Comparison of bronchopulmonary collaterals and collateral blood flow in patients with chronic thromboembolic and primary pulmonary hypertension.

Endrys, J; Hayat, Nasser; Cherian, G

doi:10.1136/hrt.78.2.171

Cited by 90 publications

(87 citation statements)

References 20 publications

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“…In a rat model of chronic pulmonary artery obstruction, Weibel (28) used a histological approach and documented proliferative changes in bronchial blood vessels with patent new vessels evident by 10 -40 days after LPAL. Furthermore, these results suggested that the response to pulmonary ischemia in the rat more closely resembles bronchial neovascularization in human subjects after pulmonary artery obstruction (6,18). Therefore, the goals of the present study were to confirm the earlier work of Weibel in a rat model of chronic pulmonary ischemia and provide a three-dimensional visualization and functional assessment of the patency of the neovasculature.…”

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confidence: 66%

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Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung

Sukkar¹,

Jenkins²,

Sánchez³

et al. 2008

Journal of Applied Physiology

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. Inhibition of CXCR 2 attenuates bronchial angiogenesis in the ischemic rat lung. J Appl Physiol 104: 1470-1475, 2008. First published March 6, 2008 doi:10.1152/japplphysiol.00974.2007.-Under conditions of chronic pulmonary ischemia, the bronchial circulation undergoes massive proliferation. However, little is known regarding the mechanisms that promote neovascularization. An expanding body of literature implicates the glutamic acid-leucine-arginine (ELRϩ) CXC chemokines and their G protein-coupled receptor, CXCR 2, as key proangiogenic components in the lung. We used a rat model of chronic pulmonary ischemia induced by left pulmonary artery ligation (LPAL) to study bronchial angiogenesis. Using a methacrylate mixture, we cast the systemic vasculature of the rat lung at weekly intervals after LPAL. Twenty-one days after LPAL, numerous large, tortuous bronchial arteries were observed surrounding the left main bronchus that penetrated the left lung parenchyma. In stark contrast, the right lung was essentially devoid of vessels. We quantified bronchial neovascularization using 15-m radiolabeled microspheres to measure systemic blood flow to the left lung (n ϭ 12 rats). Results showed that by 21 days after LPAL, bronchial blood flow to the ischemic left lung had increased Ͼ10-fold compared with controls 2 days after LPAL (P Ͻ 0.01). Focusing on the predominant rat CXC chemokine that signals through CXCR 2, we measured increased levels of cytokine-induced neutrophil chemoattractant-3 protein expression in left lung homogenates early (4 and 24 h; n ϭ 10 rats) after LPAL relative to paired right lung controls (P Ͻ 0.01). Treatment with a neutralizing antibody to CXCR 2 resulted in a significant decrease in neovascularization 21 days after LPAL (n ϭ 9 rats; P Ͻ 0.01). Our results confirm the time course of bronchial angiogenesis in the rat and suggest the importance of CXC chemokines in promoting systemic neovascularization in the lung. bronchial artery; cytokine-induced neutrophil chemoattractant-3; microspheres THE BRONCHIAL CIRCULATION is the systemic vascular supply to the lung and provides nutrient blood flow to conducting airways down to the level of the terminal bronchioles as well as nerves, lymph nodes, visceral pleura, and walls of large pulmonary vessels. It normally provides less than 1% of cardiac output to the lung but has been shown to increase to as much as 30% of the original pulmonary blood flow after chronic unilateral pulmonary artery obstruction (13). This pathological feature of bronchial angiogenesis occurs during conditions of chronic inflammation such as cystic fibrosis (4), asthma (12), pulmonary fibrosis (27), lung cancer (16), and chronic thromboembolic disease (18). In animal models, pulmonary ischemia resulting from chronic pulmonary artery obstruction has been shown to cause proliferation of the systemic circulation to the lung in sheep (5), pigs (8), dogs (13), rats (28), and mice (14). However, little is known regarding the mechanisms that promote growth of bronchial arteries in chroni...

