Endogenous Hydrogen Sulfide Regulates Pulmonary Artery Collagen Remodeling in Rats with High Pulmonary Blood Flow

2009 ◽  
Vol 234 (5) ◽  
pp. 504-512 ◽  
Author(s):  
Xiaohui Li ◽  
Hongfang Jin ◽  
Geng Bin ◽  
Li Wang ◽  
Chaoshu Tang ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hydrogen Sulfide ◽  
Pulmonary Artery ◽  
Lung Tissue ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Tissue Growth ◽  
Pulmonary Vasculature ◽  
Collagen Remodeling ◽  
Collagen Iii

The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-γ-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H2S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H2S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H2S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated ( P < 0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group ( P < 0.01). This study suggests that endogenous H2S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.

The pulmonary vasculature in a neonatal porcine model with increased pulmonary blood flow and pressure

2001 ◽  
Vol 11 (4) ◽  
pp. 420-430 ◽  
Author(s):  
Elisabeth V. Stenbøg ◽  
Daniel A. Steinbrüchel ◽  
Anne Bloch Thomsen ◽  
Ulrik Baandrup ◽  
Lene Heickendorff ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Vascular Disease ◽  
Pulmonary Blood Flow ◽  
Left Pulmonary Artery ◽  
Pulmonary Vasculature ◽  
Pulmonary Vascular Disease ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Circulating Levels

Introduction: Hypertension and hyperperfusion of the pulmonary vascular bed in the setting of congenital cardiac malformations may lead to progressive pulmonary vascular disease. To improve the understanding of the basic mechanisms of this disease, there is a need for clinically relevant animal models which reflect the disease process. Material and Results: We randomly allocated 45 newborn pigs, at the age of 48 hrs, to groups in which there was either construction of a 3 mm central aorto-pulmonary shunt, undertaken in 9, or ligation of the left pulmonary artery, achieved in 13. Controls included sham operations in 13, or no operations in 10 pigs. Follow-up was continued for three months. The interventions were compatible with survival in most pigs. The shunts resulted in an acute 85% increase in systolic pulmonary arterial pressure, and a more than twofold increase in pulmonary blood flow. By three months of age, nearly all shunts had closed spontaneously, and haemodynamics were normal. Ligation of the left pulmonary artery resulted in a normal total pulmonary blood flow, despite only the right lung being perfused, and a 33% increase in systolic pulmonary arterial pressure. These haemodynamic changes were maintained throughout the period of study. In both groups, histomorphometry revealed markedly increased muscularity of the intra-acinar pulmonary arteries. Circulating levels of endothelin were normal in the shunted animals, and elevated in those with ligation of the left pulmonary artery. Conclusion: In neonatal porcine models of pulmonary vascular disease, created by construction of 3 mm central aorto-pulmonary shunts and ligation of one pulmonary artery, we observed histopathological changes of the pulmonary vasculature similar to early hypertensive pulmonary vascular disease in humans. Elevated circulating levels of endothelin were associated with abnormal haemodynamics rather than abnormal pathology. These findings could be valuable for future studies on the pathogenesis of hypertensive pulmonary vascular disease associated with congenital cardiac malformations.

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.

In vivo support for the new concept of pulmonary blood flow-mediated CO2 gas excretion in the lungs

2015 ◽  
Vol 308 (12) ◽  
pp. L1224-L1236 ◽  
Author(s):  
Yoshiko Kawai ◽  
Kumiko Ajima ◽  
Maki Kaidoh ◽  
Masao Sakaguchi ◽  
Satoshi Tanaka ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arteries ◽  
Systemic Arterial Pressure ◽  
Maximal Velocity ◽  
Clinical Models ◽  
A Cell ◽  
Induced Changes

To further examine the validity of the proposed concept of pulmonary blood flow-dependent CO2 gas excretion in the lungs, we investigated the effects of intramediastinal balloon catheterization-, pulmonary artery catheterization-, or isoprenaline (ISP)-induced changes in pulmonary blood flow on the end-expiratory CO2 gas pressure (PeCO2), the maximal velocity of the pulmonary artery (Max Vp), systemic arterial pressure, and heart rate of anesthetized rabbits. We also evaluated the changes in the PeCO2 in clinical models of anemia or pulmonary embolism. An almost linear relationship was detected between the PeCO2 and Max Vp. In an experiment in which small pulmonary arteries were subjected to stenosis, the PeCO2 fell rapidly, and the speed of the reduction was dependent on the degree of stenosis. ISP produced significant increases in the PeCO2 of the anesthetized rabbits. Conversely, treatment with piceatannol or acetazolamide induced significant reductions in the PeCO2. Treatment with a cell surface F1/FO ATP synthase antibody caused significant reductions in the PeCO2 itself and the ISP-induced increase in the PeCO2. Neither the PeCO2 nor SAP was significantly influenced by marked anemia [%hematocrit (Ht), 70∼47%]. On the other hand, in the presence of less severe anemia (%Ht: 100∼70%) both the PeCO2 and SAP fell significantly when the rabbits' blood viscosity was decreased. The rabbits in which pulmonary embolisms were induced demonstrated significantly reduced PeCO2 values, which was compatible with the lowering of their Max Vp. In conclusion, we reaffirm the validity of the proposed concept of CO2 gas exchange in the lungs.

