Loss of Left Lung Function Following Surgical Correction of Aberrant Left Pulmonary Artery

CHEST Journal ◽  
1975 ◽  
Vol 68 (1) ◽  
pp. 129-130 ◽  
Author(s):  
Robert M. Sade
Keyword(s):  
Lung Function ◽  
Pulmonary Artery ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Surgical Correction

scholarly journals Transcatheter stenting of arterial duct in duct-dependent congenital heart disease

2013 ◽  
Vol 141 (11-12) ◽  
pp. 803-806
Author(s):  
Milan Djukic ◽  
Tamara Ilisic ◽  
Igor Stefanovic ◽  
Marija Gradinac ◽  
Irena Vulicevic ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Ductus Arteriosus ◽  
Arterial Oxygen Saturation ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Surgical Correction ◽  
Arterial Oxygen ◽  
Arterial Duct

Introduction. Critical congenital heart diseases (CHD) are mostly duct-dependent and require stable systemic-pulmonary communication. In order to maintain patency of the ductus arteriosus (DA), the first line treatment is Prostaglandin E1 and the second step is the surgical creation of aortic-pulmonary shunt. To reduce surgical risk in neonates with the critical CHD, transcatheter stenting of DA can be performed in selected cases. Case Outline. A four-month old infant was diagnosed with the pulmonary artery atresia with ventricular septal defect (PAA/VSD). The left pulmonary artery was perfused from DA, and the right lung through three major aortopulmonary collaterals (MAPCAs). A coronary stent was placed in the long and critically stenotic DA, with final arterial duct diameter of 3.5 mm, and significantly increased blood supply to the left lung. After the procedure, the infant?s status was improved with regard to arterial oxygen saturation, feeding and weight gain. During the follow-up, one year later, aortography revealed in-stent stenosis. The left pulmonary artery, as well as the branches, was well-developed and the decision was made to proceed with further surgical correction. Conclusion. Stenting of DA can be an effective alternative to primary surgical correction in selected patients with duct-dependent CHD.

Unintended Pulmonary Artery Ligation during PDA Ligation

2016 ◽  
Vol 19 (4) ◽  
pp. 187 ◽  
Author(s):  
Dohun Kim ◽  
Si-Wook Kim ◽  
Hong-Ju Shin ◽  
Jong-Myeon Hong ◽  
Ji Hyuk Lee ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Ductus Arteriosus ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Chest Ct ◽  
Mechanical Ventilator ◽  
Artery Ligation ◽  
Ventilator Support ◽  
Surgical Ligation ◽  
Emergent Operation

A 10-day-old boy was transferred to our hospital due to tachypnea. Patent ductus arteriosus (PDA), 4.8 mm in diameter, with small ASD was diagnosed on echocardiography. Surgical ligation of the ductus was performed after failure of three cycles of ibuprofen. However, the ductus remained open on routine postoperative echocardiography on the second postoperative day, and chest CT revealed inadvertent ligation of the left pulmonary artery (LPA) rather than the PDA. Emergent operation successfully reopened the clipped LPA and ligated the ductus on the same (second postoperative) day.<br />Mechanical ventilator support was weaned on postoperative day 21, and the baby was discharged on postoperative day 47 with a normal left lung shadow.

Abstract 12430: Vicious Circle Between Progressive Right Ventricular Dilatation and Pulmonary Regurgitation in Patients After Tetralogy of Fallot Repair? Right Heart Enlargement Promotes Flow Reversal in the Left Pulmonary Artery

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Atsuko Kato ◽  
Christian Drolet ◽  
Shi-Joon Yoo ◽  
Andrew Redington ◽  
Lars Grosse-Wortmann
Keyword(s):  
Pulmonary Artery ◽  
Tetralogy Of Fallot ◽  
Left Lung ◽  
Pulmonary Regurgitation ◽  
Left Pulmonary Artery ◽  
Flow Reversal ◽  
Left Hemithorax ◽  
Forward Flow ◽  
Lung Area ◽  
The Right