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confidence: 66%

“…Pulmonary arterial obstruction can lead to abnormalities in gas exchange, to inflammation of lung tissue, and in cases of chronic thromboembolic disease to angiogenesis of systemic bronchial vessels to the ischemic lung (6,18). Models of chronic pulmonary thromboembolism have been developed in a variety of animals.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung

Sukkar¹,

Jenkins²,

Sánchez³

et al. 2008

Journal of Applied Physiology

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“…In human disease, as well as in animal models, obstruction of the pulmonary vasculature results in rapid and sustained systemic neovascularization of the lung (4,6,7,10,18). Both bronchial and intercostal arteries participate by proliferating and perfusing lung vascular networks.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary ischemia induces lung remodeling and angiogenesis

Wagner

Petrache

Schofield

et al. 2006

Journal of Applied Physiology

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Mitzner. Pulmonary ischemia induces lung remodeling and angiogenesis. J Appl Physiol 100: 587-593, 2006. First published October 6, 2005 doi:10.1152/japplphysiol.00029.2005.-Cellular remodeling during angiogenesis in the lung is poorly described. Furthermore, it is the systemic vasculature of the lung and surrounding the lung that is proangiogenic when the pulmonary circulation becomes impaired. In a mouse model of chronic pulmonary thromboembolism, after left pulmonary artery ligation (LPAL), the intercostal vasculature, in proximity to the ischemic lung, proliferates and invades the lung (12). In the present study, we performed a detailed investigation of the kinetics of remodeling using histological sections of the left lung of C57Bl/6J mice after LPAL (4 h to 20 days) or after sham surgery. New vessels were seen within the thickened visceral pleura 4 days after LPAL predominantly in the upper portion of the left lung. Connections between new vessels within the pleura and pulmonary capillaries were clearly discerned by 7 days after LPAL. The visceral pleura and the lung parenchyma showed intense tissue remodeling, as evidenced by markedly elevated levels of both proliferating cell nuclear antigen and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling positive cells. Rapidly dividing cells were predominantly macrophages and type II pneumocytes. The increased apoptotic activity was further quantified by caspase-3 activity, which showed a sixfold increase relative to naive lungs, by 24 h after LPAL. Because sham surgeries had little effect on measured parameters, we conclude that both thoracic wound healing and pulmonary ischemia are required for systemic neovascularization.histology; apoptosis; caspase-3 THE PROCESS OF NEW VESSEL growth induced by tissue ischemia requires an orchestrated series of local cellular events. New vessel formation follows an organized progression of changes, including matrix dissolution, cell migration, and proliferation (3). Pulmonary ischemia resulting from chronic pulmonary embolism or other forms of pulmonary artery obstruction lead to proliferation of the systemic circulation within and surrounding the lung (4,7,8,18). The bronchial and intercostal vasculatures respond to pulmonary ischemia due to pulmonary artery obstruction with rapid neovascularization. It is interesting to note that the pulmonary vasculature appears not to be responsive in this setting. In general, the pulmonary artery is not proangiogenic, except in rare circumstances, as a secondary source of perfusion in some lung carcinomas (11). Unlike other organs, the lung is unique in that pulmonary ischemia is not accompanied by tissue hypoxia. Our laboratory previously developed a mouse model of lung angiogenesis and quantified new systemic perfusion of the lung following left pulmonary artery ligation (LPAL) (12). Rapid neovascularization occurs, and systemic perfusion of the lung can be measured 5 days after pulmonary artery ligation. However, unlike most other species, new vessel growth appear...

