Early Reperfusion Induces Alveolar Injury in Pulmonary Embolism

Fukahori, Masami; Murata, Tetsuya; Mohammed, Minhaz Uddin; Fukuyama, Naoto; Nakazawa, Hiroe

doi:10.1378/chest.111.1.198

Cited by 6 publications

(4 citation statements)

References 13 publications

(2 reference statements)

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“…Our data emphasize the importance of rapid diagnosis and shows the basis for aggressive treatment to ameliorate pulmonary vascular obstruction as quickly as possible to forestall the rapid expression in proinflammatory genes. The action of the chemokines on neutrophil trafficking may exacerbate injury, known to occur during reperfusion with treatment for PEm (63,64). Blockade of the induction of gene expression, or the synthesis or action of chemokines might help reduce injury from PEm and from reperfusion after PEm.…”

Section: Discussionmentioning

confidence: 99%

Chemokines Accumulate in the Lungs of Rats with Severe Pulmonary Embolism Induced by Polystyrene Microspheres

Zagorski

Debelak

Gellar

et al. 2003

The Journal of Immunology

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Pulmonary thromboembolism (PEm) is a serious and life threatening disease and the most common cause of acute pulmonary vascular occlusion. Even following successful treatment of PEm, many patients experience long-term disability due to diminished heart and lung function. Considerable damage to the lungs presumably occurs due to reperfusion injury following anti-occlusive treatments for PEm and the resulting chronic inflammatory state in the lung vasculature. We have used a rat model of irreversible PEm to ask whether pulmonary vascular occlusion in the absence of reperfusion is itself sufficient to induce an inflammatory response in lungs. By adjusting the severity of the vascular occlusion, we were able to generate hypertensive and nonhypertensive PEm, and then examine lung tissue for expression of CXC and C-C chemokine genes and bronchoalveolar lavage (BAL) fluid for the presence of chemokine proteins. Hypertensive and nonhypertensive PEm resulted in increased expression of both CXC and C-C chemokines genes in lung tissues. Hypertensive PEm was also associated with a 50–100-fold increase in protein content in lung BAL fluid, which included the CXC chemokines cytokine-induced neutrophil chemoattractant and macrophage-inflammatory protein 2. The presence of chemokines in BALs was reflected by a potent neutrophil chemotactic activity in in vitro chemotaxis assays. Abs to cytokine-induced neutrophil chemoattractant blocked the in vitro neutrophil chemotactic activity of BAL by 44%. Our results indicate that the ischemia and hypertension associated with PEm are sufficient to induce expression of proinflammatory mediators such as chemokines, and establish a proinflammatory environment in the ischemic lung even before reperfusion.

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Section: Discussionmentioning

confidence: 99%

Chemokines Accumulate in the Lungs of Rats with Severe Pulmonary Embolism Induced by Polystyrene Microspheres

Zagorski

Debelak

Gellar

et al. 2003

The Journal of Immunology

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“…Reperfusion of the ischemic lung tissue triggers migration of polymorphonuclear cells to alveoli, which results in the increased generation of reactive oxygen species (ROS) [17]. The main source of ROS in the lungs is activated phagocytes that are markedly increased in the BAL fluid in patients with PTE [7].…”

Section: Mechanisms Of Surfactant Alterationsmentioning

confidence: 99%

Lung surfactant alterations in pulmonary thromboembolism

Čalkovská¹,

Mokrá²,

Calkovský³

2009

Eur J Med Res

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Beside neonatal respiratory distress syndrome, secondary surfactant deficiency may occur in patients with mature lungs. Recent studies revealed quantitative and qualitative changes of lung surfactant in pulmonary thromboembolism (PTE) concerning the total phospholipids content in BAL fluid, alterations in surfactant phospholipids classes and a large-to-small aggregates ratio. Reduced expression of surfactant protein A (SP-A) mRNA and SP-A in lung tissue after pulmonary embolism was found. Serum levels of SP-A were significantly higher in patients with PTE than in other lung diseases, except COPD. Surfactant changes in PTE may result from damage of type II cells by hypoxia, leakage of plasma proteins into the airspaces and/or by reactive oxygen species. They can contribute to lung atelectasis and edema, and a further reduction in oxygen saturation as seen in clinical picture of PTE. Surfactant changes are reliable marker of lung injury that might become a prognostic indicator in patients with pulmonary thromboembolism.

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“…Another potential mechanism underlying the decreased phospholipid concentration may be the resolution of the thrombus and reperfusion of occluded lung tissue [144]. …”

Section: Postembolic Pulmonary Inflammationmentioning

confidence: 99%

Principle Mechanisms Underlying Venous Thromboembolism: Epidemiology, Risk Factors, Pathophysiology and Pathogenesis

Kroegel

Reißig²

2003

Respiration

151

102

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Deep vein thrombosis (DVT) and pulmonary embolism (PE) are distinct but related aspects of the same dynamic disease process known as venous thromboembolism (VTE). An estimated 200,000 new cases occur in the United States every year, including 94,000 with PE, resulting in an incidence of 23 per 100,000 patients per year-cases. Without treatment, pulmonary embolism is associated with a mortality rate of approximately 30%, causing nearly 50,000 deaths per year. Moreover, based on post-mortem studies, two-thirds of the patients with pulmonary emboli remain undiagnosed. Clinically, PE may present as (1) isolated dyspnea, (2) pleuritic pain and/or hemoptysis, and (3) circulatory collapse. However, clinical history and examination can be notoriously misleading in reaching a diagnosis. A number of acquired etiologic risk factors (predispositions) are associated with a tendency to develop VTE. These include increasing age, immobilization, surgery, trauma, hospital or nursing home confinement, malignancy, neurologic disease with extremity paresis, as well as certain types of oral contraception and hormone replacement therapy. In addition, a variety of genetic risk factors, such as factor V Leiden, protein S or C deficiency have also been identified. However, in at least half of the instances, no predisposing factors can be identified (idiopathic PE). In the majority of cases thromboemboli originate in the deep veins of the calf or pelvis. The pathogenic conditions for VTE comprise a triad of factors and include (1) venous stasis, (2) hypercoagulable states, and (3) vascular endothelium injury. Occlusion of pulmonary arteries has variable and transient clinical and pathophysiologic consequences, involving both mechanical and reflex effects of vascular occlusion with a consecutive perfusion defect as well as the release of vasoactive and other inflammatory mediators. The objectives of this article are to present an overview of the etiologic and pathogenic factors promoting VTE as well as the pathophysiologic and inflammatory processes following PE.

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Early Reperfusion Induces Alveolar Injury in Pulmonary Embolism

Cited by 6 publications

References 13 publications

Chemokines Accumulate in the Lungs of Rats with Severe Pulmonary Embolism Induced by Polystyrene Microspheres

Chemokines Accumulate in the Lungs of Rats with Severe Pulmonary Embolism Induced by Polystyrene Microspheres

Lung surfactant alterations in pulmonary thromboembolism

Principle Mechanisms Underlying Venous Thromboembolism: Epidemiology, Risk Factors, Pathophysiology and Pathogenesis

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