Hydraulic input impedance to aorta and pulmonary artery in dogs

1963 ◽  
Vol 18 (1) ◽  
pp. 134-140 ◽  
Author(s):  
Dali J. Patel ◽  
Flavio M. deFreitas ◽  
Donald L. Fry
Keyword(s):  
Pulmonary Artery ◽  
Physical Properties ◽  
Input Impedance ◽  
Vascular System ◽  
Electrical Networks ◽  
Pressure Flow ◽  
Logical Basis ◽  
Vascular Bed ◽  
Hydraulic Load ◽  
Complex Ratio

Pressure-flow relationships were studied at the root of the aorta and the pulmonary artery in 18 dogs. The hydraulic input impedance to the vascular bed was calculated as a complex ratio of the corresponding pressure and flow harmonics. Results indicate: a) The predominant features of the load against which the heart is pumping consists of an impedance with a magnitude that initially decreases rapidly with frequency and then increases gradually with frequency. In general, pressure tends to lag behind flow for all harmonics. b) The input impedance versus frequency patterns provided a logical basis for choosing various simple electrical networks which can be used to characterize in a compact manner the general features of the hydraulic load presented to the ventricles. c) The hazards of using such simple networks to define the physical properties of the vascular system are pointed out. Submitted on July 5, 1962 Submitted on July 30, 1962

scholarly journals The relation between the pulmonary and bronchial vascular systems

1931 ◽  
Vol 109 (763) ◽  
pp. 319-336 ◽  
Keyword(s):  
Pulmonary Artery ◽  
Vascular System ◽  
Azygos Vein ◽  
Operative Procedures ◽  
Left Auricle ◽  
Bronchial Arteries ◽  
Direct Communication ◽  
Distinctive Features ◽  
Vascular Bed ◽  
Isolated Lung

Berry, Brailsford and Daly (1931) showed that perfusion of the bronchial vascular system may be carried out ( a ) by way of the posterior bronchial arteries, or ( b ) in conjunction with the thoracic parietes and oesophagus, or with the oesophagus alone, by way of the aorta. They designated their preparations, lung-thorax-oesophagus, lung-oesophagus, or isolated lung according to the extent of the systemic vascular bed perfused. They also demonstrated that no extensive arterial or venous communications exist between the bronchial and pulmonary vascular systems, the capillaries and possibly the smallest arterioles and venules serving as the only means of direct communication. In the same paper are given in detail the operative procedures carried out prior to the perfusion experiments, together with radiographs and photomicrographs depicting the extent of the bronchial vascular bed perfused. Briefly, the method consists in simultaneous perfusion with pumps of the pulmonary artery and aorta or bronchial arteries, with collection of the blood from the left auricle and azygos vein. . It is proposed here to describe the distinctive features of the apparatus and the results of the perfusion experiments.

Effect of Ligation of Left Pulmonary Artery at Birth on Maturation of Pulmonary Vascular Bed

Respiration ◽  
1962 ◽  
Vol 19 (5) ◽  
pp. 362-369
Author(s):  
Peter E. Pool ◽  
Keith H. Averill ◽  
John H.K. Vogel
Keyword(s):  
Pulmonary Artery ◽  
Left Pulmonary Artery ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

scholarly journals Effects of acute Rho kinase inhibition on chronic hypoxia-induced changes in proximal and distal pulmonary arterial structure and function

2011 ◽  
Vol 110 (1) ◽  
pp. 188-198 ◽  
Author(s):  
Rebecca R. Vanderpool ◽  
Ah Ram Kim ◽  
Robert Molthen ◽  
Naomi C. Chesler
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Arteries ◽  
Rho Kinase ◽  
Pressure Flow ◽  
Kinase Inhibition ◽  
Pulmonary Vasoconstriction ◽  
Pulsatile Pressure ◽  
Arterial Structure ◽  
Pulmonary Arterial ◽  
Induced Changes