Sodium hydrosulfide alleviates pulmonary artery collagen remodeling in rats with high pulmonary blood flow

2008 ◽  
Vol 23 (6) ◽  
pp. 409-419 ◽  
Author(s):  
Xiaohui Li ◽  
Junbao Du ◽  
Hongfang Jin ◽  
Bin Geng ◽  
Chaoshu Tang
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Sodium Hydrosulfide ◽  
Collagen Remodeling

scholarly journals Pulmonary artery size is associated with functional clinical status in the Fontan circulation

Heart ◽  
2019 ◽  
pp. heartjnl-2019-314972 ◽  
Author(s):  
Floris-Jan S Ridderbos ◽  
Bregje E Bonenkamp ◽  
Sophie L Meyer ◽  
Graziella Eshuis ◽  
Tjark Ebels ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Independent Predictor ◽  
Clinical Status ◽  
Fontan Circulation ◽  
Pulmonary Vasculature ◽  
Cross Sectional ◽  
Fontan Patients

ObjectiveIn the Fontan circulation, non-pulsatile pulmonary blood flow is suggested to negatively affect pulmonary artery growth. The pulmonary vasculature is regarded a key determinant of outcome after Fontan completion. We hypothesised that in Fontan patients pulmonary artery size correlates with follow-up and functional clinical status.MethodsThis is a single-centre, cross-sectional cohort study. Thirty-nine paediatric and adult Fontan patients with a concomitant cardiac magnetic resonance (CMR) scan and a cardiopulmonary exercise test between 2012 and 2013 were included. CMR-derived left and right pulmonary artery cross-sectional areas were expressed as Nakata index. Functional status was defined as peak oxygen consumption (pVO2) indexed for weight, as percentage of predicted (pred) and as New York Heart Association Functional Class (NYHA-FC).ResultsAge at CMR was 18±7.2 years. Time since Fontan completion was 11.9±7.4 years. Nakata index was lower versus the reference values (238.6±78.5 vs 330±30 mm2/m2, p<0.001). Nakata index correlated negatively with age at CMR (r=−0.393, p=0.013) and time since Fontan completion (r=−0.341, p=0.034). pVO2 was 27.9±8.9 mL/min/kg and pVO2pred was 58.1%±14.1%. Nakata index correlated positively with pVO2 (r=0.468, p=0.003) and pVO2pred (r=0.353, p=0.028). Nakata index correlated negatively with NYHA-FC (r=−0.450, p=0.004). Nakata index was an independent predictor (β=0.359, p=0.007) for pVO2 (adjusted R2=0.442, with maximum heart rate and oxygen pulse at peak exercise).ConclusionsPulmonary artery size expressed as Nakata index is a novel independent predictor for functional clinical status. Nakata index negatively correlated with follow-up duration, suggesting that chronic abnormal non-pulsatile pulmonary blood flow plays a role in lagging pulmonary arterial growth in the Fontan circulation.

Transposition of the great arteries {S,D,D} and absent proximal left pulmonary artery

1995 ◽  
Vol 5 (2) ◽  
pp. 199-201
Author(s):  
Dipak Kholwadwala ◽  
Vincent A. Parnell ◽  
Rubin S. Cooper
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Left Ventricular Outflow Tract ◽  
Pulmonary Arteries ◽  
Left Pulmonary Artery ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Left Ventricular Outflow ◽  
The Right

while preferential blood flow to the rightpulmonary artery has been described in transposition of the great arteries with or without obstruction of the left ventricular outflow tract, this disparity of pulmonary blood flow is not present in newborns.1We report a newborn with transposition in whom there was discontinuity of the pulmonary arteries and ductal blood supply to the left pulmonary artery. To our knowledge, this entity has not been described in newborns with transposition of the great arteries {S,D,D}.

scholarly journals A STUDY OF THE RELATION OF PULMONARY AND BRONCHIAL CIRCULATION

1913 ◽  
Vol 18 (5) ◽  
pp. 500-506 ◽  
Author(s):  
Albert A. Ghoreyeb ◽  
Howard T. Karsner
Keyword(s):  
Pulmonary Artery ◽  
Lung Tissue ◽  
Bronchial Artery ◽  
Venous Blood ◽  
Pulmonary Arteries ◽  
The Other ◽  
Main Trunk ◽  
Intimate Contact ◽  
Bronchial Arteries ◽  
Bronchial Circulation

