PULMONARY VASCULAR ADJUSTMENTS IN THE NEONATAL PERIOD

PEDIATRICS ◽  
1961 ◽  
Vol 28 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Abraham M. Rudolph ◽  
Peter A. M. Auld ◽  
Richard J. Golinko ◽  
Milton H. Paul
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Neonatal Period ◽  
Pulmonary Arterial Pressure ◽  
Systolic Pressure ◽  
Indwelling Catheters ◽  
Pulmonary Vessels ◽  
Pulmonary Arterial ◽  
Unanesthetized Animals ◽  
Young Puppy

Pulmonary arterial or right ventricular pressures were measured repeatedly in 18 puppies and 2 goats, from 1 to 36 days of age; these pressures were measured with the use of indwelling catheters in unanesthetized animals. In puppies the systolic pressure in the pulmonary circulation decreased rapidly to near adult levels in 5 to 10 days after birth, and then more slowly to adult levels by 5 to 6 weeks of age. In goats the pressures decreased more slowly, reaching near adult levels in about 12 to 14 days. Acetylcholine produced a decrease in pulmonary arterial pressure in the puppy in the first 5 days of life, but an increase in pulmonary pressure after that time in the resting animal. In the hypoxic puppy, a reduction in pulmonary arterial pressure was induced by acetylcholine. These findings suggest that the pulmonary vessels in the young puppy are actively constricted but that relaxation occurs after the first few days of life.

Effect of surface tension on circulation in the excised lungs of dogs

1964 ◽  
Vol 19 (4) ◽  
pp. 707-712 ◽  
Author(s):  
I. Bruderman ◽  
K. Somers ◽  
W. K. Hamilton ◽  
W. H. Tooley ◽  
J. Butler
Keyword(s):  
Surface Tension ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Lung Volume ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Alveolar Pressure ◽  
Pulmonary Arterial ◽  
Air Liquid Interface ◽  
Effect Of Surface

The hypothesis that the surface tension of the fluid film which lines the lung alveoli reduces the pericapillary pressure in air-filled lungs was tested by perfusing the excised lungs of dogs with saline, 6% dextran in saline, and blood. After almost maximal inflation with air from low volumes or the degassed state (inflation state) the pulmonary arterial pressure, relative to the base of the lungs, was lower than the alveolar pressure with flows up to 50 ml/min. It was higher than the alveolar pressure at any flow when the air-liquid interface had been abolished by filling the lungs to the same volume with fluid. The pulmonary arterial pressure at the same flow and alveolar pressure was lower in the inflation state than after deflation from higher volumes (the deflation state). However, lung volume was larger in the deflation state. The possibility of some low resistance channels in the inflation state could not be excluded. However, histological examinations showed that the alveolar capillaries were patent and failed to show any airless lung. pulmonary circulation; pericapillary pressure in lungs; surface tension and pulmonary vascular resistance Submitted on July 29, 1963

scholarly journals Preoperative 2D-echocardiographic assessment of pulmonary arterial pressure in subgroups of liver transplantation recipients

2021 ◽  
Vol 16 (4) ◽  
pp. 344-352
Author(s):  
Jungchan Park ◽  
Myung Soo Park ◽  
Ji-Hye Kwon ◽  
Ah Ran Oh ◽  
Seung-Hwa Lee ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Systolic Pressure ◽  
Heart Catheterization ◽  
Predictive Values ◽  
Ventricular Systolic Pressure ◽  
2D Echocardiography ◽  
Echocardiographic Assessment ◽  
Pulmonary Arterial

Background: The clinical efficacy of preoperative 2D-echocardiographic assessment of pulmonary arterial pressure (PAP) has not been evaluated fully in liver transplantation (LT) recipients.Methods: From October 2010 to February 2017, a total of 344 LT recipients who underwent preoperative 2D-echocardiography and intraoperative right heart catheterization (RHC) was enrolled and stratified according to etiology, disease progression, and clinical setting. The correlation of right ventricular systolic pressure (RVSP) on preoperative 2D-echocardiography with mean and systolic PAP on intraoperative RHC was evaluated, and the predictive value of RVSP > 50 mmHg to identify mean PAP > 35 mmHg was estimated.Results: In the overall population, significant but weak correlations were observed (R = 0.27; P < 0.001 for systolic PAP, R = 0.24; P < 0.001 for mean PAP). The positive and negative predictive values of RVSP > 50 mmHg identifying mean PAP > 35 mmHg were 37.5% and 49.9%, respectively. In the subgroup analyses, correlations were not significant in recipients of deceased donor type LT (R = 0.129; P = 0.224 for systolic PAP, R = 0.163; P = 0.126 for mean PAP) or in recipients with poorly controlled ascites (R = 0.215; P = 0.072 for systolic PAP, R = 0.21; P = 0.079 for mean PAP). Conclusion: In LT recipients, the correlation between RVSP on preoperative 2D-echocardiography and PAP on intraoperative RHC was weak; thus, preoperative 2D-echocardiography might not be the optimal tool for predicting intraoperative PAP. In LT candidates at risk of pulmonary hypertension, RHC should be considered.

