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A quarter of the world's population experience wheezing. These sounds have been used for diagnosis since the time of the Ebers Papyrus ( ca 1500 BC). We know that wheezing is a result of the oscillations of the airways that make up the lung. However, the physical mechanisms for the onset of wheezing remain poorly understood, and we do not have a quantitative model to predict when wheezing occurs. We address these issues in this paper. We model the airways of the lungs by a modified Starling resistor in which airflow is driven through thin, stretched elastic tubes. By completing systematic experiments, we find a generalized ‘tube law’ that describes how the cross-sectional area of the tubes change in response to the transmural pressure difference across them. We find the necessary conditions for the onset of oscillations that represent wheezing and propose a flutter-like instability model for it about a heavily deformed state of the tube. Our findings allow for a predictive tool for wheezing in lungs, which could lead to better diagnosis and treatment of lung diseases.

Interactions between fluids and elastic solids are ubiquitous in applications ranging from aeronautical and civil engineering to physiological flows. Here we study the pulsatile flow through a two-dimensional Starling resistor as a simple model for unsteady flow in elastic vessels. We numerically solve the equations governing the flow and the large-displacement elasticity and show that the system responds as a forced harmonic oscillator with nonconventional damping. We derive an analytical prediction for the amplitude of the oscillatory wall deformation, and thus the conditions under which resonances occur or vanish.

In central serous chorioretinopathy (CSC), the macula is detached because of fluid leakage at the level of the retinal pigment epithelium. The fluid appears to originate from choroidal vascular hyperpermeability, but the etiology for the fluid is controversial. The choroidal vascular findings as elucidated by recent optical coherence tomography (OCT) and wide-field indocyanine green (ICG) angiographic evaluation show eyes with CSC have many of the same venous patterns that are found in eyes following occlusion of the vortex veins or carotid cavernous sinus fistulas (CCSF). The eyes show delayed choroidal filling, dilated veins, intervortex venous anastomoses, and choroidal vascular hyperpermeability. While patients with occlusion of the vortex veins or CCSF have extraocular abnormalities accounting for the venous outflow problems, eyes with CSC appear to have venous outflow abnormalities as an intrinsic phenomenon. Control of venous outflow from the eye involves a Starling resistor effect, which appears to be abnormal in CSC. Similar choroidal vascular abnormalities have been found in peripapillary pachychoroid syndrome. However, peripapillary pachychoroid syndrome has intervortex venous anastomoses located in the peripapillary region while in CSC these are seen to be located in the macular region. Spaceflight associated neuro-ocular syndrome appears to share many of the pathophysiologic problems of abnormal venous outflow from the choroid along with a host of associated abnormalities. These diseases vary according to their underlying etiologies but are linked by the venous decompensation in the choroid that leads to significant vision loss. Choroidal venous overload provides a unifying concept and theory for an improved understanding of the pathophysiology and classification of a group of diseases to a greater extent than previous proposals.

Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as “intracranial pressure sensor” played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.

A computational model of a morphologically-based alveolar capillary unit (ACU) in the rabbit is developed to relate lung fluid balance to mechanical forces between capillary surface and interstitium during development of interstitial edema. We hypothesize that positive values of interstitial liquid pressure Pliq impact on capillary transmural pressure and on blood flow. ACU blood flow, capillary recruitment and filtration are computed by modulating vascular and interstitial pressures. Model results are compared with experimental data of Pliq increasing from ~-10 (control) up to ~4cmH2O in two conditions, hypoxia and collagenase injection. For hypoxia exposure, fitting data requires a linear increase in hydraulic conductivity Lp and capillary pressure PC, that fulfils the need of increase in oxygen delivery. For severe fragmentation of capillary endothelial barrier (collagenase injection), fitting requires a rapid increase in both hydraulic and protein permeability, causing ACU de-recruitment, followed by an increase in PC as a late response to restore blood flow. In conclusion, the model allows to describe the lung adaptive response to edemagenic perturbations; the increase in Pliq, related to the low interstitial compliance, provides an efficient control of extravascular water, by limiting microvascular filtration.

We present a novel application of rotors in geometric algebra to represent the change of curvature tensor, that is used in shell theory as part of the constitutive law. We introduce a new decomposition of the change of curvature tensor, which has explicit terms for changes of curvature due to initial curvature combined with strain, and changes in rotation over the surface. We use this decomposition to perform a scaling analysis of the relative importance of bending and stretching in flexible tubes undergoing self excited oscillations. These oscillations have relevance to the lung, in which it is believed that they are responsible for wheezing. The new analysis is necessitated by the fact that the working fluid is air, compared to water in most previous work. We use stereographic imaging to empirically measure the relative importance of bending and stretching energy in observed self excited oscillations. This enables us to validate our scaling analysis. We show that bending energy is dominated by stretching energy, and the scaling analysis makes clear that this will remain true for tubes in the airways of the lung., 8 figures

