scholarly journals 952Mean pulmonary arterial pressure estimated from vortical blood flow in the main pulmonary artery: Definition of cut-off criteria for the diagnosis of pulmonary hypertension

2013 ◽  
Vol 14 (suppl_1) ◽  
pp. i17-i17
Author(s):  
G Reiter ◽  
U Reiter ◽  
G Kovacs ◽  
H Olschewski ◽  
M Fuchsjäger
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Main Pulmonary Artery ◽  
Pulmonary Arterial ◽  
Definition Of

scholarly journals Transcatheter radiofrequency pulmonary artery denervation in swine: the evaluation of lesion degree, hemodynamics and pulmonary hypertension inducibility

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Natalia S. Goncharova ◽  
Heber Ivan Condori Leandro ◽  
Aleksandr D. Vakhrushev ◽  
Elena G. Koshevaya ◽  
Yury A. Skorik ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Controlled Study ◽  
Group Iii ◽  
Group I ◽  
Before And After ◽  
Pulmonary Arterial ◽  
The Mean

Abstract Background Mechanisms of positive effects of pulmonary artery (PA) denervation (PADN) remain poorly understood. The study aimed to evaluate pulmonary hemodynamic changes after PADN and their association with the extent of PA wall damage in an acute thromboxane A2 (TXA2)-induced pulmonary hypertension (PH) model in swine. Methods In this experimental sham-controlled study, 17 normotensive male white Landrace pigs (the mean weight 36.2 ± 4.5 kg) were included and randomly assigned to group I (n = 9)—PH modeling before and after PADN, group II (n = 4)—PADN only, or group III (n = 4)—PH modeling before and after a sham procedure. Radiofrequency (RF) PADN was performed in the PA trunk and at the proximal parts of the right and left PAs. PA wall lesions were characterized at the autopsy study using histological and the immunohistochemical examination. Results In groups I and II, no statistically significant changes in the mean pulmonary arterial pressure nor systemic blood pressure were found after PADN (−0.8 ± 3.4 vs 4.3 ± 8.6 mmHg, P = 0.47; and 6.0 ± 15.9 vs -8.3 ± 7.5 mmHg, P = 0.1; correspondingly). There was a trend towards a lower diastolic pulmonary arterial pressure after PADN in group I when compared with group III during repeat PH induction (34.4 ± 2.9 vs 38.0 ± 0.8; P = 0.06). Despite the presence of severe PA wall damage at the RF application sites, S100 expression was preserved in the majority of PA specimens. The presence of high-grade PA lesions was associated with HR acceleration after PADN (ρ = 0.68, p = 0.03). No significant correlation was found between the grade of PA lesion severity and PA pressure after PADN with or without PH induction. Conclusions Extended PADN does not affect PH induction using TXA2. Significant PA adventitia damage is associated with HR acceleration after PADN. Possible delayed effects of PADN on perivascular nerves and pulmonary hemodynamics require further research in chronic experiments.

Cold-induced pulmonary hypertension in cattle

1978 ◽  
Vol 45 (3) ◽  
pp. 469-473 ◽  
Author(s):  
D. H. Will ◽  
I. F. McMurtry ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Blood Flow ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Right Heart Failure ◽  
Early Spring ◽  
Oxygen Breathing ◽  
Pulmonary Arterial ◽  
Lung Vessels

The frequency with which cattle develop right-heart failure during the winter at high altitude suggested that cold might contribute to hypoxic pulmonary hypertension. Indeed in a preliminary study conducted out-of-doors during early Spring, two calves with known hyperreactive pulmonary vessels showed elevated pulmonary arterial pressures attributed to their prior exposure to nighttime cold (-5 degrees C). In a second study five hyperreactive calves had increases in mean pulmonary arterial pressure from 29 to 45 Torr (+ 55%) during 48 h of exposure to cold (0 to -5 degrees C) in a climatic chamber. Three calves with less reactive lung vessels increased their pressures from 25 to 36 Torr (+ 44%). In a more complete study, six calves selected as potential hyperresponders showed increases in pulmonary arterial pressure (+ 60%), blood flow (+ 18%), and vascular resistance (+ 38%) during 48 h of cold exposure. Arterial PO2 decreased (-10 Torr) and PCO2 rose (+6 Torr) suggesting hypoventilation. Oxygen breathing returned pulmonary pressures and resistance to near control values, suggesting that cold had induced a hypoxic pulmonary vasoconstriction and an increased blood flow. Thus, a cold produced pulmonary hypertension in cattle at the modest altitude of 1,524 m and the pressor responses were greater in calves with more reactive lung vessels.

scholarly journals A multiscale model of vascular function in chronic thromboembolic pulmonary hypertension