Hypoxic pulmonary hypertension (HPH) is initially a disease of the small pulmonary arteries. Its severity is usually quantified by pulmonary vascular resistance (PVR). Acute Rho kinase inhibition has been found to reduce PVR toward control values in animal models, suggesting that persistent pulmonary vasoconstriction is the dominant mechanism for increased PVR. However, HPH may also cause proximal arterial changes, which are relevant to right ventricular (RV) afterload. RV afterload can be quantified by pulmonary vascular impedance, which is obtained via spectral analysis of pulsatile pressure-flow relationships. To determine the effects of HPH independent of persistent pulmonary vasoconstriction in proximal and distal arteries, we quantified pulsatile pressure-flow relationships before and after acute Rho kinase inhibition and measured pulmonary arterial structure with microcomputed tomography. In control lungs, Rho kinase inhibition decreased 0 Hz impedance (Z0), which is equivalent to PVR, from 2.1 ± 0.4 to 1.5 ± 0.2 mmHg·min·ml−1 ( P < 0.05) and tended to increase characteristic impedance (ZC) from 0.21 ± 0.01 to 0.22 ± 0.01 mmHg·min·ml−1. In HPH lungs, Rho kinase inhibition decreased Z0 ( P < 0.05) without affecting ZC. Microcomputed tomography measurements performed on lungs after acute Rho kinase inhibition demonstrated that HPH significantly decreased the unstressed diameter of the main pulmonary artery (760 ± 60 vs. 650 ± 80 μm; P < 0.05), decreased right pulmonary artery compliance, and reduced the frequency of arteries of diameter 50–100 μm (both P < 0.05). These results demonstrate that acute Rho kinase inhibition reverses many but not all HPH-induced changes in distal pulmonary arteries but does not affect HPH-induced changes in the conduit arteries that impact RV afterload.

The pulmonary vascular bed in patients with functionally univentricular physiology and a Fontan circulation

2021 ◽  
pp. 1-10
Author(s):  
Ahmed Krimly ◽  
C. Charles Jain ◽  
Alexander Egbe ◽  
Ahmed Alzahrani ◽  
Khalid Al Najashi ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Venous Hypertension ◽  
Adult Survival ◽  
Vascular Reserve ◽  
Passive Flow ◽  
Vascular Bed ◽  
Systemic Ventricle ◽  
Pharmacologic Regulation ◽  
Fontan Palliation ◽  
Pulmonary Vascular Bed

Abstract Fontan palliation represents one of the most remarkable surgical advances in the management of individuals born with functionally univentricular physiology. The operation secures adult survival for all but a few with unfavourable anatomy and/or physiology. Inherent to the physiology is passive transpulmonary blood flow, which produces a vulnerability to adequate filling of the systemic ventricle at rest and during exertion. Similarly, the upstream effects of passive flow in the lungs are venous congestion and venous hypertension, especially marked during physical activity. The pulmonary vascular bed has emerged as a defining character on the stage of Fontan circulatory behaviour and clinical outcomes. Its pharmacologic regulation and anatomic rehabilitation therefore seem important strategic therapeutic targets. This review seeks to delineate the important aspects of pulmonary artery development and maturation in functionally univentricular physiology patients, pulmonary artery biology, pulmonary vascular reserve with exercise, and pulmonary artery morphologic and pharmacologic rehabilitation.

P4685Validation of noninvasive pulmonary artery pressure/flow relationship: echocardiography vs right heart catheterization

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Caravita ◽  
P Yerly ◽  
C Baratto ◽  
C Dewachter ◽  
A Rimouche ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Doppler Echocardiography ◽  
Pulmonary Circulation ◽  
Right Heart Catheterization ◽  
Peak Exercise ◽  
Heart Catheterization ◽  
Right Heart ◽  
Pressure Flow ◽  
Relationship Of

Abstract Background Invasive pressure-flow (P/Q) relationship of the pulmonary circulation can detect the presence of pulmonary hypertension (PH) during exercise and provide information on patients' symptoms and assess disease severity. Doppler-echocardiography was reported to provide accurate but imprecise noninvasive estimates of both resting and exercise pulmonary haemodynamics. However, data on the direct comparison of invasive vs noninvasive approaches to build pressure-flow relationship are scarce. Purpose To compare echocardiographic estimates with invasive measurements of P/Q relationship of the pulmonary circulation during exercise. Methods Patients undergoing a clinically indicated right heart catheterization and echocardiography were studied at rest and during exercise. The ratio between mean pulmonary artery pressure and cardiac output at peak exercise (TPR), as well as P/Q slope throughout exercise were calculated. Both TPR and P/Q slope are abnormal when ≥3 mmHg/L/min. Echocardiographic estimates were compared with invasive measurements. Results Sixty patients were included (mean age 65±14 years, 73% female). PH was present at rest in 38 cases (63%), of precapillary origin in 23 (61%). Heart failure with preserved ejection fraction was diagnosed in 23 patients, of which 17 had no PH at rest. TPR at peak exercise and P/Q slope were abnormal (≥3 mmHg/L/min) in the majority of patients (56 and 45 subjects, respectively). Echocardiographic estimates of P/Q slope and TPR correlated significantly although weakly with invasive measurements (R2=0.38 and 0.56, respectively, p<0.001). Bias of echocardiography for P/Q slope and TPR was 1.1±4.2 and 0.4±2.9 mmHg/L/min, respectively (figure). Sensitivity of echocardiography to detect an abnormal TPR or P/Q slope (i.e. ≥3 mmHg/L/min) was 100 and 98%, respectively, faced by low specificity (0 and 33%, respectively). Figure 1 Conclusions Doppler-echocardiography can provide rather accurate and sensitive but imprecise estimates of pressure-flow relationships of the pulmonary circulation during exercise. This intrinsic imprecision may limit its use in clinical practice.

