MR imaging of the central pulmonary arterial tree in conotruncal malformation

Model arterial trees were constructed following rules consistent with morphometric data, Nj = (Dj/Da)-beta 1 and Lj = La(Dj/Da)beta 2, where Nj, Dj, and Lj are number, diameter, and length, respectively, of vessels in the jth level; Da and La are diameter and length, respectively, of the inlet artery, and -beta 1 and beta 2 are power law slopes relating vessel number and length, respectively, to vessel diameter. Simulated heterogeneous trees approximating these rules were constructed by assigning vessel diameters Dm = Da[2/(m + 1)]1/beta 1, such that m-1 vessels were larger than Dm (vessel length proportional to diameter). Vessels were connected, forming random bifurcating trees. Longitudinal intravascular pressure [P(Qcum)] with respect to cumulative vascular volume [Qcum] was computed for Poiseuille flow. Strahler-ordered tree morphometry yielded estimates of La, Da, beta 1, beta 2, and mean number ratio (B); B is defined by Nk + 1 = Bk, where k is total number of Strahler orders minus Strahler order number. The parameters were used in P(Qcum) = Pa [formula: see text] and the resulting P(Qcum) relationship was compared with that of the simulated tree, where Pa is total arterial pressure drop, Q is flow rate, Ra = (128 microLa)/(pi D4a (where mu is blood viscosity), and Qa (volume of inlet artery) = 1/4D2a pi La. Results indicate that the equation, originally developed for homogeneous trees (J. Appl. Physiol. 72: 2225–2237, 1992), provides a good approximation to the heterogeneous tree P(Qcum).

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Structure-function relationships in the pulmonary arterial tree

Journal of Applied Physiology ◽

10.1152/jappl.1999.86.2.569 ◽

1999 ◽

Vol 86 (2) ◽

pp. 569-583 ◽

Cited By ~ 52

Author(s):

Christopher A. Dawson ◽

Gary S. Krenz ◽

Kelly L. Karau ◽

Steven T. Haworth ◽

Christopher C. Hanger ◽

...

Keyword(s):

Vascular Diseases ◽

Pressure Profile ◽

Vessel Diameter ◽

Morphometric Parameters ◽

Morphometric Data ◽

Arterial Tree ◽

Pulmonary Hemodynamics ◽

Pressure Flow ◽

Pulmonary Arterial ◽

And Function

Knowledge of the relationship between structure and function of the normal pulmonary arterial tree is necessary for understanding normal pulmonary hemodynamics and the functional consequences of the vascular remodeling that accompanies pulmonary vascular diseases. In an effort to provide a means for relating the measurable vascular geometry and vessel mechanics data to the mean pressure-flow relationship and longitudinal pressure profile, we present a mathematical model of the pulmonary arterial tree. The model is based on the observation that the normal pulmonary arterial tree is a bifurcating tree in which the parent-to-daughter diameter ratios at a bifurcation and vessel distensibility are independent of vessel diameter, and although the actual arterial tree is quite heterogeneous, the diameter of each route, through which the blood flows, tapers from the arterial inlet to essentially the same terminal arteriolar diameter. In the model the average route is represented as a tapered tube through which the blood flow decreases with distance from the inlet because of the diversion of flow at the many bifurcations along the route. The taper and flow diversion are expressed in terms of morphometric parameters obtained using various methods for summarizing morphometric data. To help put the model parameter values in perspective, we applied one such method to morphometric data obtained from perfused dog lungs. Model simulations demonstrate the sensitivity of model pressure-flow relationships to variations in the morphometric parameters. Comparisons of simulations with experimental data also raise questions as to the “hemodynamically” appropriate ways to summarize morphometric data.

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Regional and Global Biventricular Function in Pulmonary Arterial Hypertension: A Cardiac MR Imaging Study

Radiology ◽

10.1148/radiol.12111599 ◽

2013 ◽

Vol 266 (1) ◽

pp. 114-122 ◽

Cited By ~ 47

Author(s):

Monda L. Shehata ◽

Ahmed A. Harouni ◽

Jan Skrok ◽

Tamer A. Basha ◽

Danielle Boyce ◽

...

Keyword(s):

Pulmonary Arterial Hypertension ◽

Mr Imaging ◽

Arterial Hypertension ◽

Imaging Study ◽

Cardiac Mr ◽

Biventricular Function ◽

Pulmonary Arterial

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176 METHOD FOR LONG-TERM CULTURE OF THE PULMONARY ARTERIAL TREE DISSECTED FROM CHICK EMBRYOS.

Journal of Investigative Medicine ◽

10.1136/jim-52-suppl1-176 ◽

2004 ◽

Vol 52 (Suppl 1) ◽

pp. S109.6-S110

Author(s):

N. Gundersen ◽

J. Sweeley ◽

M. Williams ◽

M. J. Dahl ◽

G. C. Schoenwolf ◽

...