The most striking point brought out in this study is that as long as a definite pressure is maintained in either the pulmonary or bronchial circulations, the admixture of bloods is extremely limited. It is easily conceivable that more mixture occurs normally than under the conditions of the experiment, but there is no reason for considering this to be a large difference. If, however, in either system the pressure sinks to zero the possibility of supply by the other system becomes evident. It takes much longer for the mass injected through the bronchial arteries to penetrate to all parts of the lung than when the mass is injected through the pulmonary artery; but when accomplished, the injection reaches to all capillaries including those of the pleura, the only vessels remaining uninjected being the larger trunks of the pulmonary artery. On the other hand, the injection of the bronchial vessels by way of the pulmonary arteries is not complete with normal pressure, but occurs rapidly when a high pulmonary pressure is employed. It is therefore probable that either circulation can suffice for the simple nutritive demands of the lung if the other system is interfered with. It has been shown that embolism of the pulmonary artery, without other circulatory disturbance, does not lead to necrosis of the affected area of the lung, but it is probable that the preservation of circulation is not due to collateral bronchial circulation so much as to the free anastomosis and early division into capillaries of the pulmonary artery. In support of this statement is the fact that the appearance is not altered when the bronchials are ligated at their origin. The same ligation shows no subsequent interference with the nutrition of the bronchi up to a period of five weeks, demonstrating that the pulmonary circulation is sufficient to provide for the nutrition of the bronchi. If, however, as Virchow has shown, the pulmonary artery supplying an entire lobe be occluded, the bronchial circulation can and does suffice for the nutrition of the lobe. In the case of the occlusion of a branch of the pulmonary artery the pressure in the area interfered with does not sink to zero because of the collateral circulation in this area; whereas, if the main trunk is occluded no collateral supply is available, the pressure sinks to zero, and the bronchial artery becomes available as a source of blood supply. It must be remembered that the lung tissue, as a whole, has ready access to oxygen and this gas is the nutritive element acquired by the blood in the lungs. From these studies it would appear that the part of the lung tissue not in intimate contact with oxygen in the air is supplied by oxygenated blood of the bronchial arteries, and that the tissues through which the pulmonary blood circulates take up whatever organized nutriment they need from the pulmonary blood and possibly provide for their oxygen and carbon dioxide interchange (which must be very slight) either directly with the alveolar air, or by finding sufficient oxygen in the venous blood of the pulmonary artery. The studies of the injected specimens confirm Küttner's findings of a very rapid breaking up of the pulmonary artery into capillaries. In all the specimens studied it was found that although the pleural vessels can be injected by way of the bronchial arteries when there is zero pressure in the pulmonary arteries, yet when the two sets of vessels are injected simultaneously in the dog, the pleural vessels invariably derive their supply of injection mass from the pulmonary artery.

scholarly journals Pulmonary Blood Flow Measurements Following Vena Cava-to-Pulmonary Artery Anastomosis

1973 ◽  
Vol 15 (2) ◽  
pp. 128-134 ◽  
Author(s):  
Francis Robicsek ◽  
Walter P. Scott ◽  
Norris B. Harbold ◽  
Harry K. Daugherty ◽  
Donald C. Mullen
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Vena Cava ◽  
Flow Measurements ◽  
Blood Flow Measurements

Dilatable Pulmonary Artery Banding Palliation in Congenital Heart Disease

2021 ◽  
Vol 12 (2) ◽  
pp. 213-219
Author(s):  
R. Allen Ligon ◽  
Larry A. Latson ◽  
Mark M. Ruzmetov ◽  
Kak-Chen Chan ◽  
Immanuel I. Turner ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Blood Flow ◽  
Heart Disease ◽  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Congenital Heart ◽  
Balloon Dilation ◽  
Retrospective Chart Review ◽  
Pulmonary Artery Banding ◽  
Surgical Removal

Background: Surgical pulmonary artery banding (PAB) has been limited in practice because of later requirement for surgical removal or adjustment. The aim of this study is to describe our experience creating a dilatable PAB via transcatheter balloon dilation (TCBD) in congenital heart disease (CHD) patients. Methods: Retrospective chart review of adjustable PAB—outline anatomical variants palliated and patient outcomes. Results: Sixteen patients underwent dilatable PAB—median age 52 days (range 4-215) and weight 3.12 kg (1.65-5.8). Seven (44%) of the patients were premature, 11 (69%) had ventricular septal defect(s) with pulmonary over-circulation, four (25%) atrioventricular septal defects, and four (25%) single ventricle physiology. Subsequent to the index procedure: five patients have undergone intracardiac complete repair, six patients remain well palliated with no additional intervention, and four single ventricles await their next palliation. One patient died from necrotizing enterocolitis (unrelated to PAB) and one patient required a pericardiocentesis postoperatively. Five patients underwent TCBD of the PAB without complication—Two had one TCBD, two had two TCBD, and another had three TCBD. The median change in saturation was 14% (complete range 6-22) and PAB diameter 1.7 mm (complete range 1.1-5.2). Median time from PAB to most recent outpatient follow-up was 868 days (interquartile range 190-1,079). Conclusions: Our institution has standardized a PAB technique that allows for transcatheter incremental increases in pulmonary blood flow over time. This methodology has proven safe and effective enough to supplant other institutional techniques of limiting pulmonary blood flow in most patients—allowing for interval growth or even serving as the definitive palliation.

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