A purely hydraulic mechanism consisting in the pulsatile cuff-compression effect, by the cerebrospinal fluid displacement induced by the arterial pulsation, on the final portion of the bridging veins, has recently been hypothesized. This mechanism is able to maintain the constancy of cerebral blood flow (CBF) within the autoregulatory range, thus implying an exact balance between arterial inflow and venous outflow. In this study, we correlated arterial inflow and venous outflow during an experimentally induced condition of intracranial hypertension in pigs.Mock cerebrospinal fluid (CSF) was progressively infused until a condition of brain tamponade was reached. Blood flow velocities at middle cerebral artery and sagittal sinus sites were evaluated simultaneously.Mean intracranial arterial blood flow velocity (IABFV), mean sagittal sinus blood flow velocity (SSBFV), and pulsatile-IABFV remained almost constant until cerebral perfusion pressure (CPP) dropped below 60-70 mmHg; then, a progressive decrease in mean IABFV and SSBFV, together with an increase in pulsatile-IABFV, was evident.The strict similarity between mean IABFV and SSBFV patterns suggests that CBF decrement is mainly due to a decrease in the venous outflow, which, in turn, produces an obstacle to the arterial inflow. The correspondent increase in pulsatile-IABFV confirms the presence of a distal outflow obstruction. All these findings point towards a purely hydraulic mechanism underlying the cerebral autoregulation which acts at the level of the so-called Starling resistor.

In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation.We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa.A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP=1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces.

“Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures” by J. B. West, C. T. Dollery, and A. Naimark ( J Appl Physiol 19: 713–724, 1964) is a classic paper, although it has not yet been included in the Essays on the American Physiological Society Classic Papers Project ( http://www.the-aps.org/publications/classics/ ). This is the paper that originally described the “zones of the lung.” The final figure in the paper, which synthesizes the results and discussion, is now seen in most textbooks of physiology or respiratory physiology. The paper is also a model of clear, concise writing. The paper and its final figure can be used to teach or review a number of physiological concepts. These include the effects of gravity on pulmonary blood flow and pulmonary vascular resistance; recruitment and distention of pulmonary vessels; the importance of the transmural pressure on the diameter of collapsible distensible vessels; the Starling resistor; the interplay of the pulmonary artery, pulmonary vein, and alveolar pressures; and the vascular waterfall. In addition, the figure can be used to generate discovery learning and discussion of several physiological or pathophysiological effects on pulmonary vascular resistance and the distribution of pulmonary blood flow.

We developed electrical circuit based model for the different components of the cerebral circulation, what allowed us to simulate cerebral blood flow in a variety of cerebrovascular disorders. This approach allowed us to derive a set of equations by which relative maximum, or fractional flow reserve, can be defined and calculated in three relevant sites: the stenotic artery, in the veins related to the stenotic artery, and in the collateral circulation of the affected region of the brain. Our results create theoretical basis for the entirely new approach to cerebrovascular disorders that currently emphasise anatomical identification of the disease to guide the treatment, such as the degree of arterial luminal stenosis obtained from various imaging modalities. In doing so, we directly address an urgent need for stroke experts to advance the care of their patients, since current approach of stroke treatment has not been meaningfully successful. DOI: http://dx.doi.org/10.5755/j01.eee.20.10.8877

The upper airway is often modeled as a classical Starling resistor, featuring a constant inspiratory airflow, or plateau, over a range of downstream pressures. However, airflow tracings from clinical sleep studies often show an initial peak before the plateau. To conform to the Starling model, the initial peak must be of small magnitude or dismissed as a transient. We developed a method to simulate fast or slow inspirations through the human upper airway, to test the hypothesis that this initial peak is a transient. Eight subjects [4 obstructive sleep apnea (OSA), 4 controls] slept in an "iron lung" and wore a nasal mask connected to a continuous/bilevel positive airway pressure machine. Downstream pressure was measured using an epiglottic catheter. During non-rapid eye movement (NREM) sleep, subjects were hyperventilated to produce a central apnea, then extrathoracic pressure was decreased slowly (∼2-4 s) or abruptly (

The upper airway is often modeled as a Starling resistor, which predicts that flow is independent of inspiratory effort during flow limitation. However, while some obstructive sleep apnea (OSA) patients exhibit flat, Starling resistor-like flow limitation, others demonstrate considerable negative effort dependence (NED), defined as the percent reduction in flow from peak to mid-inspiration. We hypothesized that the variability in NED could be due to differences in phasic pharyngeal muscle activation between individuals. Therefore, we induced topical pharyngeal anesthesia to reduce phasic pharyngeal muscle activation to see if it increased NED. Twelve subjects aged 50±10 years with a BMI of 35±6 kg/m(2) and severe OSA (apnea-hypopnea index=52±28 events/h) were studied. NED and phasic genioglossus muscle activity (EMG(GG)) of flow limited breaths were determined before and after pharyngeal anesthesia with lidocaine. Pharyngeal anesthesia led to a 33% reduction in EMG(GG) activity (p