Loss of endothelium-dependent vasodilation in the pulmonary vessels of sheep after prolonged endotoxin

1994 ◽  
Vol 76 (1) ◽  
pp. 361-369 ◽  
Author(s):  
J. A. Spath ◽  
P. J. Sloane ◽  
M. H. Gee ◽  
K. H. Albertine
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Prolonged Exposure ◽  
Pulmonary Arterial Pressure ◽  
Necrosis Factor Alpha ◽  
Pulmonary Vessels ◽  
Endotoxin Infusion ◽  
Pulmonary Arterial ◽  
Endothelium Dependent Relaxation

We examined the hemodynamic response of awake sheep to prolonged endotoxin infusion (10 ng.kg-1 x min-1 for 12 h) and the in vitro endothelium-dependent relaxation of pulmonary arterial vessels excised 12 h after the end of endotoxin infusion to determine whether the development of pulmonary hypertension after endotoxin is associated with loss of endothelium-dependent relaxation. In seven of nine sheep, there was a maintained increase (4–68% of baseline) in pulmonary arterial pressure 24 h after the beginning of endotoxin infusion. The greater the increase in pulmonary arterial pressure in vivo, the greater was the in vitro deficit in endothelium-dependent relaxation of the pulmonary vessels. The maximum in vitro vessel dilation was 59% for pulmonary artery rings isolated from sheep without a sustained increase in pulmonary arterial pressure 24 h after endotoxin. Prolonged endotoxin infusion did not alter the in vitro response of pulmonary arterial vessels to KCl or 10(-5) M norepinephrine. Force development, response to 10(-5) M norepinephrine, and vasodilation in response to acetylcholine were also not altered in pulmonary vessels taken from control sheep and exposed in vitro to tumor necrosis factor-alpha (400 U/ml). Our results suggest that loss of endothelium-dependent relaxation in pulmonary vessels supports the sustained pulmonary hypertension that develops after prolonged exposure to endotoxin.

Pregnancy blunts pulmonary vascular reactivity in dogs

1980 ◽  
Vol 239 (3) ◽  
pp. H297-H301 ◽  
Author(s):  
L. G. Moore ◽  
J. T. Reeves
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Acute Hypoxia ◽  
Limited Data ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Pregnancy decreases systemic vascular reactivity but comparatively little is known about the effects of pregnancy on the pulmonary circulation. Pulmonary vascular resistance (PVR) during acute hypoxia was lower (P < 0.01) in eight intact anesthetized pregnant dogs compared to the same animals postpartum. Mean pulmonary arterial pressure (Ppa) and PVR during infusion of prostaglandin (PG) F2 alpha were also reduced during pregnancy. Nonpregnant female dogs (n = 5) treated with estrogen (0.001 mg x kg-1 x da-1) for 2 wk had decreased Ppa (P < 0.01) during acute hypoxia compared to control measurements, but PVR was unchanged during hypoxia and PGF2 alpha infusion. Treatment with progesterone in four dogs had no effect on pulmonary vascular reactivity to hypoxia or PGF2 alpha. Inhibition of circulating PG with meclofenamate in four dogs during pregnancy did not appear to restore pulmonary vascular reactivity. Blunted pulmonary vascular reactivity is suggested by the limited data available for women, but is not seen in pregnant cows. We conclude that pregnancy decreases pulmonary as well as systemic vascular reactivity in the dog, but the mechanism is unclear.

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.

Hyperventilation, alkalosis, prostaglandins, and pulmonary circulation of the newborn

1986 ◽  
Vol 61 (6) ◽  
pp. 2088-2094 ◽  
Author(s):  
F. C. Morin
Keyword(s):  
Carbon Dioxide ◽  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Respiratory Alkalosis ◽  
Newborn Lamb ◽  
Mechanical Factors ◽  
Pulmonary Arterial ◽  
Carbon Dioxide Co2 ◽  
Normal Ventilation

This study was designed to determine whether the effects of hyperventilation on the pulmonary circulation of the newborn lamb were 1) due to mechanical factors or to respiratory alkalosis; and 2) mediated by prostaglandins. Six control lambs were studied during normal ventilation and during hyperventilation with, and without, decreased carbon dioxide (CO2). Five lambs were given indomethacin and studied similarly. In control lambs, hyperventilation with decreased CO2 decreased pulmonary arterial pressure from 26 +/- 2.2 to 18 +/- 1.0 (SE) Torr (P less than or equal to 0.005) and pulmonary vascular resistance from 0.099 +/- 0.035 to 0.070 +/- 0.011 Torr X kg-1 X min-1 (P less than or equal to 0.015). Hyperventilation with normal CO2 did not affect the pulmonary circulation. Hyperventilation with decreased CO2 increased pulmonary arterial concentrations of 6-ketoprostaglandin F1 alpha, a major metabolite of prostacyclin, in control lambs but not in the indomethacin-treated lambs. However, it affected the pulmonary circulation of the control- and indomethacin-treated lambs similarly. In conclusion, hyperventilation affected the pulmonary circulation by respiratory alkalosis not by mechanical factors and prostaglandins did not mediate its effects.

