Chronic airway infection leads to angiogenesis in the pulmonary circulation

Hopkins, Natalie; Cadogan, Elaine; Giles, Shay; McLoughlin, Paul

doi:10.1152/jappl.2001.91.2.919

Cited by 43 publications

(52 citation statements)

References 20 publications

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“…The left lung was isolated and fixed for morphometric examination as previously described (25,26). The extent of histologic lung damage was determined using quantitative stereological techniques by blinded assessors as previously described (27).…”

Section: In Vivo Experimental Ventilation-induced Alimentioning

confidence: 99%

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB–dependent mechanism

Contreras

Ansari

Curley

et al. 2012

Critical Care Medicine

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Section: In Vivo Experimental Ventilation-induced Alimentioning

confidence: 99%

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB–dependent mechanism

Contreras

Ansari

Curley

et al. 2012

Critical Care Medicine

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“…The point counting grid was used for volume density analysis. The relative wall thickness of each artery (VWT) was calculated by the formula: VWT5(Ro-Ri)/Ro [30]. Three sections of each mouse lung from five to six animals per group were analysed.…”

Section: Vessel Wall Thickness Measurementmentioning

confidence: 99%

Treprostinil inhibits the recruitment of bone marrow-derived circulating fibrocytes in chronic hypoxic pulmonary hypertension

Nikam

Schermuly²,

Dumitrascu³

et al. 2010

European Respiratory Journal

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A unique subpopulation of peripheral blood mononuclear cells that exhibit a parallel expression of haematopoietic and mesenchymal markers has been described as ''circulating fibrocytes''. These cells were demonstrated to obtain a fibroblastic phenotype in tissues or cell culture and contribute to pulmonary fibrotic disorders and tissue remodelling processes.The aim of our study was to characterise the recruitment of circulating fibrocytes in vivo in the model of chronic hypoxic pulmonary hypertension in mice and to analyse the therapeutic effect of the stable prostacyclin analogue trepostinil with respect to this cell population.To track circulating fibrocytes in vivo, we transplanted wild-type mice with bone marrow from ubiquitously eGFP expressing mice and subjected them to chronic hypoxia. We observed significantly increased recruitment of circulating fibrocytes to the remodelled pulmonary resistance arteries in response to hypoxia. Treatment with treprostinil significantly reduced the recruitment of these cells compared to normoxic mice. Treprostinil also reduced right ventricular systolic pressure and slightly reduced the vascular remodelling but failed to reverse the right ventricular hypertrophy.In summary, we show that circulating fibrocytes contribute to hypoxic pulmonary vascular remodelling and may be specifically targeted by a prostacyclin analogue. Further investigations of cellular and paracrine mechanisms are warranted to decipher their role in pulmonary hypertension.

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“…In adult dogs after pneumonectomy there is growth of new alveolar septa and alveolar capillaries in the residual left lung. 23 Schraufnagel et al have reported evidence of pulmonary angiogenesis in the rat lung after induction of biliary cirrhosis. 24 Schraufnagel has also suggested there is new vessel formation in the lungs of a patient with pulmonary venoocclusive disease.…”

mentioning

confidence: 99%

Vascular Remodeling Versus Vasoconstriction in Chronic Hypoxic Pulmonary Hypertension

Stenmark

McMurtry

2005

Circulation Research

118

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C hronic or sustained pulmonary hypertension is a complication of residence at high altitudes and chronic lung diseases such as chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, asthma, and sleep apnea. Alveolar hypoxia is an important (though probably not exclusive) contributor to the pulmonary hypertension observed in these conditions. Further, it is widely accepted that secondary hypoxic pulmonary hypertension is strongly associated with increased morbidity and reduced survival. 1,2 These facts have led to intense research efforts to identify the underlying mechanisms contributing to this condition, with the ultimate goal of identifying and developing novel therapeutic interventions. This work has relied heavily on the use of animal models, and one of the most commonly used is exposure of rats to chronic-hypoxic conditions by nitrogen dilution or hypobaria. Observations, predominately in this model, have led to the longstanding and widely accepted theory that chronic hypoxic pulmonary hypertension results from a combination of sustained vasoconstriction and vascular remodeling. It is generally believed that the contribution of vasoconstriction is greatest early in the disease process and that structural remodeling of the pulmonary vascular bed becomes progressively more important over time. That structural change is an important determinant of increased resistance and pressure in chronic pulmonary hypertension is supported by observations that over time of exposure to hypoxia, acute reexposure to normal or even high levels of inspired oxygen becomes progressively less effective in reducing the pulmonary arterial pressure. This lack of responsiveness to oxygen, or even to other pulmonary vasodilators such as Ca 2ϩ channel blockers, has led to the concept that chronic hypoxic pulmonary hypertension is associated with a "fixed" structural component responsible for the increased pulmonary vascular resistance. The structural changes thought to contribute to the increased vascular resistance have been broadly characterized into 2 processes: (1) inward remodeling of the pulmonary artery wall and (2) a reduction in the total number of small peripheral pulmonary arteries (a process referred to as rarefaction or pruning of the pulmonary vasculature).The work presented by Hyvel et al challenges, at least in certain ways, both of these concepts. 3 Pulmonary vascular remodeling refers to a process that causes thickening of the arterial wall and is thought to increase resistance by physical encroachment of the lumen of small peripheral pulmonary arteries and arterioles. Because intimal thickening is not usually observed in hypoxic pulmonary hypertension, this reduction in luminal area is believed to be attributable largely to constrictive medial and adventitial thickening. However, using different lung preparation techniques than have been used in most other hypoxic studies (ie, the pulmonary vasculature was "maximally" vasodilated by perfusion with calcium-free plus EGTA physiological saline solution...

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Chronic airway infection leads to angiogenesis in the pulmonary circulation

Cited by 43 publications

References 20 publications

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB–dependent mechanism

Hypercapnic acidosis attenuates ventilation-induced lung injury by a nuclear factor-κB–dependent mechanism

Treprostinil inhibits the recruitment of bone marrow-derived circulating fibrocytes in chronic hypoxic pulmonary hypertension

Vascular Remodeling Versus Vasoconstriction in Chronic Hypoxic Pulmonary Hypertension

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