Background and ObjectivesThe origin and the presence of negative pressure in the epidural space as well as the relationship of the extent of epidural anesthesia to epidural pressure has long been a subject of controversy. To further elucidate epidural pressure and its time course, the pressure at the needle tip was continuously measured as it traversed the interspinous ligament and the ligamentum flavum.MethodsIn a group of 22 patients, fluid was infused under gravity, and in a second group of 25 patients, boluses of fluid were administered at controlled infusion rates and under gravity. The volume-pressure-flow relationship was thus measured in one of two ways, either with a manual syringe and pressure transducer or with a pressure-monitoring-computer-controlled volumetric infusion pump.ResultsNatural pressure, (i.e., pressure in the epidural space before instrumentation is applied) could be approached when the space was first entered before fluid was infused (initial pressure); or after fluid had been infused (residual pressure). Epidural pressure could be extrapolated from the upsweep of the volume-pressure-flow relationship by projecting it back to just before the first injection. The extrapolated pressure lay between the initial and residual pressures. Medicinal solution placed in the barrel of the syringe did not infuse under gravity until the syringe barrel was lifted to a certain height, at which flow began and continued at a perceptible rate, with very little or no further increase in height required to maintain flow. The pressure at which flow began was the critical opening pressure, a characteristic of a Starling resistor. Furthermore, resistance to inflow of fluid was related to the presence or absence of natural or surgical disease in the epidural space. Resistance was significantly higher in the diseased than in the surgical group, at 114 (range, 22-226) mm Hg/L/h versus 46 (range, 8-86) mm Hg/L/h. Three phases were seen in the pressure-time recordings.ConclusionsVolume-pressure-flow relationships in the epidural space can be explained by a model in which epidural and subarachnoid pressures are inextricably related with the Starling pressure, dependent on the subarachnoid pressure. This model suggests reasons why spread of anesthetics might be difficult to predict.

Beard & Feigl's call for the removal of Guyton's venous return curve from teaching materials (referred to here as the Guyton–Levy venous pressure curve, VPC), is not based on any deficiency of the VPC itself but purely on Guyton's own conceptual misinterpretations thereof (Beard & Feigl, 2013). Levy resolved these misinterpretations in 1979 (Levy, 1979) and there is today no valid remaining misinterpretation. Yet Beard & Feigl, evidently unaware of the full power of the VPC when combined with the Frank-Starling cardiac output (CO) curve to form Guyton's Graphical Analysis (GGA; Guyton et al. 1973), to this day unsurpassed in its ability to model the central haemodynamics of any circulatory state, would have the baby (GGA) thrown out with the bathwater (Guyton's misinterpretations). Hoping not to put too fine a point on the matter, Beard & Feigl assert that in Guyton's original VPC experiment (Guyton et al. 1957) the artificial pump was the independent variable. In fact, the pump was downstream to the Starling resistor (SR) thus rendering pump output dependent on the hydrostatic height of the SR relative to the canine surrogate mid right atrium. The pump was adjusted manually simply to insure quantitative transfer to the canine left heart of whatever flow emerged through the SR; how much flow was entirely dependent on the throttling effect of the SR. Accordingly, the SR, not the pump, was the true independent variable governing the experiment. This in no way alters the reality that CO was the independent variable controlling right atrial pressure (RAP). As cited (Beard & Feigl, 2013), Grodins and Levy used preparations essentially identical to Guyton's (the SR was excluded) and they varied CO by simply changing the pump rate. Their VPC was similar. This not only supported the validity of Guyton's experiment and the VPC itself, but it also helped disprove Guyton's backpressure premise – if the VPC is the same with or without a SR (which is a simulated tricuspid stenosis intuitively implying backpressure), then RAP must vary due to something other than backpressure. Beard & Feigl imply the VPC and GGA are deficient for their failure to model peripheral tissue–organ haemodynamics. The VPC/GGA are models of the central circulation. Irrespective of the sundry nuances of peripheral perfusion, spent blood is presented back to the heart by the vasculature in aggregate, not in particular, and this is faithfully represented by the VPC/GGA. GGA, properly understood, exposes clinical decision making based on considerations of ‘venous return’ as the conceptual distraction it is. GGA accurately provides all the central circulatory information needed to optimally comprehend and manage clinical cardiovascular disorders. There is no clinical circumstance compelling considerations of venous return in lieu of venous pressure as all changes in venous return translate into proportionate changes in venous pressure.

The development of intelligent medical systems, electronic monitoring systems required for physiological models. The proposed model of venous blood flow realized on the electric circuit basis can be used to support the development of blood pressure, real-time devices. Designed for venous blood nonlinear dynamic model is an extension of Starling resistor model. When the tissue pressure increased, static models are not suitable. Suggested non-linear dynamic model allows determining the threshold pressure, when blood flow returns to normal in damaged blood vessels. The integrated model can be used for blood pressure support biomedical devices., Kuriant medicinines intelektualias elektronines monitoringo sistemas reikalingi fiziologinių sistemų modeliai. Pasiūlytas elektros grandinių pagrindu sukurtas veninės kraujotakos modelis gali būti panaudotas kuriant kraujo spaudimo palaikymo realaus laiko įrenginius. Sukurtas veninės kraujotakos dinaminis netiesinis modelis yra Starlingo rezistoriaus modelio patobulinimas. Esami statiniai modeliai netinka, kai audinių spaudimas padidėjęs. Sukurtas dinaminis netiesinis modelis leidžia nustatyti spaudimo slenkstį, kai kraujotaka pažeistose kraujagyslėse atsinaujina. Integruotą modelį galima naudoti biomedicininiuose kraujo spaudimo palaikymo įrenginiuose.