Nitric oxide inhalation: effects on the ovine neonatal pulmonary and systemic circulations

1996 ◽  
Vol 8 (3) ◽  
pp. 431 ◽  
Author(s):  
V DeMarco ◽  
JW Skimming ◽  
TM Ellis ◽  
S Cassin
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Minimum Concentration ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Inhaled No

Others have shown that inhaled nitric oxide causes reversal of pulmonary hypertension in anaesthetized perinatal sheep. The present study examined haemodynamic responses to inhaled NO in the normal and constricted pulmonary circulation of unanaesthetized newborn lambs. Three experiments were conducted on each of 7 lambs. First, to determine a minimum concentration of NO which could reverse acute pulmonary hypertension caused by infusion of the thromboxame mimic U46619, the haemodynamic effects of 5 different doses of inhaled NO were examined. Second, the effects of inhaling 80 ppm NO during hypoxic pulmonary vasoconstriction were examined. Finally, to determine if tachyphalaxis occurs during NO inhalation, lambs were exposed to 80 ppm NO for 3 h during which time pulmonary arterial pressure was doubled by infusion of U46619. Breathing NO (80 ppm) caused a slight but significant decrease in pulmonary vascular resistance (PVR) in lambs with normal pulmonary arterial pressure (PAP). Nitric oxide, inhaled at concentrations between 10 and 80 ppm for 6 min (F1O2 = 0.60), caused decreases in PVR when PAP was elevated with U46619. Nitric oxide acted selectively on the pulmonary circulation, i.e. no changes occurred in systemic arterial pressure or any other measured variable. Breathing 80 ppm NO for 6 min reversed hypoxic pulmonary vasoconstriction. In the chronic exposure study, inhaling 80 ppm NO for 3 h completely reversed U46619-induced pulmonary hypertension. Although arterial methaemoglobin increased during the 3-h exposure to 80 ppm NO, there was no indication that this concentration of NO impairs oxygen loading. These data demonstrate that NO, at concentrations as low as 10 ppm, is a potent, rapid-action, and selective pulmonary vasodilator in unanaesthetized newborn lambs with elevated pulmonary tone. Furthermore, these data support the use of inhaled NO for treatment of infants with pulmonary hypertension.

Effects of chronically elevated pulmonary arterial pressure and flow on right ventricular afterload

1994 ◽  
Vol 267 (1) ◽  
pp. H155-H165 ◽  
Author(s):  
B. Ha ◽  
C. L. Lucas ◽  
G. W. Henry ◽  
E. G. Frantz ◽  
J. I. Ferreiro ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Arterial Pressure ◽  
Right Ventricle ◽  
Pulmonary Arterial Pressure ◽  
Systolic Pressure ◽  
Arterial Blood Flow ◽  
Pulmonary Hemodynamics ◽  
Reflected Wave ◽  
Arterial Blood ◽  
Pulmonary Arterial

The effects of pulsatile hemodynamics on right ventricle-pulmonary circulation interactions were studied in control lambs and in two lamb models of altered pulmonary hemodynamics induced at infancy: elevated pulmonary arterial pressure (PAP) was created by the infusion of monocrotaline pyrrole (MCTP), and elevated pulmonary arterial blood flow was obtained by the creation of an arteriovenous fistula (Shunt). High-fidelity PAP, midvessel Doppler blood velocity (PAV), and cardiac output (CO) were measured in open-chest, anesthetized lambs. PAV waveforms were normalized to match the measured CO. Measured pressure and flow signals were separated in the time domain into forward and backward components. Pulmonary input impedance and indexes quantifying the timing of the reflected wave pulse (beginning of reflected pulse, duration of reflected pulse in systole, and duration of reflected wave in diastole) were calculated for each group. Results indicate that in control animals the reflected wave returned late in systole and extended through much of diastole, thereby increasing diastolic pressure like a counterpulsation balloon. No significant differences in the timing indexes were found between Shunt and control animals. In the MCTP group, the reflected wave returned significantly earlier than normal with the peak reflected pulse occurring before valve closure. The resulting augmentation of systolic pressure and, therefore, large pulse pressure is consistent with pressure waveforms observed in clinical pulmonary hypertension. We conclude that early wave reflection exerts a detrimental effect in pulmonary hypertension by unfavorably loading the still-ejecting right ventricle.

Enhanced systolic function of the right ventricle during respiratory distress syndrome in newborn lambs

2001 ◽  
Vol 280 (1) ◽  
pp. H392-H400 ◽  
Author(s):  
Maartje De Vroomen ◽  
Paul Steendijk ◽  
Robbert H. Lopes Cardozo ◽  
Hens H. A. Brouwers ◽  
Frank Van Bel ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Distress Syndrome ◽  
Pulmonary Arterial Pressure ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular Systolic Function ◽  
Left Ventricular ◽  
Ventricular Systolic Function ◽  
Pulmonary Arterial ◽  
The Right

Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 ± 0.6 ml at baseline and 6.1 ± 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 ± 2.3 ml at baseline to 7.7 ± 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.

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