Introduction: The left pulmonary artery (LPA) contributes more than the right (RPA) to total pulmonary regurgitation (PR) in patients after tetralogy of Fallot (TOF) repair, but the mechanism of this difference is not well known. We hypothesized that unilaterally increased pulmonary vascular resistance (PVR), resulting from lung compression by the enlarged and levorotated heart leads to greater PR in the LPA. This study aimed to analyze the interplay between heart and lung size, mediastinal geometry, and differential PR. Methods: This is a single-center retrospective analysis of 50 magnetic resonance studies in patients after TOF repair. Patients with more than mild discrete branch pulmonary artery stenosis were excluded. Blood flow was measured by phase-contrast velocity encoding within the branch pulmonary arteries. On the axial image with the largest total cardiac surface area, cardiac angle (α) between the thoracic anterior-posterior line and the interventricular septum, right and left lung areas as well as right and left hemithorax areas were measured (Figure). Results: There was no difference in LPA and RPA diameters. The LPA showed significantly less total forward flow (p=0.04), smaller net forward flow (p=<0.001), and greater RF (p=0.001) than the RPA. Left lung area was smaller than the right (p<0.001). RVEDVi correlated with LPA RF (R=0.48, p<0.001), but not with RPA RF. Larger RVEDVi correlated with a larger α angle (R=0.46, p<0.001), i.e. a more leftward cardiac axis and with smaller left lung area (R=-0.58, p<0.001). LPA RF, but not RPA RF, correlated inversely with left lung area indexed to the left hemithorax area (R=-0.34, p=0.02). Conclusions: An enlarged and levorotated heart - as a result of PR - is associated with smaller left lung size, and augments diastolic flow reversal in the LPA, presumably via increased left PVR. By imposing a further volume load on the RV, LPA regurgitation may thus close a positive feed-back loop of PR and RV dilatation.

Effect of pulmonary artery occlusion and reperfusion on extravascular fluid accumulation

1981 ◽  
Vol 50 (1) ◽  
pp. 102-106 ◽  
Author(s):  
P. S. Barie ◽  
T. S. Hakim ◽  
A. B. Malik
Keyword(s):  
Pulmonary Artery ◽  
Water Content ◽  
Left Atrial ◽  
Left Lung ◽  
Weight Ratio ◽  
Dry Weight ◽  
Left Pulmonary Artery ◽  
Artery Occlusion ◽  
Lung Water ◽  
The Right

We determined the effect of pulmonary hypoperfusion on extravascular water accumulation in anesthetized dogs by occluding the left pulmonary artery for 3 h and then reperfusing it for 24 h. The lung was reperfused either at normal left atrial pressure (Pla) or during increased Pla induced by a left atrial balloon. In each case the extravascular water content-to-bloodless dry weight ratio (W/D) of the left lung was compared with that of the right lung. The W/D of the left lung of 3.26 +/- 0.49 ml/g was not significantly different from the value of 2.87 +/- 0.37 for the right lung after the reperfusion at normal Pla. However, the W/D of the left lung of 5.10 +/- 0.38 ml/g was greater (P less than 0.05) than the value of 4.42 +/- 0.34 for the right lung after reperfusion at Pla of 25 Torr. This difference could not be prevented by pretreatment with heparin, suggesting that the increase in lung water content was not due to activation of intravascular coagulation secondary to stasis occurring during the occlusion. Because the left lung was more edematous than the right one, even though both lungs had been subjected to the same increase in Pla, the results suggest that a period of pulmonary hypoperfusion causes an increase in the interstitial protein concentration.

scholarly journals The role of CXCR2 in systemic neovascularization of the mouse lung

2007 ◽  
Vol 103 (2) ◽  
pp. 594-599 ◽  
Author(s):  
Jesús Sánchez ◽  
Aigul Moldobaeva ◽  
Jessica McClintock ◽  
John Jenkins ◽  
Elizabeth Wagner
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Left Lung ◽  
Neutralizing Antibody ◽  
Left Pulmonary Artery ◽  
Endothelial Cell Proliferation ◽  
Antibody Treatment ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction ◽  
Deficient Mice