We studied the impact of wall strain and surrounding pressure on the onset of airflow limitation in a thin-walled “floppy” tube model. A vacuum source-generated steady-state (baseline) airflow (0–350 ml/s) through a thin-walled latex tube (length 80 mm, wall thickness 0.23 mm) enclosed within a rigid, sealed, air-filled, cylindrical chamber while upstream minus downstream pressure, chamber pressure (Pc), and lumen geometry [in-line digital camera; segmentation (Amira 5.2.2) and analysis (Rhinoceros 4) software] were monitored. Longitudinal strain (S; 0–62.5%) and Pc (0–20 cmH2O) combinations were imposed, and Pc associated with onset of 1) reduced airflow and 2) fully developed airflow limitation recorded. At any strain, increasing Pc resulted in a decrease in airflow. Across all baseline airflow, threshold pressure was 1–7 cmH2O for S < 25%, 6–8 cmH2O at S = 25% and 37.5%, and 5–7 cmH2O at S = 50% and 62.5%. Pc associated with fully developed airflow limitation was 4–6 cmH2O for S < 25%, >20 cmH2O at S = 25% (i.e., no flow limitation), 18 cmH2O at S = 37.5%, and 8–12 cmH2O at S = 50% and 62.5%. Lumen area decreased with increasing Pc but was 1) larger at S = 25% and 2) characterized by bifold narrowing at S < 25% and trifold narrowing at S ≥ 25%. In conclusion, tube function was modulated by Pc vs. S interactions, with S = 25% producing trifold lumen narrowing, maximal patency, and no airflow limitation. Findings may have implications for understanding peripharyngeal tissue pressure and pharyngeal wall strain effects on passive pharyngeal airway function in humans.

Understanding the mechanics of the upper airway is critical to the research on the pathophysiology of upper airway obstruction. This article will review the determinants of upper airway patency including the upper airway dilating muscles, the transmural pressure across the airway, pharyngeal compliance, and craniofacial structure. During sleep, loss of the wakefulness stimulus to breathe results in decreased upper airway caliber and increased resistance. Models that characterize the relationship between pressure and flow of the upper airway during sleep and that explain upper airway collapsibility during sleep will be presented. Finally, a proposed scheme of the pathophysiology of upper airway collapse during sleep will be presented. Keywords: upper airway resistance; collapsiblity; nasopharynx; sleep; upper airway dilators; inspiratory flow limitation; sleep-disordered breathing; Starling resistor

The aim of this paper is to test a new infusion system prototype which is intended to recover the normal venous return and lost blood quantity in hypovolemic patients. For this purpose a bolus of fluid is injected at a high speed in the vena cava, accelerating and dragging the stagnating flow upstream the catheter. In order to improve the effects of the injection and to avoid damage to heart valves, the injection is synchronized with the heart cycle and should be controlled by the electrocardiogram track of the patient in such a way that the maximum flow rate injected occurs when the tricuspid valve is open. An in-vitro experimental apparatus — simulating the vena cava and its environment — has been built and used to measure velocity and pressure fields in the vena cava during the high velocity injection. In a first embodiment, the experimental apparatus consists of two reservoirs arranged, respectively, upstream and downstream a Starling Resistor, but at different heights. A constant flow rate inside the vena cava is maintained, thus simulating the diastolic phase of the heart. In a second embodiment of the experimental apparatus, two electrical valves, arranged downstream the Starling Resistor, generate an oscillating pressure wave along the vena cava, thus simulating the human central venous pressure. By varying the flow rate inside the vena cava and the opening rate of the valves, it has been possible to evaluate the dragging effect of the new injection system and the mechanical behavior of the vena cava during both continuous and pulsating infusion.Copyright © 2006 by ASME

1988).Initssimplestform,a Starling resistor is a compliant tube; theinlet and outlet pressures are specified, as isthepressureexteriortothetube.Becausetheexteriorpressureandtheupstreampressureare coupled (e.g. through lung recoil) suchasystemtypicallydisplaysthephenomenonof flow limitation. Increases in drivingand exterior pressure lead to increasesin flow, but only up to a point beyondwhich flow is constant: the system is flowlimited.Thisphenomenonhasbeenexplainedandinterpreted on a number of grounds: theequalpressurepointconceptofMead(Mead

