Inflammation and intimal hyperplasia associated with experimental pulmonary embolism

Eagleton, Matthew J.; Henke, Peter K.; Luke, Catherine E.; Hawley, Angela E.; Bedi, Asheesh; Knipp, Brian S.; Wakefield, Thomas W.; Greenfield, Lazar J.

doi:10.1067/mva.2002.126556

Cited by 57 publications

(64 citation statements)

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“…The total leukocyte count reduces at 45 times the normal value. At 14 days after the pulmonary embolism, the wall of the pulmonary arteries is similar to the onset of pulmonary embolism, with no significant differences concerning the leukocyte number [27,28]. Beginning with the fourth day after the pulmonary embolism, an increase in the intima thickness is found, associated with an increase in the cellularity within the intimal layer compared to control animals.…”

Section: The Pulmonary Artery Wallmentioning

confidence: 67%

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

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et al. 2017

Revista Romana De Medicina De Laborator

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Inflammation of the venous wall is involved in thrombogenesis, thrombus resolution, wall remodeling and the post-thrombotic syndrome. Different mechanisms are involved in both arterial and venous thrombosis and patients with atherothrombosis hold a higher risk of venous thrombosis. Although inflammation may represent the connection between arterial and venous thrombosis, it is not yet sure if it is the cause or consequence of venous thrombosis. Consequently, the relationships between inflammation markers as indicators of the inflammatory process and clinical venous thromboembolism need to be investigatd. For example, inflammation mediators such as the pro-inflammatory cytokines interleukin 8 (IL-8), IL-6, monocyte chemotactic protein 1 (MCP-1), C Reactive Protein (CRP), vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), matrix metalloproteinases and tumor necrosis factor alpha (TNF alpha)

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Section: The Pulmonary Artery Wallmentioning

confidence: 67%

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Cocoi

Pop

Cocoi³

et al. 2017

Revista Romana De Medicina De Laborator

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“…PEm produces multiple stimuli that are capable of inciting an inflammatory response, including pulmonary artery hypertension (26,27), ischemia (28), hypoxia (29), and interaction of embolized material with vascular endothelium (30). A common feature of these stimuli is the potential to induce expression and release of additional proinflammatory molecules and to initiate a cascade of events resulting in a state of chronic inflammation and tissue remodeling.…”

mentioning

confidence: 99%

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

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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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“…In particular, neutrophils are the first leukocytes to be found in the damaged intravascular area. Pro-coagulants are secreted locally by leukocytes that contribute to oxidative and proteolytic injury especially in case of pulmonary embolism [11,12].…”

Section: Discussionmentioning

confidence: 99%

Clinical value of neutrophil to lymphocyte ratio in the region of lower extremity deep venous thrombosis

et al. 2016

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Objectives. Many studies have demonstrated a significant association between cardiovascular disease and neutrophil to lymphocyte ratio (NLR). To our knowledge, no study has been reported in patients with deep venous thrombosis (DVT) which affecting proximal or distal leg. In this study we analyzed proximal and distal DVT according to the NLR. Methods. This retrospective study was obtained from patients' records of a tertiary university hospital between May 2011 to January 2014. A total of 57 patients with the diagnosis of acute primary DVT and 30 patients as control group included in the study. All of them were confirmed with lower extremity venous duplex examinations. Of these, 37 examinations with the diagnosis of proximal DVT were compared to 20 examinations with distal DVT. The groups compared regarding to complete blood counter values. Results. Mean eosinophil level was higher in the distal DVT group (0.28±0.24 vs. 0.12±0.01, p=0.001), whereas median NLR were higher in the proximal DVT group than the distal DVT group (3.5 [0.5-4.3] vs. 2.3 [1.2-9.7], respectively; p=0.002). In addition, median NLR, leukocyte and neutrophil counts were statistically lower in the control group than the others (p=0.014, p=0.027 and p=0.004, respectively). Conclusion. NLR, an inexpensive and easily measurable laboratory variable, was independently and significantly associated with the presence and severity of DVT, especially acute proximal DVT.

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Inflammation and intimal hyperplasia associated with experimental pulmonary embolism

Cited by 57 publications

References 0 publications

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

Involvement of inflammatory markers in pathogenesis of venous thromboembolism

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

Clinical value of neutrophil to lymphocyte ratio in the region of lower extremity deep venous thrombosis

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