Adult Case of Ductus arteriosus Aneurysm Complicated with Left Pulmonary Artery Obstruction

1994 ◽  
Vol 8 (2) ◽  
pp. 109-111
Author(s):  
Yasushi Sunaga ◽  
Kayo Hayashi ◽  
Tetsuro Sugiura ◽  
Nobuyuki Tsuda ◽  
Torn Seki ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Ductus Arteriosus ◽  
Left Pulmonary Artery ◽  
Adult Case ◽  
Ductus Arteriosus Aneurysm ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction

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 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.

Giant Left Atrium as Cause of Left Pulmonary Artery Obstruction

1987 ◽  
Vol 43 (3) ◽  
pp. 329-331 ◽  
Author(s):  
A. Jorge S. Serra ◽  
Kathleen W. McNicholas ◽  
Gerald M. Lemole
Keyword(s):  
Pulmonary Artery ◽  
Left Atrium ◽  
Left Pulmonary Artery ◽  
Giant Left Atrium ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction

scholarly journals Juxtaductal left pulmonary artery obstruction in pulmonary atresia.

Heart ◽  
1986 ◽  
Vol 55 (1) ◽  
pp. 39-44 ◽  
Author(s):  
K Momma ◽  
A Takao ◽  
M Ando ◽  
M Nakazawa ◽  
G Satomi ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Atresia ◽  
Left Pulmonary Artery ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction
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