer. Depending on the flow parameters of the two layers, the slip rate of the boundary, and the dip and thickness of the shear zone, a shear sense in reverse to the relative movement of the shear zone boundaries may develop. These models can decipher thermo-kinematics of layered shear zones in plate-scale hot orogens.

Fluid flow due to collective non-reciprocal motion of symmetrically-beating artificial cilia

Using a magneto-mechanical solid-fluid numerical model for permanently magnetic artificial cilia, we show that the metachronal motion of symmetrically beating cilia establishes a net pressure gradient in the direction of the metachronal wave, which creates a unidirectional flow. The flow generated is characterised as a function of the cilia spacing, the length of the metachronal wave, and a dimensionless parameter that characterises the relative importance of the viscous forces over the elastic forces in the cilia.

Mechanism of a flow-gated angiogenesis switch: early signaling events at cell–matrix and cell–cell junctions

A bias towards angiogenesis from the venous circulation has long been known, but its cause remains unclear. Here we explore the possibility that high interstitial pressure in tumors and the resultant net filtration pressure gradient that would induce flow from the interstitium into the venous circulation or lymphatics could also be an important mechanical regulator of angiogenesis. The objective of this study was to test the hypothesis that basal-to-apical (B-A) transendothelial flow promotes angiogenesis and to investigate potential mechanisms. Macro- and microvascular endothelial monolayers were cultured on type I collagen gels in a microfluidic cell culture device and subjected to apical-to-basal (A-B) and B-A transendothelial flows. Samples were perfusion fixed and analyzed for morphological responses, localization and degree of phosphorylation of certain signaling proteins. Application of B-A, but not A-B flow, to cultured endothelial monolayers was found to promote capillary morphogenesis and resulted in distinct localization patterns of VE-cadherin and increased FAK phosphorylation. These results suggest that B-A flow triggers the transition of vascular endothelial cells from a quiescent to invasive phenotype and that the flow-mediated response involves signaling at cell-cell and cell-matrix interfaces. These results support the hypothesis that transendothelial pressure gradients resulting in B-A flow promotes sprouting angiogenesis and are consistent with early observations that tumor angiogenesis occurs from the venous side of the circulation.

Modeling the impact of concomitant aortic stenosis and coarctation of the aorta on left ventricular workload

Coarctation of the aorta (COA) is an obstruction of the aorta and is usually associated with bicuspid and tricuspid aortic valve stenosis (AS). When COA coexists with AS, the left ventricle (LV) is facing a double hemodynamic load: a valvular load plus a vascular load. The objective of this study was to develop a lumped parameter model, solely based on non-invasive data, allowing the description of the interaction between LV, COA, AS and the arterial system. First, a formulation describing the instantaneous net pressure gradient through the COA was introduced and the predictions were compared to in vitro results. The model was then used to determine LV work induced by coexisting AS and COA with different severities. The results show that LV stroke work varies from 0.98 J (no-AS; no-COA) up to 2.15 J (AS: 0.61 cm 2+COA: 90%). Our results also show that the proportion of the total flow rate that will cross the COA is significantly reduced with the increasing COA severity (from 85% to 40%, for a variation of COA severity from 0% to 90%, respectively). Finally, we introduced simple formulations capable of, non-invasively, estimating both LV peak systolic pressure and workload. As a conclusion, this study allowed the development of a lumped parameter model, based on non-invasive measurements, capable of accurately investigating the impact of coexisting AS and COA on LV workload. This model can be used to optimize the management of patients with COA and AS in terms of the sequence of lesion repair.

Observations of the velocity profile of a fast and deep oceanic density current constrained in a gully

The southwestern side of the Wyville Thomson Ridge transports cold Faroe‐Shetland Channel Bottom Water in a narrow cascade from a depth of 500 m down to 1700 m. An upward looking acoustic Doppler current profiler located at a depth of 1200 m measured its currents to a height of 500 m for 6 months. The westward flowing deep density current (mean thickness 343 m) extended well above the bottom Ekman layer (of order 20 m) and had a profile with a bullet nose shape that had a peak velocity at a height that was about of its thickness. The mean maximum speed was about 60 cm s−1, although there was significant variability in velocity with 90% of the variance explained by mode 1 that had a similar bullet nose shape. From the downstream momentum balance it is estimated that the vertical eddy viscosity in the overflow was of order 0.5 m2 s−1 through most of its depth but somewhat larger near the interface. A full description of the velocity profile requires an opposing surface slope and current, with zero net pressure gradient within the overflow. The transverse circulation (mean speed ∼3 cm s−1) had southward flows at the interface and seabed and a return flow at middepth. This circulation is driven by imbalances between Coriolis forcing from the downstream current and the transverse pressure gradient. Its overturning scales suggest a bulk eddy viscosity of order 2 m2 s−1 and may indicate a feedback between the downstream and transverse currents.

