Acute effects of partial compression of ductus arteriosus on fetal pulmonary circulation

1989 ◽  
Vol 257 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Base Line ◽  
Acute Effects ◽  
Artery Pressure

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

The Use of Histamine Questioned

PEDIATRICS ◽  
1976 ◽  
Vol 58 (5) ◽  
pp. 776-777
Author(s):  
Shyamal K. Sanyal
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Cardiac Catheterization ◽  
Pulmonary Blood Flow ◽  
Pathogenetic Mechanism ◽  
Artery Pressure

The pathogenetic mechanism proposed by Levin et al.1 to explain the persistence of fetal cardiopulmonary circulatory pathway (PFCCP) during infancy if of interest. However, their suggestion that use of histamine injected directly into the pulmonary artery may be beneficial in such patients raises some questions. The initial cardiac catheterization data in their patient at the age of 33 days show hypoxia and hypercarbia. The authors have indicated in Table II that both of these factors could produce a decrease in pulmonary blood flow as well as an increase in pulmonary artery pressure and pulmonary vascular resistance.

scholarly journals Progressive dysfunction of nitric oxide synthase in a lamb model of chronically increased pulmonary blood flow: a role for oxidative stress

2008 ◽  
Vol 295 (5) ◽  
pp. L756-L766 ◽  
Author(s):  
Peter E. Oishi ◽  
Dean A. Wiseman ◽  
Shruti Sharma ◽  
Sanjiv Kumar ◽  
Yali Hou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Lung Tissue ◽  
Pulmonary Blood Flow ◽  
Artery Pressure ◽  
Oxide Synthase ◽  
Inhaled No

Cardiac defects associated with increased pulmonary blood flow result in pulmonary vascular dysfunction that may relate to a decrease in bioavailable nitric oxide (NO). An 8-mm graft (shunt) was placed between the aorta and pulmonary artery in 30 late gestation fetal lambs; 27 fetal lambs underwent a sham procedure. Hemodynamic responses to ACh (1 μg/kg) and inhaled NO (40 ppm) were assessed at 2, 4, and 8 wk of age. Lung tissue nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), neuronal NOS (nNOS), inducible NOS (iNOS), and heat shock protein 90 (HSP90), lung tissue and plasma nitrate and nitrite (NOx), and lung tissue superoxide anion and nitrated eNOS levels were determined. In shunted lambs, ACh decreased pulmonary artery pressure at 2 wk ( P < 0.05) but not at 4 and 8 wk. Inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). In control lambs, ACh and inhaled NO decreased pulmonary artery pressure at each age ( P < 0.05). Total NOS activity did not change from 2 to 8 wk in control lambs but increased in shunted lambs (ANOVA, P < 0.05). Conversely, NOxlevels relative to NOS activity were lower in shunted lambs than controls at 4 and 8 wk ( P < 0.05). eNOS protein levels were greater in shunted lambs than controls at 4 wk of age ( P < 0.05). Superoxide levels increased from 2 to 8 wk in control and shunted lambs (ANOVA, P < 0.05) and were greater in shunted lambs than controls at all ages ( P < 0.05). Nitrated eNOS levels were greater in shunted lambs than controls at each age ( P < 0.05). We conclude that increased pulmonary blood flow results in progressive impairment of basal and agonist-induced NOS function, in part secondary to oxidative stress that decreases bioavailable NO.

Physiological alterations in increased pulmonary blood flow with and without pulmonary hypertension

1961 ◽  
Vol 16 (2) ◽  
pp. 305-308 ◽  
Author(s):  
Lois T. Ellison ◽  
David P. Hall ◽  
Thomas Yeh ◽  
H. Mobarhan ◽  
Joseph Rossi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Function ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Artery Hypertension ◽  
Systolic Pulmonary Artery Pressure ◽  
Venous Admixture ◽  
Artery Pressure ◽  
Physiological Alterations

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960

Inhibition of 20-HETE abolishes the myogenic response during NOS antagonism in the ovine fetal pulmonary circulation

2005 ◽  
Vol 289 (2) ◽  
pp. L261-L267 ◽  
Author(s):  
Thomas A. Parker ◽  
Theresa R. Grover ◽  
John P. Kinsella ◽  
John R. Falck ◽  
Steven H. Abman
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Ductus Arteriosus ◽  
Combined Treatment ◽  
Specific Inhibitor ◽  
Fetal Lung ◽  
Myogenic Response ◽  
Fetal Sheep ◽  
Artery Pressure