We previously showed increased expression of the ELR+, CXC chemokines in the lung after left pulmonary artery obstruction. These chemokines have been shown in other systems to bind their G protein-coupled receptor, CXCR2, and promote systemic endothelial cell proliferation, migration, and capillary tube formation. In the present study, we blocked CXCR2 in vivo using a neutralizing antibody and also studied mice that were homozygous null for CXCR2. To estimate the extent of neovascularization in this model, we measured systemic blood flow to the left lung 14 days after left pulmonary artery ligation (LPAL). We found blood flow significantly reduced (67% decrease) with neutralizing antibody treatment compared with controls. However, blood flow was not altered in the CXCR2-deficient mice compared with wild-type controls after LPAL. To test for ligand availability, we measured macrophage inflammatory protein (MIP)-2 in lung homogenates after LPAL, because this is the predominant CXC chemokine previously shown to be increased after LPAL ( 22 ). MIP-2 protein was two- to fourfold higher in the left lung relative to the right lung in all treatment groups 4 h after LPAL and this increase did not differ among groups. We speculate that the CXCR2-deficient mice have compensatory mechanisms that mitigate their lack of gene expression and conclude that CXCR2 contributes to chemokine-induced systemic angiogenesis after pulmonary artery obstruction.

scholarly journals Left Lung and Pulmonary Artery Hypoplasia: A Rare Case of Hemoptysis

2020 ◽  
Author(s):  
Guiomar Pinheiro ◽  
Ana Margarida Alves ◽  
Isabel Neves ◽  
Teresa Sequeira
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Hypoplasia ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Pulmonary Infections ◽  
Rare Congenital Disorder ◽  
History Of ◽  
Pulmonary Artery Hypoplasia

Pulmonary hypoplasia or agenesis is a rare congenital disorder that results in lung underdevelopment. This disease is usually found in children but rarely encountered in adults. We describe the case of an 84-year-old woman diagnosed with a unilateral pulmonary hypoplasia presenting simultaneously with left pulmonary artery hypoplasia. Due to this condition, the patient had a lifelong history of pulmonary infections that resulted in several bronchiectases in the affected lung. Moreover, the pulmonary artery hypoplasia led to the development of pulmonary hypertension and collateral circulation causing hemoptysis, giving rise to the patient attending the emergency department. Although we were able to medically manage the hemoptysis, it can be fatal and require surgical intervention. Hence, an early diagnosis is essential so that appropriate follow-up and prompt prevention and treatment of complications, such as pulmonary infections, hemoptysis and pulmonary hypertension, are achieved.

scholarly journals Role of ROS in ischemia-induced lung angiogenesis

2010 ◽  
Vol 299 (4) ◽  
pp. L535-L541 ◽  
Author(s):  
Julie Nijmeh ◽  
Aigul Moldobaeva ◽  
Elizabeth M. Wagner
Keyword(s):  
Pulmonary Artery ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Wild Type ◽  
Systemic Blood Flow ◽  
Artery Ligation ◽  
Underlying Mechanisms ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction

Pulmonary artery obstruction and subsequent lung ischemia have been shown to induce systemic angiogenesis despite preservation of normoxia. The underlying mechanisms, however, remain poorly understood. In a mouse model of lung ischemia induced by left pulmonary artery ligation (LPAL), we showed previously, the formation of a new systemic vasculature to the ischemic lung. We hypothesize that LPAL in the mouse increases reactive oxygen species (ROS) production, and these molecules play an initiating role in subsequent lung neovascularization. We used oxidant-sensitive dyes (DHE and H2DCF-DA) to quantify ROS and measured the antioxidant-reduced glutathione (GSH) and its oxidized form (GSSG) as indicators of ROS levels after LPAL. The magnitude of systemic neovascularization was determined by measuring systemic blood flow to the left lung with radiolabeled microspheres 14 days after LPAL. An increase in ROS was observed early (30 min: 55% increase in H2DCF-DA) after LPAL, with a return to baseline by 24 h. GSH/GSSG was decreased (∼50%) 4 h after LPAL, suggesting earlier ROS upregulation. Mice treated with the antioxidant N-acetylcysteine showed attenuated angiogenesis (62% of wild-type LPAL), and mice lacking Nrf2, a transcription factor important for antioxidant synthesis, resulted in increased neovascularization (207% of wild-type LPAL). Overall, GSH/GSSG was inversely associated with the magnitude of neovascularization. These results demonstrate that LPAL induces an early and transient ROS upregulation, and ROS appear to play a role in promoting ischemia-induced angiogenesis.