Molecular Regulation of Lymphatic Contractility

The lymphatic system plays critical roles in body fluid and macromolecular homeostasis, lipid absorption, immune function, and metastasis. To accomplish these tasks, the lymphatics must move lymph and its contents from the interstitial space through the lymph vessels and nodes and into the great veins. Contrary to popular belief, lymph does not passively "drain" down this pathway, because the net pressure gradients oppose flow. Instead, the lymphatics must act as both the conduits that direct and regulate lymph flow and the pumps that generate the lymph flow. Thus, to regulate lymph transport and function, both lymphatic pumping and flow resistance must be controlled. Both of these processes occur via regulation of lymphatic muscle contractions, which are classically thought to occur via the interaction of cell calcium with regulatory and contractile proteins. However, our knowledge of this regulation of lymphatic contractile function is far from complete. In this chapter we review our understanding of the important molecular mechanisms, the calcium regulation, and the contractile/regulatory proteins that control lymphatic contractions. A better understanding of these mechanisms could provide the basis for the development of better diagnostic and treatment modalities for lymphatic dysfunction. While progress has been made in our understanding of the molecular biology of lymphangiogenesis as a result of the development of potential lymphangiogenic therapeutic targets, there are currently no therapeutic agents that specifically modulate lymphatic pump function and lymph flow via lymphatic muscle. However, their development will not be possible until the molecular basis of lymphatic contractility is more fully understood.

Modeling South China Sea circulation: Response to seasonal forcing regimes

A three‐dimensional ocean model has been utilized to study circulation and its seasonal variation in the South China Sea (SCS) in response to the forcing of the Asian monsoon and the Kuroshio intrusion. The SCS ocean model has a resolution of approximately 10 km horizontal spacing and 30 vertical levels with a realistic bottom topography. The model is forced with time‐dependent wind stress and heat flux from National Center for Environmental Prediction Reanalysis data as well as with lateral fluxes from a Pacific Ocean model of 40 km horizontal resolution. This study reports on the analysis of the mean seasonal circulation and dynamic processes in response to monsoonal wind stress, the Kuroshio intrusion, and other intrinsic forcing processes. It is found that the seasonal circulation in the SCS is mainly driven by the monsoonal wind stress and greatly influenced by the inflow from the Kuroshio intrusion. Strong currents along the continental margin of the SCS form mean basin‐wide cyclonic and anticyclonic circulations in the winter and summer, respectively. Multiscale eddies are embedded in the general circulation across the basin. While mainstream of the Kuroshio passes through the Luzon Strait without intruding into the SCS, partial intrusion occurs in the upper 200 m near the shelf margin southwest of Taiwan at times when winter dynamic conditions prevail in the north SCS. The intrusion of the Kuroshio into the SCS also occurs at depths in all seasons, mainly along the continental slope. The coastal current separation to the east off southern Vietnam and the associated eddy formations characterize the circulation in the south SCS. The simulated results compare well with the corresponding observed fields. Dynamical processes involved in the forced flow fields are investigated by examination of the momentum balances. The analyses reveal that the circulation in the SCS is generally dominated by the geostrophic currents. North of the Luzon Strait, positive nonlinearity in the zonal direction is locally intensified, which leads to the formation of centripetal acceleration for the mainstream of the Kuroshio to turn eastward. The Kuroshio intrusion at depths is governed by the ageostrophic flows and highly associated with the net westward pressure gradient force. Coastal jet separation to the east off Vietnam is mainly associated with the local wind stress field and with the shelf topography in the summer and winter, respectively. Sensitivity study reveals that the weakening of the Kuroshio markedly enhances Kuroshio's intrusion and forms an anticyclonic eddy west of the Luzon Strait.

Lowering of interstitial fluid pressure in rat submandibular gland: a novel mechanism in saliva secretion

The submandibular gland transports fluid at a high rate through the interstitial space during salivation, but the exact level of all forces governing transcapillary fluid transport has not been established. In this study, our aim was to measure the relation between interstitial fluid volume (V(i)) and interstitial fluid pressure (P(if)) in salivary glands during active secretion and after systemically induced passive changes in gland hydration. We tested whether interstitial fluid could be isolated by tissue centrifugation to enable measurement of interstitial fluid colloid osmotic pressure. During control conditions, V(i) averaged 0.23 ml/g wet wt (SD 0.014), with a corresponding mean P(if) measured with micropipettes of 3.0 mmHg (SD 1.3). After induction of secretion by pilocarpine, P(if) dropped by 3.8 mmHg (SD 1.5) whereas V(i) was unchanged. During dehydration and overhydration of up to 20% increase of V(i) above control, a linear relation was found between volume and pressure, resulting in a compliance (DeltaV(i)/DeltaP(if)) of 0.012 ml.g wet wt(-1).mmHg(-1). Interstitial fluid was isolated, and interstitial fluid colloid osmotic pressure averaged 10.4 mmHg (SD 1.2), which is 64% of the corresponding level in plasma. We conclude that P(if) drops during secretion and, thereby, increases the net transcapillary pressure gradient, a condition that favors fluid filtration and increases the amount of fluid available for secretion. The reduction in P(if) is most likely induced by contraction of myoepithelial cells and suggests an active and new role for these cells in salivary secretion. The relatively low interstitial compliance of the organ will enhance the effect of the myoepithelial cells on P(if) during reduced V(i).

Hemodialysis: Techniques and Prescription

Hemodialysis: Techniques and Prescription