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“…In fact, systemic collateral arterial flow volume can easily be calculated by subtracting the pulmonary arterial flow volume from the pulmonary venous flow volume (Qspa ϭ Qpv Ϫ Qpa). Accurate measurement of systemic collateral flow to the lungs is also useful in differentiating secondary from primary pulmonary hypertension (16,18,19).…”

Section: Clinical Applications Of Mr Quantification Of Pulmonary Venomentioning

confidence: 99%

Phase‐contrast magnetic resonance quantification of normal pulmonary venous return

Goo

Alotay

Grosse-Wortmann

et al. 2009

Magnetic Resonance Imaging

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Purpose:To assess the feasibility of phase-contrast magnetic resonance (PCMR) in quantifying the pulmonary venous return in normal subjects. Materials and Methods:PCMR was performed in 12 healthy adult volunteers (mean age 38 years, range 27-60 years; 9 men; body surface area 1.81 Ϯ 0.15 m 2 ) for the ascending and descending aorta, caval veins, main and branch pulmonary arteries, and pulmonary veins. Two readers independently quantified blood flow in all subjects.Results: Intraobserver differences were Ϫ2.0% (95% confidence interval [CI]: Ϫ9.9% to 5.9%), Ϫ4.5% (95% CI: Ϫ15.6% to 6.5%), and Ϫ0.7% (95% CI: Ϫ4.5% to 3.0%) for all vessels, pulmonary veins, and other great vessels, respectively. Interobserver differences were Ϫ2.0% (95% CI: Ϫ10.6% to 6.6%), Ϫ3.1% (95% CI: Ϫ16.0% to 9.9%), and Ϫ1.4% (95% CI: Ϫ6.4% to 3.5%) for all vessels, pulmonary veins, and other great vessels, respectively. Pulmonary venous flow volume showed high correlations with the volumes of the pulmonary arterial flow, systemic arterial flow, and systemic venous flow (r ϭ 0.76 -0.92, P Ͻ 0.005). Conclusion:Flow quantification of normal pulmonary venous return using PCMR is feasible with high reproducibility and accuracy. FLOW QUANTIFICATION using the phase-contrast (or velocity-encoded) technique is a central part of comprehensive cardiac magnetic resonance (MR) imaging for congenital heart disease in children and adults. Phasecontrast MR imaging (PCMR) has been validated as accurate in evaluating velocity, volume, and pattern of pulsatile blood flow (1-5). Flow measurements using PCMR have been used at various great vessels, including the aorta, the pulmonary artery, and the superior and inferior vena cavae, in various clinical settings (6 -10). In contrast, feasibility of flow quantification of the pulmonary veins using PCMR has not been evaluated. As in systemic circulation, information on pulmonary venous flow in addition to pulmonary arterial flow is crucial for the full understanding of pulmonary circulation.Measurement of pulmonary venous flow is important in the following clinical scenarios: direct measurement of systemic collateral arterial flow to the lung; shunting involving the pulmonary vein; and alternative measurement of pulmonary arterial flow when it is not available for any reason. Attention with regard to evaluation of pulmonary vein abnormalities after radiofrequency ablation has also increased recently. However, it is very difficult to provide accurate quantification of pulmonary venous flow when using echocardiography and the catheter technique. This fact motivated our study because noninvasive PCMR has great potential in offering such pulmonary venous flow data. A few clinical studies have demonstrated the usefulness of quantification of pulmonary venous flow volume with PCMR in patients with anomalous pulmonary venous connection, stenotic pulmonary artery with or without a stent, and systemic collateral arteries supplying the lungs (11-13). The amount of systemic collateral arterial supply to the lungs can be calcula...

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Comparison of bronchopulmonary collaterals and collateral blood flow in patients with chronic thromboembolic and primary pulmonary hypertension.

Cited by 90 publications

References 20 publications

Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung

Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung

Pulmonary ischemia induces lung remodeling and angiogenesis

Phase‐contrast magnetic resonance quantification of normal pulmonary venous return

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Comparison of bronchopulmonary collaterals and collateral blood flow in patients with chronic thromboembolic and primary pulmonary hypertension.

Cited by 90 publications

References 20 publications

Inhibition of CXCR2attenuates bronchial angiogenesis in the ischemic rat lung

Inhibition of CXCR2attenuates bronchial angiogenesis in the ischemic rat lung

Pulmonary ischemia induces lung remodeling and angiogenesis

Phase‐contrast magnetic resonance quantification of normal pulmonary venous return

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Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung

Inhibition of CXCR₂attenuates bronchial angiogenesis in the ischemic rat lung