2021 ◽  
Author(s):  
Mitchel J. Colebank ◽  
M. Umar Qureshi ◽  
Sudarshan Rajagopal ◽  
Richard A Krasuski ◽  
Mette S. Olufsen
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Main Pulmonary Artery ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Large Artery ◽  
Wave Reflections ◽  
Thromboembolic Pulmonary Hypertension ◽  
Optimal Target ◽  
Pulmonary Arterial

Chronic thromboembolic pulmonary hypertension (CTEPH) is caused by recurrent or unresolved pulmonary thromboemboli, leading to perfusion defects and increased arterial wave reflections. CTEPH treatment aims to reduce pulmonary arterial pressure and reestablish adequate lung perfusion, yet patients with distal lesions are inoperable by standard surgical intervention. Instead, these patients undergo balloon pulmonary angioplasty (BPA), a multi-session, minimally invasive surgery that disrupts the thromboembolic material within the vessel lumen using a catheter balloon. However, there still lacks an integrative, holistic tool for identifying optimal target lesions for treatment. To address this insufficiency, we simulate CTEPH hemodynamics and BPA therapy using a multiscale fluid dynamics model. The large pulmonary arterial geometry is derived from a computed tomography (CT) image, whereas a fractal tree represents the small vessels. We model ring- and web-like lesions, common in CTEPH, and simulate normotensive conditions and four CTEPH disease scenarios; the latter includes both large artery lesions and vascular remodeling. BPA therapy is simulated by simultaneously reducing lesion severity in three locations. Our predictions mimic severe CTEPH, manifested by an increase in mean proximal pulmonary arterial pressure above 20 mmHg and prominent wave reflections. Both flow and pressure decrease in vessels distal to the lesions and increase in unobstructed vascular regions. We use the main pulmonary artery (MPA) pressure, a wave reflection index, and a measure of flow heterogeneity to select optimal target lesions for BPA. In summary, this study provides a multiscale, image-to-hemodynamics pipeline for BPA therapy planning for inoperable CTEPH patients.

Enhanced endothelin-1 and endothelin receptor gene expression in chronic hypoxia

1994 ◽  
Vol 77 (3) ◽  
pp. 1451-1459 ◽  
Author(s):  
H. Li ◽  
S. J. Chen ◽  
Y. F. Chen ◽  
Q. C. Meng ◽  
J. Durand ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Chronic Hypoxia ◽  
Pulmonary Arterial Pressure ◽  
Mrna Levels ◽  
Hypoxic Pulmonary Hypertension ◽  
Receptor Mrna ◽  
Etb Receptor ◽  
Pulmonary Arterial

To test the hypothesis that endothelin (ET)-1 synthesis and ET receptor levels are increased selectively in the lung of rats with chronic hypoxic pulmonary hypertension, the current study examined the effects of exposure to chronic hypoxia (10% O2, 1 atm, 4 wk) on pulmonary arterial pressure, ET-1 levels in plasma and lung, and ET-1 and ETA and ETB receptor mRNA levels in lung, heart, pulmonary artery, aorta, kidney, spleen, and liver. Hypoxic exposure was associated with increases in pulmonary arterial pressure, plasma ET-1 levels, ET-1 mRNA in lung and pulmonary artery, and ET-1 stores and ETA and ETB receptor mRNA levels in lung. In thoracic aorta and the four heart chambers, ETA and ETB receptor mRNA levels were increased, but ET-1 mRNA levels were unchanged from air control levels. No change in ET-1 or ET receptor mRNA levels was seen in organs perfused by the systemic vascular bed, except in liver, where ETA receptor mRNA levels were decreased. The findings of concomitant increases in gene transcript levels for ET-1 and the ETA and ETB receptors in lung, but not in the great vessels or any other organ examined, are consistent with the hypothesis that increased ET-1 synthesis in the lung contributes to pulmonary vascular remodeling and the maintenance of chronic hypoxic pulmonary hypertension.

scholarly journals Intima Sarcoma of the Pulmonary Artery Mimicking Takayasu Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
C. Belge ◽  
I. Renckens ◽  
R. Van Puijenbroek ◽  
W. Wuyts ◽  
B. Meyns ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Takayasu Arteritis ◽  
Pulmonary Arterial Pressure ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Thin Walled ◽  
Takayasu Disease

Pulmonary artery intima sarcoma is an uncommon but fatal tumor, which often masquerades chronic thromboembolic pulmonary hypertension (CTEPH) and in the present case Takayasu arteritis. Pulmonary arterial pressure is mildly elevated in the presence of extensive proximal lesions. A parenchyma thin-walled cavitary lesion may be a sign of pulmonary extravasation of the tumor.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

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