Effect of tetanic myocardial contraction on coronary pressure-flow relationships

1993 ◽  
Vol 265 (4) ◽  
pp. H1215-H1226 ◽  
Author(s):  
J. Z. Livingston ◽  
J. R. Resar ◽  
F. C. Yin
Keyword(s):  
Coronary Flow ◽  
Pressure Range ◽  
Interventricular Septum ◽  
Myocardial Contraction ◽  
Cardiac Contraction ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
Vascular Bed ◽  
Butanedione Monoxime ◽  
Intact Heart

Cardiac contraction causes a decrease in coronary flow. Despite many studies, it is still not clear what mechanism or mechanisms are responsible for this flow decrease. The phasic nature of myocardial contraction and the complexities intrinsic to intact heart preparations make it difficult to elucidate the mechanisms. We therefore studied coronary pressure-flow relationships during steady-state (tetanic) contractions in the maximally vasodilated isolated canine interventricular septum to see whether waterfall-type behavior is present. Using ryanodine and electrical stimulation allowed the production of reproducible and reversible tetani. This preparation minimizes the difficulties associated with transmural variations and also the effects of intramyocardial capacitance. Two separate protocols were performed to delineate the pressure-flow relationships in the passive and tetanized states. The first compared diastolic and tetanized pressure-flow relationships. In the second protocol, 2,3-butanedione monoxime was added to obtain an intermediate contractile level, thus allowing the comparison of two contractile states. Both the diastolic and tetanized pressure-flow relationships were curvilinear in the low-pressure range. Linear and nonlinear fits to the data showed that the primary effect of contraction was a shift of the pressure-flow relationships to higher pressures at a given flow. This effect was graded by the level of contractility and was independent of developed stress. Although other mechanisms may also be operative, these results support the presence of waterfall behavior in the coronary vascular bed.

A hemodynamic model representation of the dog lung

1991 ◽  
Vol 70 (1) ◽  
pp. 15-26 ◽  
Author(s):  
S. T. Haworth ◽  
J. H. Linehan ◽  
T. A. Bronikowski ◽  
C. A. Dawson
Keyword(s):  
Steady State ◽  
Dynamic Modeling ◽  
Power Law ◽  
Transmural Pressure ◽  
Morphometric Data ◽  
Pressure Flow ◽  
Average Ratio ◽  
Vascular Bed ◽  
Hemodynamic Model ◽  
Arteries And Veins

The published morphometric data from human, cat, and dog lungs suggest that the power-law relationships between the numbers (Na and Nv) and diameters (Da and Dv) of arteries and veins and between the lengths (La and Lv) and diameters of the arteries and veins could be used as scaling rules for assigning dimensions and numbers to the intrapulmonary vessels of the arterial and venous trees of the dog lung. These rules, along with the dimensions of the extrapulmonary arteries and capillary sheet and the distensibility coefficients of the vessels obtained from the literature, were used to construct a steady-state hemodynamic model of the dog lung vascular bed. The model can be characterized approximately by 15 orders of arteries with Na approximately 2.07 Da-2.58 and 13 orders of veins with Nv approximately 2.53 Dv-2.61. For the intrapulmonary vessels (orders 1–12), La approximately 4.85 Da1.01, and Lv approximately 6.02 Da1.07. The average ratio of the numbers of vessels in consecutive orders is approximately 3.2 for the arteries and veins. These arterial and venous trees are connected by the capillary sheet with an undistended thickness of approximately 3.5 microns and an area of 33 m2. The average distensibility (% increase in diameter over the undistended diameter/Torr increase in transmural pressure) for the model arteries and veins is approximately 2.4%/Torr, and the distensibility of the capillary sheet (% increase in thickness over the undistended thickness/Torr increase in transmural pressure) is approximately 3.6%/Torr. The calculated arterial-capillary-venous volumes and compliances of the model agree well with experimental estimates of these variables in dogs. In addition, the model appears consistent with certain aspects of the pressure-flow relationships measured in dog lungs. The model appears to be a useful summary of some of the available data on pulmonary morphometry and vessel properties. It is anticipated that the model will provide the basis for dynamic modeling of the dog lung in the future.

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