Clinical evidence suggests that increased amniotic fluid volume due to polyhydrarnnios increases placental vascular resistance. We have sought to model the possible effects of an increased amniotic fluid volume oil the net fetofetal transfusion in monochorionic twin pregnancies. We wanted to compare these effects with the results of previous simulations, which aimed to explain why the twin-twin transfusion syndrome (TTTS) placentas more often include bidirectional arteriovenous (AV) rather than AV plus arterioarterial (AA) anastomoses. We extended our mathematical model of TTTS by simulating two different mechanisms that increase the placental vascular resistance as a consequence of polyhydramnios. First, there is an increase in the placental capillary resistance and hence in deep AV and opposite AV (denoted as VA) resistances due to polyhydramnios. Second, there is an increase in the resistance of chorionic veins due to polyhydramnios, assuming that these veins act as Starling resistors. We then simulated the effects of polyhydramnios on different placental anastomotic patterns. The results were as follows. In the first mechanism (polyhydramnios affects AV-VA resistances), an increased amniotic fluid volume hardly affected bidirectional AV, but slightly decreased fetofetal transfusion in AV plus AA anastomoses. However, for these effects to change the natural development of the pregnancy, polyhydramnios needed to persist for approximately 4 weeks, and by comparing the effects of polyhydramnios with the effects of amnioreduction, amnioreduction was more beneficial for normalizing the donor amniotic fluid volume. Therefore, these beneficial effects due to polyhydramnios have no practical clinical significance. In the second mechanism (Starling resistor for chorionic veins), polyhydramnios slightly increased fetofetal transfusion and hence slightly increased TTTS severity in bidirectional AV and AV plus VV, but did not affect AV plus AA anastomoses. In conclusion, we hypothesize that the simulated effects of polyhydramnios are not the primary cause of the fact that TTTS placentas more often include bidirectional AV than AV plus AA anastomoses. Rather, the more likely explanation is the previously identified larger range of AA than VA anastomotic diameters that adequately compensate for the effects of the AV

Retinal venous pressure was examined in six pigs using a balanced servo-nulling micropuncture technique. The mean transmural venous pressure was 0.95 mmHg (SD 1.50 mmHg). The transmural venous pressure was lower at the optic disc than away from the disc (0.32 +/- 1.46 mmHg vs 1.69 +/- 1.19 mmHg, P < 0.01). At the disc a transmural pressure of zero or less (0 to -0.5 mmHg) was demonstrated in 10/21 (48%) of the disc readings. Over an intraocular pressure range of 15-26 mmHg there was a strong correlation between intraocular pressure and retinal venous pressure (Pearson coefficient r = 0.92). The results are compatible with the Starling resistor theory of venous outflow from the eye.

Overdrainage from siphoning, a result of negative distal pressure, has been a major problem with the existing differential pressure shunt devices. The antisiphon/ siphon control devices used to reduce siphoning often malfunction owing to fibrous scar formation around the valve. Similarly, the functioning of gravity-actuated systems is adversely affected by body movements. Constant flow shunt systems may not be superior to existing differential pressure valves, as has been shown in a recent multicenter study. In view of these difficulties, we investigated the possibility of developing a shunt valve based on the Starling resistor concept of flow regulation that allows proximal pressure-dependent and distal pressure-independent flow. The valve designed is capable of proximal pressure-dependent and distal pressure-independent flow. The valve allows for adjustable negative pressure in the vertical position.

We challenge the arguments presented in the ‘PRO’ side of this debate by our friends and colleagues, Schwartz & Smith (2013), in two important areas. (1) They claim that the effective peripharyngeal pressure is Pcrit. We dispute this on several grounds. Pcrit itself is a construct, most often measured by extrapolation to the intraluminal pressure that would be required to effect near or complete obstruction (Gleadhill et al. 1991). The appropriate peripharyngeal pressure for a Starling resistor would be analogous to peribronchial pressure in intrathoracic airways, which is a relatively well defined concept (Mead et al. 1970). But absent a significant stress jump across the air/tissue interface in the pharynx, there is a continuous pressure variation in the tissues from intraluminal pressure to atmospheric pressure at the body surface (Strohl et al. 2012). Thus, the very concept of an extraluminal (or tissue) pressure is vague and Fig. 1 in Schwartz & Smith (2013) is potentially misleading. (2) For infinitely compliant conduits, their claim is that, as downstream pressure decreases, flow increases up to a point of flow limitation; beyond this, flow remains constant at a plateau (Elliott & Dawson, 1977). This is true in some individuals. In others, increasingly negative downstream pressures do cause the flows to decrease, often substantially, and even, in some, to complete or near occlusion (Schwartz et al. 1988; Owens et al. 2012). This behaviour is inconsistent with the properties of a Starling resistor. When negative effort dependence (NED) is marked, their interpretation is that somehow nasal or upstream pressure (Pus) must have decreased below Pcrit. While Pus Pcrit. These ideas may suffice for a simple floppy tube, but are unable to explain the profound reductions in inspiratory airflow observed frequently in sleep apnoea patients. Finally, we remark that clinical Pcrit features (pressure gradients determining severity of obstruction, efficacy of CPAP, decreases in neuromuscular tone leading to obstruction, phenotypic factors of age, weight, sex, etc.) do not constitute evidence for Starling resistor behaviour, insofar as other models (e.g. the distributed tippy tongue model) also fits these variations as well. For us, the important features are these: (a) the simple Starling resistor does not explain the flow/pressure relationship of the upper airways in individuals with marked NED, and (b) NED is important clinically and woefully underappreciated.