Microvascular injury distal to unilateral pulmonary artery occlusion

1981 ◽  
Vol 51 (4) ◽  
pp. 845-851 ◽  
Author(s):  
R. L. Johnson ◽  
S. S. Cassidy ◽  
M. Haynes ◽  
R. L. Reynolds ◽  
W. Schulz
Keyword(s):  
Pulmonary Artery ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Artery Occlusion ◽  
Diffusing Capacity ◽  
Pulmonary Capillary Blood Flow ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Blood ◽  
Rebreathing Method ◽  
Unilateral Pulmonary Artery Occlusion

We explored three questions: 1) does edema fluid accumulate distal to temporary unilateral pulmonary artery occlusion (TUPAO); 2) if so how rapidly does it accumulate; and 3) how is it affected by positive end-expiratory pressure (PEEP)? Using a tracheal divider we measured pulmonary capillary blood flow (Qc), tissue volume (Vt), and diffusing capacity (DLCO) in each lung with a rebreathing method. After control measurements in 12 dogs, the left pulmonary artery was occluded and measurements were repeated at intervals during 4 h of occlusion and 30 min after release of the occlusion. Six of the dogs were ventilated with 10 cmH2O PEEP. Finally the lungs were removed, weighed, and fixed for histology. TUPAO caused a 29% increase in Vt of the left lung without PEEP and a 59% increase with PEEP. After release of the occlusion, Qc and DLCO in the left lung returned to control levels within 30 min in dogs not on PEEP but remained depressed in dogs ventilated with PEEP even though PEEP was removed. At postmortem the left lung weighed more than expected in both groups of dogs but was significantly heavier in those on PEEP. Histology confirmed bronchovascular cuffing with edema and hemorrhage.

Pulmonary hypertension and arterial changes in calves with a systemic-to-left pulmonary artery connection

1994 ◽  
Vol 77 (2) ◽  
pp. 867-875 ◽  
Author(s):  
J. W. Fasules ◽  
F. Tryka ◽  
C. W. Chipman ◽  
S. H. Van Devanter
Keyword(s):  
Pulmonary Artery ◽  
Structural Changes ◽  
Heart Defects ◽  
Left Lung ◽  
Left Pulmonary Artery ◽  
Pulmonary Vascular Disease ◽  
Vascular Changes ◽  
Small Vessels ◽  
Arteriolar Diameter ◽  
Increased Pressure

The pathogenic mechanisms by which increased pressure and flow lead to pulmonary vascular disease are poorly understood, especially in newborns. To study the pathophysiological correlations and timing of the development of structural changes in response to high flow in nonhypoxic neonates, a model of high pulmonary flow was developed in newborn calves by anastomosis of the isolated left pulmonary artery (LPA) to the aorta. LPA pressure and flow increased acutely. LPA pressure reached near-systemic levels by 10 wk, whereas LPA flow was maximally increased at 1 mo before decreasing in several calves. Right pulmonary arterial pressure remained normal, and ventricular hypertrophy did not develop. Morphometric evaluation of the left lung demonstrated decreased arteriolar diameter, increased medial thickness, muscularization of arterioles at the bronchoalveolar junction, luminal obliteration of small arteries, and dilation lesions. The LPA pressure and vascular changes were greater and developed over a shorter time period than did prior models of nonhypoxic flow-induced pulmonary vascular changes. Lesser degrees of decreased arteriolar diameter and muscularization of small vessels were seen in the right lung, indicating a difference in the vascular response to moderately increased flow vs. increased pressure and flow. Thus, calves with an isolated LPA-to-aortic anastomosis simulate the hemodynamic and pulmonary vascular changes seen in newborns with congenital heart defects. Such calves may serve as models to assess effects of mechanical stresses on a newborn's vasculature.

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