Mechanisms that maintain high pulmonary vascular resistance (PVR) and oppose vasodilation in the fetal lung are poorly understood. In fetal lambs, increased pulmonary artery pressure evokes a potent vasoconstriction, suggesting that a myogenic response contributes to high PVR in the fetus. In adult systemic circulations, the arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) has been shown to modulate the myogenic response, but its role in the fetal lung is unknown. We hypothesized that acute increases in pulmonary artery pressure release 20-HETE, which causes vasoconstriction, or a myogenic response, in the fetal lung. To address this hypothesis, we studied the hemodynamic effects of N-methylsufonyl-12,12-dibromododec-11-enamide (DDMS), a specific inhibitor of 20-HETE production, on the pulmonary vasoconstriction caused by acute compression of the ductus arteriosus (DA) in chronically prepared fetal sheep. An inflatable vascular occluder around the DA was used to increase pulmonary artery pressure under three study conditions: control, after pretreatment with nitro-l-arginine (l-NA; to inhibit shear-stress vasodilation), and after combined treatment with both l-NA and a specific 20-HETE inhibitor, DDMS. We found that DA compression after l-NA treatment increased PVR by 44 ± 12%. Although intrapulmonary DDMS infusion did not affect basal PVR, DDMS completely abolished the vasoconstrictor response to DA compression in the presence of l-NA (44 ± 12% vs. 2 ± 4% change in PVR, l-NA vs. l-NA + DDMS, P < 0.05). We conclude that 20-HETE mediates the myogenic response in the fetal pulmonary circulation and speculate that pharmacological inhibition of 20-HETE might have a therapeutic role in neonatal conditions characterized by pulmonary hypertension.

Pressure-Flow Relationships in the Dog Lung During Acute, Subtotal Pulmonary Vascular Occlusion

1958 ◽  
Vol 192 (3) ◽  
pp. 613-619 ◽  
Author(s):  
Michael T. Lategola
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Vascular Occlusion ◽  
Percentage Change ◽  
Artery Pressure ◽  
Vascular Bed ◽  
Change In Mean ◽  
Pulmonary Vascular Bed

The relationship of pulmonary artery pressure to pulmonary blood flow was studied in the dog by means of occlusive shifting of blood flow within the pulmonary vascular bed. All experiments were performed using the closed-chest preparation. The range of blood flow increases studied was 25–388%. A graphical plot of the percentage change in blood flow versus the percentage change in mean pulmonary artery pressure is presented. A visually estimated curve of this latter data is presented, discussed and compared to four other curves from previous pulmonary vascular studies. A comparison of these curves suggests that the relative maximum capacity of the pulmonary vascular bed of man and dog are similar. These curves plus certain assumptions allow the speculative delineation of a graphical area representing the ‘active’ vasomotor component of exercise at different levels of pulmonary blood flow increase.

Effect of Unilateral Carbon Dioxide Breathing on Pulmonary Blood Flow

1957 ◽  
Vol 191 (2) ◽  
pp. 399-403 ◽  
Author(s):  
Richard M. Peters
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Vascular Resistance ◽  
Pulmonary Blood Flow ◽  
Control Period ◽  
Air Breathing ◽  
Fick Principle

The effect of breathing increased concentrations of carbon dioxide was studied in dogs. Each lung was independently ventilated with the chest open. The pulmonary artery pressure was recorded and blood flow determined for each lung by the Fick principle during room air breathing. After this control period, increased concentrations of carbon dioxide were substituted for room air in one lung and the above determinations repeated. In all but 2 of 11 animals the pulmonary vascular resistance fell in the CO2 lung and the blood flow to this lung increased.

Hemodynamic effects of endothelin-1 on ovine fetal pulmonary circulation

1991 ◽  
Vol 261 (1) ◽  
pp. R182-R187 ◽  
Author(s):  
B. A. Chatfield ◽  
I. F. McMurtry ◽  
S. L. Hall ◽  
S. H. Abman
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Ductus Arteriosus ◽  
Left Lung ◽  
Hemodynamic Effects ◽  
Fetal Sheep ◽  
Flow Transducer ◽  
Artery Pressure ◽  
Endothelin 1

