Analysis of blood flow in cat's lung with detailed anatomical and elasticity data

Zhuang, Fengyuan; Fung, Y. C.; Yen, R. T.

doi:10.1152/jappl.1983.55.4.1341

Cited by 101 publications

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“…Models relating hemodynamic function and pulmonary arterial tree structure have often employed Strahler-ordered data to construct symmetrical trees wherein all vessels within an order are assigned the mean diameter of the order (2,5,8,9,14,26,48). To help put Figs.…”

Section: Methodsmentioning

confidence: 99%

Branching exponent heterogeneity and wall shear stress distribution in vascular trees

Karau¹,

Krenz

Dawson

2001

American Journal of Physiology-Heart and Circulatory Physiology

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is the parent vessel diameter and D 2 and D 3 are the two daughter vessel diameters at a bifurcation]. Because wall shear stress is a physiologically transducible force, shear stress-dependent control over vessel diameter would appear to provide a means for preserving this optimal structure through maintenance of uniform shear stress. A mean z of 3 has been considered confirmation of such a control mechanism. The objective of the present study was to evaluate the consequences of a heterogeneous distribution of z values about the mean with regard to this uniform shear stress hypothesis. Simulations were carried out on model structures otherwise conforming to the criteria consistent with uniform shear stress when z ϭ 3 but with varying distributions of z. The result was that when there was significant heterogeneity in z approaching that found in a real arterial tree, the coefficient of variation in shear stress was comparable to the coefficient of variation in z and nearly independent of the mean value of z. A systematic increase in mean shear stress with decreasing vessel diameter was one component of the variation in shear stress even when the mean z ϭ 3. The conclusion is that the influence of shear stress in determining vessel diameters is not, per se, manifested in a mean value of z. In a vascular tree having a heterogeneous distribution in z values, a particular mean value of z (e.g., z ϭ 3) apparently has little bearing on the uniform shear stress hypothesis. mathematical model; pulmonary arterial tree; vascular morphometry; Murray's Law; complexity SHEAR STRESS on the vascular endothelial surface is a physiologically transducible force that influences vascular function in several ways. In the short term, shear stress affects vessel tone, and, in the longer term, it affects the vascular architecture generated during the vasculo-and angiogenesis and vascular remodeling associated with vascular adaptation and disease (3,4,7,20,21,33). Thus there has been considerable interest in the concept that the form of a vascular network reflects shear stress optimization operating during the network construction and maintenance. The complexity of vascular tree structures, in terms of both the branching network and the local contour of the vessel wall (1, 4), contributes to the difficulty in evaluating this concept. One simplification that has been used as a reference point in such evaluations is "Murray's Law," which provides a vascular design criterion for minimizing the power required to operate a distribution network constructed of cylindrical vessels with convective transport via Poiseuille flow (34). According to Murray's Law, power is minimized if flow throughout the network is proportional to the cube of the vessel diameters. This is also a condition that can produce uniform shear stress throughout the network. Thus shear stress control over vessel diameter would appear to be a means of developing and/or maintaining optimal vascular structure (23,28,29,38,45,47). One implication of Murray's Law is that, for a bif...

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Section: Methodsmentioning

confidence: 99%

Branching exponent heterogeneity and wall shear stress distribution in vascular trees

Karau¹,

Krenz

Dawson

2001

American Journal of Physiology-Heart and Circulatory Physiology

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“…intravascular pressure, which apparently contradicts the fact that all pulmonary vessels are very thin-walled and distensible [26]. An alternative approach to explain the shape of the P/Q' curves, originating from the work of ZHUANG et al [27], takes vascular distensibility into account. In this model, the P/Q ' nonlinearity is acknowledged and explained by the decrease in resistance caused by vessel distension with rising flow (and thus also pressure), resulting in a smaller increase in pressure with each subsequent rise in flow.…”

Section: Discussionmentioning

confidence: 99%

Chronic infusion of nitric oxide in experimental pulmonary hypertension: pulmonary pressure-flow analysis

