Pulmonary arterial resistance and compliance in preterm infants

2017 ◽  
Vol 244 ◽  
pp. 265-270 ◽  
Author(s):  
Seigo Okada ◽  
Jun Muneuchi ◽  
Yusaku Nagatomo ◽  
Mamie Watanabe ◽  
Chiaki Iida ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Arterial Resistance ◽  
Pulmonary Arterial

Relationship Between Pulmonary Arterial Resistance and Compliance in Patients with Down Syndrome

2019 ◽  
Vol 40 (4) ◽  
pp. 841-847 ◽  
Author(s):  
Yuka Iwaya ◽  
Jun Muneuchi ◽  
Yuka Inoue ◽  
Mamie Watanabe ◽  
Seigo Okada ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Arterial Resistance ◽  
Pulmonary Arterial

Distribution of lung vascular resistance after chronic systemic-to-pulmonary shunts

1985 ◽  
Vol 249 (6) ◽  
pp. H1106-H1113 ◽  
Author(s):  
R. P. Michel ◽  
T. S. Hakim ◽  
R. E. Hanson ◽  
A. R. Dobell ◽  
F. Keith ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Morphometric Measurements ◽  
Arterial Resistance ◽  
Pulmonary Arterial ◽  
The Right

Congenital cardiac shunts produce pathological lesions on the arterial side of the lung vasculature. We examined the effects of chronic shunts (14.2 +/- 1.2 mo) in 10 young dogs, between the left subclavian and the left lower lobe (LLL) artery, on pulmonary vascular pressure and flow (P-Q) relationships, segmental resistance with arterial and venous occlusion (AVO), and sensitivity to drugs. At final thoracotomy, mean LLL pulmonary arterial pressure (Ppa) was 23.2 +/- 4.3 mmHg compared with 11.9 +/- 0.9 in the right lung (P less than 0.05); two animals had LLL Ppa of 41 and 48 mmHg. The LLL artery and vein were cannulated, and pressure-flow (P-Q) and AVO measurements were made and compared with previous control LLL (n = 11) and contralateral right lower lobe (RLL, n = 5). Responses to serotonin, histamine, and vasodilators (diltiazem and isoproterenol) were evaluated. Comparisons of morphometric measurements were made between LLL and RLL. We found a significant increase in arterial resistance as measured with AVO and a hypersensitivity to serotonin in the shunt LLL, without changes in total pulmonary vascular resistance or P-Q measurements; vasodilators had a small effect only in the hypertensive lobes. Our data suggest that chronic shunts to the pulmonary circulation increase arterial resistance and sensitivity to serotonin, even in the absence of discernible morphometric changes, and that vasoconstriction may be an important precursor to the development of morphological lesions.

Pulmonary Arterial Resistance: Noninvasive Measurement with Indexes of Pulmonary Flow Estimated at Velocity-encoded MR Imaging—Preliminary Experience

Radiology ◽  
1999 ◽  
Vol 212 (3) ◽  
pp. 896-902 ◽  
Author(s):  
Elie Mousseaux ◽  
Jean Pierre Tasu ◽  
Odile Jolivet ◽  
Gérard Simonneau ◽  
Jacques Bittoun ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Noninvasive Measurement ◽  
Arterial Resistance ◽  
Pulmonary Flow ◽  
Pulmonary Arterial

Therapeutic hypercapnia prevents chronic hypoxia-induced pulmonary hypertension in the newborn rat

2006 ◽  
Vol 291 (5) ◽  
pp. L912-L922 ◽  
Author(s):  
Crystal Kantores ◽  
Patrick J. McNamara ◽  
Lilian Teixeira ◽  
Doreen Engelberts ◽  
Prashanth Murthy ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Vascular Remodeling ◽  
Chronic Hypoxia ◽  
Antioxidant Properties ◽  
Ventricular Performance ◽  
Pulmonary Vascular Remodeling ◽  
Beneficial Effects ◽  
Arterial Resistance ◽  
Pulmonary Arterial

Induction of hypercapnia by breathing high concentrations of carbon dioxide (CO2) may have beneficial effects on the pulmonary circulation. We tested the hypothesis that exposure to CO2 would protect against chronic pulmonary hypertension in newborn rats. Atmospheric CO2 was maintained at <0.5% (normocapnia), 5.5%, or 10% during exposure from birth for 14 days to normoxia (21% O2) or moderate hypoxia (13% O2). Pulmonary vascular and hemodynamic abnormalities in animals exposed to chronic hypoxia included increased pulmonary arterial resistance, right ventricular hypertrophy and dysfunction, medial thickening of pulmonary resistance arteries, and distal arterial muscularization. Exposure to 10% CO2 (but not to 5.5% CO2) significantly attenuated pulmonary vascular remodeling and increased pulmonary arterial resistance in hypoxia-exposed animals ( P < 0.05), whereas both concentrations of CO2 normalized right ventricular performance. Exposure to 10% CO2 attenuated increased oxidant stress induced by hypoxia, as quantified by 8-isoprostane content in the lung, and prevented upregulation of endothelin-1, a critical mediator of pulmonary vascular remodeling. We conclude that hypercapnic acidosis has beneficial effects on pulmonary hypertension and vascular remodeling induced by chronic hypoxia, which we speculate derives from antioxidant properties of CO2 on the lung and consequent modulating effects on the endothelin pathway.

Cardiopulmonary Dynamics during Arteriovenous Perfusion: Cardiac Output, Pulmonary Arterial Resistance, and Right Ventricular Stroke Work

1980 ◽  
Vol 29 (1) ◽  
pp. 49-56 ◽  
Author(s):  
Bartley P. Griffith ◽  
Harvey S. Borovetz ◽  
Robert L. Hardesty ◽  
Tin-Kan Hung ◽  
Henry T. Bahnson
Keyword(s):  
Cardiac Output ◽  
Right Ventricular ◽  
Stroke Work ◽  
Arterial Resistance ◽  
Pulmonary Arterial ◽  
Right Ventricular Stroke Work

Effects of angiotensin on pulmonary and systemic hemodynamics

1962 ◽  
Vol 202 (4) ◽  
pp. 690-694 ◽  
Author(s):  
John E. Chimoskey ◽  
Pedro C. Blaquier ◽  
A. C. Taquini ◽  
David F. Bohr
Keyword(s):  
Heart Rate ◽  
Renin Angiotensin System ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Pulmonary Resistance ◽  
Angiotensin System ◽  
Arterial Resistance ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial

In ten morphine-urethan anesthetized dogs single injections of 2.0 µg/kg of synthetic valine 5 angiotensin II amide elevated systemic and pulmonary arterial pressures and depressed heart rate. Thirty-minute intravenous infusions of angiotensin (0.4 and 1.0 µg/kg/min) in eight dogs elevated systemic arterial pressure and diminished heart rate. Pulmonary arterial, pulmonary wedge, left ventricular end-diastolic, and right atrial pressures were all slightly elevated; mean cardiac output did not change. Calculated total pulmonary resistance and pulmonary arterial resistance were diminished; central blood volume was elevated. These findings suggest that elevated systemic pressure and resistance increase myocardial work and induce reflex bradycardia, thereby elevating left ventricular end-diastolic, pulmonary wedge, and pulmonary arterial pressures. Systemic vasoconstriction also contributes to the elevated right atrial pressure and distention of the pulmonary vascular bed, which diminishes total pulmonary and pulmonary arterial resistance. These findings are not incompatible with the theory that the renin-angiotensin system is active in essential hypertension.

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