Background: Brain arteriovenous malformations (AVMs) produce circulatory and functional disturbances in adjacent as well as in remote areas of the brain, but their physiological effect on the cerebrospinal fluid (CSF) pressure is not well known. Methods: The hypothesis of an intrinsic disease mechanism leading to increased CSF pressure in all patients with brain AVM is outlined, based on a theory of hemodynamic control of intracranial pressure that asserts that CSF pressure is a fraction of the systemic arterial pressure as predicted by a two-resistor series circuit hydraulic model. The resistors are the arteriolar resistance (that is regulated by vasomotor tonus), and the venous resistance (which is mechanically passive as a Starling resistor). This theory is discussed and compared with the knowledge accumulated by now on intravasal pressures and CSF pressure measured in patients with brain AVM. Results: The theory provides a basis for understanding the occurrence of pseudotumor cerebri syndrome in patients with nonhemorrhagic brain AVMs, for the occurrence of local mass effect and brain edema bordering unruptured AVMs, and for the development of hydrocephalus in patients with unruptured AVMs. The theory also contributes to a better appreciation of the pathophysiology of dural arteriovenous fistulas, of vein of Galen aneurismal malformation, and of autoregulation-related disorders in AVM patients. Conclusions: The hydraulic hypothesis provides a comprehensive frame to understand brain AVM hemodynamics and its effect on the CSF dynamics.

Although the flow-through catheter (FTC) system has been useful and satisfactorily accurate for gastrointestinal manometry, we hypothesized that a cylindrical, liquid-filled balloon would also accurately reflect stress imposed by a sphincter. Latex balloons were fitted over the side ports of a closed-end catheter. The responses of the balloon and FTC system were compared in a cylindrical chamber commonly identified as a Starling resistor. Independent, constant-pressure sources were used to control both the inwardly directed "contact pressure" of the Starling resistor (Ps) and the intraluminal fluid pressure (Plum). The balloon transducers responded linearly and accurately (slope = 1) to changes in both Ps and Plum within the test range (0–200 mmHg, 0–26.7 kPa). When either Plum or Ps was held constant and the other changed, the balloon transducers always accurately measured the higher of the two pressures. Although the performance of the FTC system was improved after the Starling resistor was lubricated, the FTC system sometimes responded inaccurately to changes in Ps. The ability of the balloon transducers to measure the contractions of the lower esophageal sphincter and of the esophagus was demonstrated. We conclude that the balloon transducer can measure sphincter pressure accurately and suggest that, in certain circumstances, it might be advantageous relative to the FTC system.Key words: balloon manometry, flow-through catheter system, Starling resistor, lower esophageal sphincter, contact pressure.

To further explore the mechanism of hypoxic pulmonary vasoconstriction, we studied the mean pulmonary arterial pressure (Ppa)/left atrial pressure (Pla) relationship at fixed cardiac index (Q) and the Ppa/Q relationship at several levels of fixed Pla in pentobarbital sodium-anesthetized dogs ventilated alternately in hyperoxia [fraction of inspired O2 (FIO2) 0.4 or 1.0] and in hypoxia (FIO2 0.1). In all experimental conditions, Ppa/Q plots were linear with extrapolated pressure intercepts (Pi) not significantly different from Pla. Hypoxia increased the slope of Ppa/Q plots and did not affect Pi. In hyperoxia, increasing Pla (3 to 26 mmHg) induced approximately equal increases in Ppa at fixed Q and shifted Ppa/Q plots toward higher pressures in a parallel manner. In hypoxia, increasing Pla (4 to 25 mmHg) did not affect Ppa at fixed Q until Pla exceeded 16 mmHg and shifted Ppa/Q plots toward higher pressures with a decrease in slope. Consequently, the hypoxia-induced increases in Ppa at constant Q and constant Pla were attenuated at higher Pla. Thus, in anesthetized dogs, hypoxia increases the slope of Ppa/Q plots without affecting Pi at fixed Pla, and an increase in Pla inhibits hypoxic pulmonary vasoconstriction. These results can be explained without invoking a hypoxia-induced Starling resistor mechanism in the pulmonary circulation.

This study was designed to investigate the effect of stenosis on wall motion and collapse in a latex tube model. Much work has been reported on the collapse of veins and other thin-walled tubes within Starling resistor chambers [1,2]. These papers identify critical controlling factors such as the transmural pressure, upstream and downstream pressure and longitudinal tension. Additionally, they report choking, the waterfall phenomenon, and dynamic behavior such as flutter. None of these articles specifically address the problem of wall excursion and collapse distal to a high grade stenosis. However, Elad et al [3] report on the increased likelihood of transition to supercritical flow with a local area constriction in a model of the pulmonary system which suggests that stenoses may cause collapse. In this article, we report theoretical and experimental physiologic conditions under which arterial wall collapse may occur distal to an atherosclerotic stenosis.