Hampl¹,

Tristani‐Firouzi²,

Nelson³

et al. 1996

European Respiratory Journal

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Inhaled-nitric oxide (NO) is a selective pulmonary vasodilator in shortterm clinical studies. Use of NO inhalation in chronic pulmonary hypertension is complicated by potential problems with ambulatory NO delivery. We hypothesized that long-term infusion of NO solution into the central venous circulation, which did not suffer from this drawback, might reduce chronic pulmonary hypertension.Saturated NO solution was infused in chronically hypoxic rats by implantable minipumps at a rate which was effective in reducing acute hypoxic vasoconstriction in isolated, Krebs' albumin perfused lungs (2.5 µL·h -1 ). Pulmonary haemodynamics and the pressure-flow relationship were studied after 4 weeks of infusion.NO was still present in the minipumps at the end of the infusion period. Despite causing methaemoglobinaemia, NO infusion did not significantly attenuate pulmonary arterial pressure, pulmonary vascular resistance, right ventricular hypertrophy, or the parameters of the pulmonary vascular pressure-flow relationship. Pressure-flow curves, analysed with the nonlinear, distensible vessel model, indicated increased near-zero pressure resistance (Ro) in chronic hypoxia. The tendency of chronic NO infusion to reduce Ro did not reach statistical significance.Long-term infusion of nitric oxide solution is technically feasible but does not effectively reverse chronic pulmonary hypertension. The failure of infused NO to reduce pulmonary hypertension is explained by the fact that the inactivation of NO by haemoglobin is much faster than anticipated. Eur Respir J., 1996Respir J., , 9, 1475 The study was supported by the American Heart Association-Minnesota Affiliate GrantIn-Aid, US Department of Veterans Affairs, Minnesota Medical Foundation, and the National Institutes of Health Grant #1R29-HL45735.Pulmonary hypertension is a leading cause of morbidity and mortality in association with chronic obstructive pulmonary disease (COPD), adult respiratory distress syndrome (ARDS), or congenital heart disease, and as a primary disorder [1]. Nitric oxide (NO) is a potent pulmonary vasodilator [2][3][4]. When inhaled, NO selectively dilates the pulmonary vasculature [3,4]. In situations requiring acute and subacute treatment, such as neonatal pulmonary hypertensive crisis or ARDS, inhaled NO is highly effective in reducing pulmonary hypertension [5][6][7][8]. In these situations, the patient is typically intubated and continuously attended by specially trained medical staff, and the duration of the treatment is relatively short. The usefulness of inhaled NO in chronic diseases, such as COPD, has not been systematically clinically tested, partly due to fears of NO toxicity, and particularly due to technical difficulties related to the ambulatory delivery of inhaled NO gas. Nevertheless, the ability of long-term NO inhalation to reduce chronic hypoxic pulmonary hypertension and related right ventricular hypertrophy has been demonstrated in adult and neonatal rats [9,10].Chronic NO inhalation in humans would require very strict sa...

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“…Each lung vascular compartment is subject to a hydrostatic blood pressure P H = c B h i , depending on its height h i relative to the pulmonary artery, assuming the subject is vertical in the water, and blood density c B is equal to that of water. The pulmonary arteries and veins were set up in a spreadsheet as a segmented-branch model (Zhuang et al 1983;Krishnan et al 1986;Horsfield 1989;Huang et al 1996), and then simplified to single equivalent nonlinear volume-dependent resistors denoted as R 2 and R 3 for each subunit Pulmonary vascular resistance R P is the sum of all subunits calculated in parallel. The alveolar capillaries are adapted from the tapering sheet flow model of Fung Sobin 1969, 1972).…”

Section: Methodsmentioning

confidence: 99%

Computer simulation of human breath-hold diving: cardiovascular adjustments

Fitz‐Clarke

2007

Eur J Appl Physiol

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The world record for a sled-assisted human breath-hold dive has surpassed 200 m. Lung compression during descent draws blood from the peripheral circulation into the thorax causing engorgement of pulmonary vessels that might impose a physiological limitation due to capillary stress failure. A computer model was developed to investigate cardiopulmonary interactions during immersion, apnea, and compression to elucidate hemodynamic responses and estimate vascular stresses in deep human breath-hold diving. The model simulates active and passive cardiovascular adjustments involving blood volumes, flows, and pressures during apnea at diving depths up to 200 m. Redistribution of blood volume from peripheral to central compartments increases with depth. Pulmonary capillary transmural pressures in the model exceed 50 mm Hg at record depth, producing stresses in the range known to cause alveolar capillary damage in animals. Capillary pressures are partially attenuated by blood redistribution to compliant extra-pulmonary vascular compartments. The capillary pressure differential is due mainly to a large drop in alveolar air pressure from outward elastic chest wall recoil. Autonomic diving reflexes are shown to influence systemic blood pressures, but have relatively little effect on pulmonary vascular pressures. Increases in pulmonary capillary stresses are gradual beyond record depth.

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Analysis of blood flow in cat's lung with detailed anatomical and elasticity data

Cited by 101 publications

References 0 publications

Branching exponent heterogeneity and wall shear stress distribution in vascular trees

Branching exponent heterogeneity and wall shear stress distribution in vascular trees

Chronic infusion of nitric oxide in experimental pulmonary hypertension: pulmonary pressure-flow analysis

Computer simulation of human breath-hold diving: cardiovascular adjustments

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