Keyword(s):

Chick Embryos ◽

Arterial Tree ◽

Long Term Culture ◽

Pulmonary Arterial

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Ca(2+)-activated Cl- currents in pulmonary arterial myocytes

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.270.5.h1577 ◽

1996 ◽

Vol 270 (5) ◽

pp. H1577-H1584 ◽

Cited By ~ 10

Author(s):

L. H. Clapp ◽

J. L. Turner ◽

R. Z. Kozlowski

Keyword(s):

Pulmonary Artery ◽

Flash Photolysis ◽

Main Pulmonary Artery ◽

Free Calcium ◽

Patch Clamp Technique ◽

Arterial Tree ◽

Small Vessels ◽

Electrophysiological Recordings ◽

Pulmonary Arterial ◽

Response Current

Currents from smooth muscle cells isolated from the pulmonary arterial tree of the rat were recorded under voltage clamp using the whole cell configuration of the patch-clamp technique. Rapid increases in cytosolic free calcium evoked by flash photolysis of Nitr-5 activated a current that, following ion substitution and pharmacological experiments, proved to be carried by Cl-. This current [ICl(Ca)] was evoked independently of photolytic by-products and, although smaller, was still activated in the absence of pipette ATP. Experiments revealed that ICl(Ca) was evoked in 80% in the cells isolated from the main pulmonary artery but only in 43% of the cells isolated from small vessels (200-400 microns ID). Application of caffeine also resulted in activation of ICl(ca), although the response current magnitude was larger in the main pulmonary artery. Photolysis of Nitr-5 still activated ICl(ca) in the presence of caffeine, suggesting that Ca2-release is not a prerequisite for activation of ICl(ca). These results represents in the first electrophysiological recordings of Cl- currents from small pulmonary arterial vessels and indicate that their Ca2+ regulation and/or distribution may be different throughout the pulmonary circulation.

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Transit time dispersion in the pulmonary arterial tree

Journal of Applied Physiology ◽

10.1152/jappl.1998.85.2.565 ◽

1998 ◽

Vol 85 (2) ◽

pp. 565-574 ◽

Cited By ~ 27

Author(s):

Anne V. Clough ◽

Steven T. Haworth ◽

Christopher C. Hanger ◽

Jerri Wang ◽

David L. Roerig ◽

...

Keyword(s):

Transit Time ◽

Mean Transit Time ◽

Arterial Tree ◽

Lung Lobe ◽

Transit Times ◽

Pulmonary Capillary ◽

Time Dispersion ◽

Pulmonary Arterial ◽

The Difference ◽

In Transit

Knowledge of the contributions of arterial and venous transit time dispersion to the pulmonary vascular transit time distribution is important for understanding lung function and for interpreting various kinds of data containing information about pulmonary function. Thus, to determine the dispersion of blood transit times occurring within the pulmonary arterial and venous trees, images of a bolus of contrast medium passing through the vasculature of pump-perfused dog lung lobes were acquired by using an X-ray microfocal angiography system. Time-absorbance curves from the lobar artery and vein and from selected locations within the intrapulmonary arterial tree were measured from the images. Overall dispersion within the lung lobe was determined from the difference in the first and second moments (mean transit time and variance, respectively) of the inlet arterial and outlet venous time-absorbance curves. Moments at selected locations within the arterial tree were also calculated and compared with those of the lobar artery curve. Transit times for the arterial pathways upstream from the smallest measured arteries (200-μm diameter) were less than ∼20% of the total lung lobe mean transit time. Transit time variance among these arterial pathways (interpathway dispersion) was less than ∼5% of the total variance imparted on the bolus as it passed through the lung lobe. On average, the dispersion that occurred along a given pathway (intrapathway dispersion) was negligible. Similar results were obtained for the venous tree. Taken together, the results suggest that most of the variation in transit time in the intrapulmonary vasculature occurs within the pulmonary capillary bed rather than in conducting arteries or veins.

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A fractal continuum model of the pulmonary arterial tree

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.6.2225 ◽

1992 ◽

Vol 72 (6) ◽

pp. 2225-2237 ◽

Cited By ~ 49

Author(s):

G. S. Krenz ◽

J. H. Linehan ◽

C. A. Dawson

Keyword(s):

Fractal Structure ◽

Cumulative Distribution ◽

Total Resistance ◽

Arterial Tree ◽

Vascular Volume ◽

Capillary Bed ◽

Pulmonary Arterial ◽

Self Similar ◽

The Mean ◽

Level Order

The extant morphometric data from the intrapulmonary arteries of dog, human, and cat lungs produce graphs of the log of the vessel number, (N) or length (l) in each level vs. the log of the mean diameter (D) in each level that are sufficiently linear to suggest that a scale-independent self-similar or fractal structure may underlie the observed relationships. These data can be correlated by the following formulas: Nj = a1Dj-beta 1, and lj = a2Dj beta 2, where j denotes the level (order or generation) number measured from the largest vessel at the entrance to the arterial tree to the smallest vessel at the entrance to the capillary bed. With the hemodynamic resistance (R) represented by Rj = 128 microliterj/(Nj pi Dj4) and the vascular volume (Q) by Qj = Nj pi Dj2lj/4, the continuous cumulative distribution of vascular resistance (Rcum) vs. cumulative vascular volume (Qcum) (where Rcum and Qcum represent the total resistance or volume, respectively, upstream from the jth level) can be calculated from [formula: see text] where r = Dj/Dj+1 is a constant independent of j. Analogous equations are developed for the inertance and compliance distributions, providing simple formulas to represent the hemodynamic consequences of the pulmonary arterial tree structure.

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