The applicability of the waterfall model was tested using the Starling resistor and different viscosities of fluids to vary the Reynolds number. The waterfall model proved adequate to describe flow in the Starling resistor model only at very low Reynolds numbers (Reynolds number less than 1). Blood flow characterized by such low Reynolds numbers occurs only in the microvasculature. Thus, it is inappropriate to apply the waterfall model indiscriminately to flow through large collapsible veins.

In 1976 Dent (Gastroenterology 71: 263–267) introduced a sleeve-catheter device for obtaining continuous recording of lower esophageal sphincter pressure. The infused sleeve accommodates for axial sphincter movement by providing a large surface of collapsible membrane that is capable of sensing maximal sphincter pressure at any point along the sleeve. Although sleeve performance was tested previously, the precise physical principal of its function has not been delineated. This study tests the hypothesis that the sleeve device functions as a Starling resistor. The term “Starling resistor” is an eponym that designates the physics of fluid flow through collapsible tubes. When pressure at any point along an infused collapsible conduit is greater than the intraluminal pressure at the distal end of the conduit, partial collapse occurs at some axial location along the conduit where the transmural pressure equals zero. The location of zero transmural pressure is termed the “equal pressure point” (EPP). The partial collapse at the EPP causes a local change in luminal resistance that is directly related to the magnitude of the external pressure at the EPP and accompanied by a corresponding change in the pressure upstream from the EPP. A correlate to the performance of Starling resistors is that the pressure upstream to the EPP is not affected by the downstream pressure, so long as the downstream pressure is less than the external pressure. To test our hypothesis, we evaluated sleeve performance in vitro using a two-chambered model that allowed application of static or oscillatory pressures at one or two sites along the sleeve.(ABSTRACT TRUNCATED AT 250 WORDS)

Since 1964, when Fishman and Richards published Circulation of the Blood: Men and Ideas, Guyton's model of the circulation, in which mean circulatory pressure serves as the upstream pressure for venous return, has been extended, and the concept of vascular smooth muscle tone acting like the pressure surrounding a Starling resistor has been postulated. According to this scheme, the positive zero flow intercepts of rapidly determined arterial pressure-flow curves are the effective downstream pressures for arterial flow to different tissues. The arterioles, like Starling resistors, determine the downstream pressures and are followed by abrupt pressure drops, or "waterfalls." Capillary pressures are closely linked to those of the venules into which they flow. Capillary-venular pressures are the upstream pressures for venous return. In exercising muscles, reduced arteriolar tone lowers arteriolar pressure and increases arterial flow. This, in turn, raises capillary-venular pressure and increases venous flow. The arteriolar-capillary waterfall is decreased or eliminated. Total blood flow is increased by diversion of blood from tissues with slow venous drainage to muscles with fast venous drainage (low resistance X compliance). The heart pumps away the increased venous return by shifting to a new ventricular function curve.

The application of the Starling resistor concept of the lungs during continuous positive pressure ventilation (CPPV) was evaluated. Ventilation and hemodynamics were studied in eight anesthetized and paralyzed dogs before and during the use of CPPV. CPPV resulted in an increase in transpulmonary pressure and functional residual capacity (FRC), and a decrease in arterial pH and mixed venous oxygen tension (PvO2). Cardica index decreased 32% (p less than 0.01) and stroke volume 51% (p less than 0.01). Neither right nor left transmural pressures changed but pulmonary vascular resistance increased 189% (p less than 0.01). This study supports the concept that the pulmonary vasculature behaves as a Starling resistor during the use of CPPV. The increase in pulmonary vascular resistance must be considered when transpulmonary pressure is raised by CPPV.

Nasal obstruction has been shown to increase the number of apneas during sleep in normal subjects and in some may actually cause the sleep apnea syndrome. We postulated that the pharynx may act as a Starling resistor, where increases in negative inspiratory pressure result in elevated resistance across a collapsible pharyngeal segment. To test this theory in normal subjects we studied 10 men and 10 women during wakefulness. Pharyngeal resistance (the resistance across the airway segment between the choanae and the epiglottis) was determined in the normal state and with three inspiratory loads added externally. Flow was measured using a pneumotachometer and a sealed face mask; epiglottic pressure by a latex balloon placed just above the epiglottis and choanal pressure by anterior rhinometry. Pharyngeal resistance (measured at 300 ml/s) could thus be determined. Base-line inspiratory pharnygeal resistance was 1.6 +/- 0.2 cmH2O . l-1 . s. This increased to 2.3 +/- 0.3, 2.8 +/- 0.4, and 2.9 +/- 0.4 cmH2O . l-1 . s, respectively, with the addition of 1.3, 2.7, and 6.7 cmH2O . l-1 . s inspiratory load. The resistance at each level of load was significantly different from the base-line resistance determination (P less than 0.05) but not different from each other. We conclude that added nasal resistive loads during inspiration cause an increase in pharyngeal resistance during wakefulness but that this resistance does not increase further with additional increments of load.

