Distensible behavior of pulmonary artery

Frasher, Wallace G.; Sobin, Sidney S.

doi:10.1152/ajplegacy.1960.199.3.472

Cited by 5 publications

(5 citation statements)

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“…Studies of the pulmonary circulation in the 1960s began to measure proximal PVS (or its inverse, pulmonary vascular compliance) in animal models and in humans with PH. 15–21 These studies clearly demonstrated that the PA significantly stiffens in disease and that these increases in stiffness were associated with increased right ventricular afterload. 20,21 Clinically, PVS was measured as a component of impedance, using a pressure transducer and electromagnetic velocity sensor or using intravascular ultrasound during catheterization.…”

Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 79%

“…7 Historically, global in vivo stiffness of the pulmonary vascular bed was estimated with the total volumetric compliance (ΔV/ΔP), where V is the total pulmonary vascular volume and P is the pressure, in both animals and humans. [15][16][17][18][19]21 Later, input impedance modulus, a characterization of distal load at a specific location, was used as an indicator of PVS and quantified both the static and the dynamic components of right ventricle (RV) afterload. Many groups recognized the importance of this totalafterload measurement that included the impacts of PVR and PVS.…”

Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 99%

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Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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Recent studies have indicated that systemic arterial stiffening is a precursor to hypertension and that hypertension, in turn, can perpetuate arterial stiffening. Pulmonary artery (PA) stiffening is also well documented to occur in pulmonary hypertension (PH), and there is evidence that pulmonary vascular stiffness (PVS) may be a better predictor of outcome than pulmonary vascular resistance (PVR). We have hypothesized that the decreased flow-damping function of elastic PAs in PH likely initiates and/or perpetuates dysfunction of pulmonary microvasculature. Recent studies have shown that large-vessel stiffening increases flow pulsatility in the distal pulmonary vasculature, leading to endothelial dysfunction within a proinflammatory, vasoconstricting, and profibrogenic environment. The intricate role of stiffening-stimulated high pulsatile flow in endothelial cell dysfunction includes stepwise molecular events underlying PA hypertrophy, inflammation, endothelial-mesenchymal transition, and fibrosis. In addition to contributing to microenvironmental alterations of the distal vasculature, disordered proximal-distal PA coupling likely also plays a role in increasing ventricular afterload, ultimately causing right ventricle (RV) dysfunction and death. Current therapeutic treatments do not provide a realistic approach to destiffening arteries and, thus, to potentially abrogating the effects of high pulsatile flow on the distal pulmonary vasculature or the increased work imposed by stiffening on the RV. Scrutinizing the effect of PA stiffening on high pulsatile flow-induced cellular and molecular changes, and vice versa, might lead to important new therapeutic options that abrogate PA remodeling and PH development. With a clear understanding that PA stiffening may contribute to the progression of PH to an irreversible state by contributing to chronic microvascular damage in lungs, future studies should be aimed first at defining the underlying mechanisms leading to PA stiffening and then at improved treatment approaches based on these findings.Keywords: pulmonary hypertension, arterial stiffening, wave reflection, smooth muscle cell, endothelial cell, inflammation, right ventricle, treatment. Arterial stiffening is increasingly recognized as a risk factor of cardiovascular events as well as a guide for pharmacological treatment of cardiovascular diseases. Yet its exact role in the development and progression of cardiovascular diseases such as hypertension remains elusive. A recent study, however, presented convincing data supporting the possibility of a cause-effect relationship between arterial stiffness and systemic hypertension: higher levels of arterial stiffness and central pressures preceded and were associated with an increased risk of hypertension, but hypertension did not cause arterial stiffness. 1This work demonstrated that increased vascular stiffness could be a precursor to hypertension. A key implication from these observations is that arterial stiffness, when used as a measure of cardiovascula...

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Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 79%

Section: Measurement Of Pvs In Ph: Historical Perspectivementioning

confidence: 99%

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

et al. 2014

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“…In particular, the effect of hypoxia should be investigated. In all the experiments named in the foregoing [3][4][5][6][7], including this one, excised lungs were used which had no blood flow and hence were hypoxic. Since the effect of hypoxia is a complex one, of which the vessel compliance is only one aspect, a thorough study would require careful in vivo experiments and mathematical analysis.…”

Section: (C) Nonlinearity Of the Pressure-diameter Relationshipmentioning

confidence: 99%

“…Patel, et al [3] have determined the distensibility of major pulmonary artery of the dog by direct measurement of vessel diameter using an electrical recording caliper; Frasher and Sobin [4] have measured the pulmonary artery diameter of the dog as a function of the pressure using silicone polymer casts obtained under different pressures. The elasticity of pulmonary vessels in the size range of 1-4 mm was studied by Caro and Saffman [5] using X-ray techniques on the rabbit lung.…”

Section: Introductionmentioning

confidence: 99%

Elasticity of Small Pulmonary Arteries in the Cat

Yen

Fung

Bingham

1980

Journal of Biomechanical Engineering

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When synthesizing the available data of vessel elasticity of mammalian lung from the literature, the lack of data in the intermediate range of vessel sizes becomes evident. In an effort to fill this gap, the distensibility of pulmonary arteries of cats, in the range of 100 -1600 \t.m diameter was studied as a function of the perfusion pressure. The resulting percentage changes in vessel diameter (D) were expressed as polynomials of "transmural"pressure, which is taken to be the difference between the perfusion pressure and the pleural pressure, p a -p PL , in the formwhere D 0 is the value of D when p a = p PL , and a. and /3 are constants. Our results show that for vessels whose diameters D 0 are in the range of 100-200 /xm, the mean values of D/D 0 are represented by a = 2.02 percent per cm H 2 0 or 0.202 (KPa) -', |8 = 0.046 percent per (cm H 2 0) 2 or 0.046 (KPa) ~2. For vessels with diameter D 0 greater than 200 pm, the pressure-diameter relationship is linear in the ranges tested, so that (3 = 0. The values of the compliance constant a (slopes of the curves) for vessels in the diameter (D 0

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“…Early investigations quantified the global in vivo stiffness of the pulmonary vascular tree with the total volumetric compliance ( DV / DP , where V is total pulmonary tree volume and P is pressure) in both animal models (42, 52, 133) and in man (121, 134). …”

Section: Measurement Of Pulmonary Vascular Stiffnessmentioning

confidence: 99%

Pulmonary Vascular Stiffness: Measurement, Modeling, and Implications in Normal and Hypertensive Pulmonary Circulations

Hunter

Lammers

Shandas

2011

Comprehensive Physiology

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This article introduces the concept of pulmonary vascular stiffness, discusses its increasingly recognized importance as a diagnostic marker in the evaluation of pulmonary vascular disease, and describes methods to measure and model it clinically, experimentally, and computationally. It begins with a description of systems-level methods to evaluate pulmonary vascular compliance and recent clinical efforts in applying such techniques to better predict patient outcomes in pulmonary arterial hypertension. It then progresses from the systems-level to the local level, discusses proposed methods by which upstream pulmonary vessels increase in stiffness, introduces concepts around vascular mechanics, and concludes by describing recent work incorporating advanced numerical methods to more thoroughly evaluate changes in local mechanical properties of pulmonary arteries.

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Distensible behavior of pulmonary artery

Cited by 5 publications

References 0 publications

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Vascular Stiffening in Pulmonary Hypertension: Cause or Consequence? (2013 Grover Conference Series)

Elasticity of Small Pulmonary Arteries in the Cat

Pulmonary Vascular Stiffness: Measurement, Modeling, and Implications in Normal and Hypertensive Pulmonary Circulations

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