To determine the hemodynamic effects of endothelin-1 (ET-1) in the fetal pulmonary circulation, we studied pulmonary vascular responses to brief and prolonged intrapulmonary infusions of the peptide in nine chronically prepared late-gestation fetal sheep. Left pulmonary artery (LPA) blood flow was measured with an electromagnetic flow transducer, and a catheter placed in the LPA allowed ET-1 infusion directly into the left lung. Brief (10-min) infusions of ET-1 (12.5-100 ng/min) increased flow up to 212% of baseline without changing pulmonary artery pressure. With prolonged (120-min) infusion of ET-1 (50 ng/min), flow increased from 69 +/- 8 to 164 +/- 23 ml/min at 10 min (P less than 0.05) but then declined and was not different from baseline at 120 min. The gradient between mean pulmonary artery and aortic pressures did not change, suggesting no constriction of the ductus arteriosus. Systemic (vena caval) infusion of ET-1 (100 ng/min for 30 min) caused systemic and pulmonary hypertension, as mean pulmonary artery pressure increased from 43 +/- 1 to 51 +/- 2 mmHg (P less than 0.05) and remained elevated for 30 min after cessation of the ET-1 infusion. We conclude that intrapulmonary ET-1 is a potent fetal pulmonary vasodilator, but its dilator effect is transient during prolonged infusion. In contrast, systemic infusion causes sustained hypertension, suggesting differential effects of ET-1 on the pulmonary and systemic circulations. These findings demonstrate marked vasoactivity of ET-1 in the fetus, suggesting a potential role in the normal or abnormal transitional circulation.

A fetal-instrumented model to study age-specific responses to leukotriene D4 and prostaglandin D2 in unsedated newborn lambs

1989 ◽  
Vol 67 (6) ◽  
pp. 587-593
Author(s):  
J. Y. Coe ◽  
P. M. Olley ◽  
F. Coceani
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Main Pulmonary Artery ◽  
Right Atrial ◽  
Prostaglandin D2 ◽  
Leukotriene D4

Sequential studies of the pulmonary vascular response to leukotriene D4 (LTD4) and prostaglandin D2 (PGD2) in the immediate newborn period were performed in lambs, instrumented in utero and delivered vaginally. Compounds were tested in fully conscious 1.5-day-old lambs and the study was repeated 1 week later. Bolus injections of PGD2 (0.05–2.0 μg/kg) or LTD4 (0.01–1.0 μg/kg) were made into the main pulmonary artery or aorta while pulmonary blood flow and aortic, pulmonary artery, and left and right atrial pressures were monitored continuously. PGD2 was a systemic constrictor regardless of age. In lambs 1.5 days of age, it decreased pulmonary vascular pressure and resistance by 6% (p < 0.05) and 15% (p < 0.05), respectively, while 1 week later it increased pulmonary vascular resistance by 18% (p < 0.05). In contrast, LTD4 was a pulmonary and systemic vasoconstrictor in both the early and late newborn, the threshold dose being between 0.01 and 0.05 μg/kg at either age. The decrease in pulmonary blood flow and the increase in pressure and resistance were greater in older animals. In lambs 1.5 days of age, LTD4 (1 μg/kg) increased pulmonary vascular resistance by 66.1% (p < 0.05) and 1 week later by 210% (p < 0.001). These sequential observations in the same animal indicate that unlike PGD2, LTD4 is a pulmonary vasoconstrictor regardless of age, and its effectiveness increases significantly with age. These results support previous reports that PGD2 action in the pulmonary circulation changes shortly after birth from dilation to constriction.Key words: pulmonary circulation, newborn lamb, prostaglandin D2, leukotriene D4.

VENTILATION-PERFUSION RELATIONSHIPS IN CHILDREN WITH HEART DISEASE AND DIMINISHED PULMONARY BLOOD FLOW

PEDIATRICS ◽  
1968 ◽  
Vol 42 (5) ◽  
pp. 778-785
Author(s):  
Martin H. Lees ◽  
Richard H. Burnell ◽  
Clarence L. Morgan ◽  
Benjamin B. Ross
Keyword(s):  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Pulmonary Function ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Blood Flow ◽  
Alveolar Ventilation ◽  
Uneven Distribution ◽  
Artery Pressure ◽  
Major Abnormality

Pulmonary function of infants and children with diminished pulmonary blood flow was studied by measurement of alveolar ventilation and alveolar-arterial gas tension differences of O2, CO2, and N2. The increased ventilation of these subjects was found to be effective in CO2 elimination (arterial CO2 tension, 31 mm Hg), but there was evidence of considerable unevenness of distribution of ventilation/perfusion ratios (VAQ). A measure of the degree of VA/Q unevenness was obtained by use of the urine-alveolar nitrogen tension difference. It is likely, under the prevailing conditions of hyperventilation and hypoperfusion, that maldistribution of perfusion is the major abnormality. Uneven distribution of perfusion is most probably due to the effects of gravity enhanced by low pulmonary artery pressure and blood flow—an exaggenation of the normal physiologic relative overperfusion of the lower-most parts of the lung.

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