Although there is present agreement that intrapleural pressure is not uniform throughout the thoracic cavity there is disagreement both as to the magnitude of this difference and as to its significance. A new method has been employed (flow through a Starling resistor) for measuring pleural and esophageal pressure. There appears to be an area in the cephalad thorax, both in the horizontal and vertical head up position, in which end expiratory esophageal and pleural pressure are more negative than in the remainder of the thoracic cavity. The method employed and the possible significance of the findings are discussed.

One of the major aims of treatment for intracranial hypertension is the prevention of plateau waves. Our investigation of this phenomenon supposes an inherent nonlinear reversible physiological mechanism as the cause of the abrupt onset and resolution of these waves. We hypothesise that under certain conditions, the cerebral bridging veins exhibit a characteristic Starling resistor behavior sufficient to explain the increase in cerebral blood volume and the simultaneous decrease in blood flow associated with the onset of a plateau wave and that a modest reduction of CSF pressure due to CSF absorption causes a reversal of this process.

A hydraulic model of the cerebrovascular bed is presented. The model consists of a Starling resistor in series with an upstream resistance. Volume-pressure tests were performed on the model by injecting fluid into the rigid shell of the Starling resistor. An exponential pressure response to the increase in fluid volume was observed, which supports the hypothesis that the origin of the in vivo exponential pressure response to a transient increase in cerebrospinal fluid (CSF) volume can be attributed to compression of the cerebral vessels, most probably the veins. Mathematical expressions for the dependence of pressure on volume change were derived from the model and applied to in vivo volume-pressure data. The correlation between the model and in vivo experiments suggests that the CSF pressure is coupled to cerebral venous pressure and that the volume-pressure test is an indirect measure of the cerebral venous volume and is not a measure of intracranial elastance. The physical basis for the volume-pressure test is clarified, and expressions are derived to improve the utility of the test.

Mechanical properties and pressure-flow relationships of tracheae excised from very premature lambs were studied in a plethysmograph. Control (Group I) data revealed the tracheae to be extremely compliant, collapsible airways, with an inflation compliance (Si) of 0.033 (+/- 0.004 SE) mmHg-1, collapsing compliance (Sc) of 0.026 (+/- 0.001 SE) mmHg-1, and pressure-flow relationships similar to those of a Starling resistor. Acetylcholine administration (Group II) lowered both Si, 0.026 (+/- 0.003 SE) mmHg-1 and Sc, 0.022 (+/- SE) mmHg-1, as did longitudinal stretch (Group III): Si, 0.021 (+/- .003 SE) mmHg-1, and Sc, 0.017 (+/- 0.002 SE) mmHg-1. Alterations in tracheal collapsibility were also evidenced by significant reductions in resistance to airflow when the tracheae were subjected to compressive forces. Altering both smooth muscle tone (acetylcholine administration) and longitudinal length simultaneously (Group IV) produced results similar to those obtained for Group III. These data help to define the functional characteristics of immature airways and may provide insight for more effective clinical management of the premature infant.

Intracerebral pulse waves were recorded in cat and monkey while intracranial pressure (ICP) manipulations were performed. The intracerebral pulse waves appeared comparable to cerebrospinal fluid (CSF) pulsations. The wave forms were divided into multiple smaller waves, designated P1 to P4. The P1 component was primarily of arterial origin and was accentuated by increasing ICP unrelated to increased venous pressure, most commonly from a mass lesion. Bilateral carotid occlusion resulted in decreased amplitude of P7. Venous hypertension from jugular venous or sagittal sinus occlusion, on the other hand, accentuated waves P2 and P3 more than P7. This is consistent with a Starling resistor model of the cerebral venous system in which mass lesions may compress low-pressure veins and accentuate the arterial pressure-dependent P1 wave, whereas venous hypertension causes increased prominence of the later P2 and P3 waves.

A technique is described for reliably producing quantifiable impairment of microvascular reperfusion of the brain after ischemia in dogs. The technique is derived from an analysis of the cerebrospinal fluid compression ischemia model as a Starling resistor. It is proposed that this model would be useful in systematic study of post-ischemic impairment of reperfusion.

The purpose of this study is to clarify the origin of the intracranial exponential pressure-volume curve observed in vivo. Pressure-flow properties of a Starling resistor in a rigid container were investigated. A Starling resistor is a collapsible tube in which the pressure external to the tube exceeds the outflow pressure. The basis for this study was the work by several investigators (Yada et al. 1973, Nakagawa et al. 1974, Portnoy et al. 1982) who have shown that the cerebral vascular bed acts as a Starling resistor, and Lofgren’s (Lofgren 1973) model of the cerebral vascular bed as a series circuit consisting of an inflow resistor corresponding to resistance vessels and an outflow resistor corresponding to the collapsible veins.