Ultrastructure of the alveolar‐capillary wall in mitral stenosis

Jm, Kay; Fr, Edwards

doi:10.1002/path.1711110404

Cited by 79 publications

(43 citation statements)

References 13 publications

(13 reference statements)

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“…In addition, lung weight changes were due to tissue and vascular changes rather than extravascular lung water 17 . These features are reminiscent of the extracellular matrix thickening reported in patients with mitral stenosis and pulmonary venous pressure elevation 18,19 in whom it accounts for the structural changes observed and might be viewed a safety mechanism against excessive fluid leakage from the capillaries. An increase in collagen content not observed in pre-capillary PH but typical of post-capillary PH is mediated by proliferation of A C C E P T E D M A N U S C R I P T…”

mentioning

confidence: 74%

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Guazzi¹,

Phillips²,

Arena³

et al. 2015

Progress in Cardiovascular Diseases

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Cardiac dysfunction of both systolic and diastolic origin leads to increased left atrial pressure, lung capillary injury and increased resistance to gas transfer. Acutely, pressure-induced trauma disrupts the endothelial and alveolar anatomical configuration and definitively causes an impairment of cellular pathways involved in fluid-flux regulation and gas exchange efficiency, a process well identified as stress failure of the alveolarcapillary membrane. In chronic heart failure (HF), additional stimuli other than pressure may trigger the true remodeling process of capillaries and small arteries characterized by endothelial dysfunction, proliferation of myofibroblasts, fibrosis and extracellular matrix deposition. In parallel there is a loss of alveolar gas diffusion properties due to the increased path from air to blood (thickening of extracellular matrix) and loss of fine molecular mechanism involved in fluid reabsorption and clearance. Deleterious changes in gas transfer not only reflect the underlying lung tissue damage but also portend independent prognostic information and may play a role in the pathogenesis of exercise limitations and ventilatory abnormalities observed in these patients. Few currently approved treatments for chronic HF have the potential to positively affect structural remodeling of the lung capillary network; angiotensin-converting enzyme inhibitors are one of the few currently established options. Recently, more attention has been paid to novel therapies specifically targeting the nitric oxide pathway as a suitable target to improve endothelial function and permeability as well as alveolar gas exchange properties.

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confidence: 74%

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Guazzi¹,

Phillips²,

Arena³

et al. 2015

Progress in Cardiovascular Diseases

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“…These specimens also showed that lymphatic vessels undergo compensatory changes including dilation and occasionally muscularization due to chronically increased edema clearance. [14][15][16][17][18][19] Other mechanisms have also been proposed that are adaptive to increased hydrostatic pressure and prevent pulmonary edema. 20 It is probable that several of these mechanisms occur in different degrees…”

Section: Resultsmentioning

confidence: 99%

Mediastinal Lymphadenopathy in Patients Undergoing Cardiac Transplant Evaluation

Pastis

Bakel

Brand

et al. 2011

Chest

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Mediastinal lymphadenopathy (MLA) is not commonly recognized as associated with congestive heart failure (CHF). However, recent case series have reported a 35% to 81% incidence of MLA in different patient populations with CHF. [1][2][3][4] However, the true incidence remains unknown as these reports analyzed different heart failure populations.The lymphatic circulation is primarily responsible for regulating pulmonary fl uid homeostasis. The lymphatic system is highly recruitable and, with time to adapt, can increase clearance of pulmonary edema fl uid by . 10-fold. This system enables low-pressure drainage of excessive fl uid from the interstitium through lymph nodes (LNs) and into collecting ducts. Lymphatic Abbreviations: CHF 5 congestive heart failure; CO 5 cardiac output; EBUS 5 endobronchial ultrasound; EF 5 ejection fraction; EUS 5 endoscopic ultrasound; HT 5 heart transplantation; LN 5 lymph node; MLA 5 mediastinal lymphadenopathy; MPAP 5 mean pulmonary artery pressure; MR 5 mitral regurgitation; MUGA 5 multigated acquisition scan; PCWP 5 pulmonary capillary wedge pressure; RAP 5 right atrial pressure; RVG 5 radionuclide ventriculography; TR 5 tricuspid regurgitation

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“…Lungs of heart failure patients undergo extensive remodeling (18,25,26), resulting in architectural changes such as pulmonary artery and vein wall thickening, pulmonary arteriole muscularization, and capillary endothelial and alveolar epithelial basement membrane thickening (18). Collectively, such remodeling results in increased alveolocapillary barrier thickness, correlating with reduced microvascular fluid and protein permeabilities (11,20,45).…”

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confidence: 99%

“…Collectively, such remodeling results in increased alveolocapillary barrier thickness, correlating with reduced microvascular fluid and protein permeabilities (11,20,45). In addition to the aforementioned changes, alveolar epithelial type II cell proliferation may occur in these lungs (25,26). Hence, the hypothesis that alveolar epithelial type II cell hyperplasia increases Na absorption and accelerates alveolar fluid clearance (48) seems plausible because these cells contain the needed Na transport machinery.…”

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confidence: 99%

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

Maron

Luther²,

Pilati³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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We thus hypothesized that its function might be upregulated in rats with heart failure, a condition that severely challenges the lung's ability to maintain fluid balance. Heart failure was induced by left coronary artery ligation. Echocardiographic and cardiovascular hemodynamics confirmed its development at 16 wk postligation. At that time, alveolar fluid clearance was measured by an increase in protein concentration over 1 h of a 5% albumin solution instilled into the lungs. Baseline alveolar fluid clearance was similar in heart failure and age-matched control rats. Terbutaline was added to the instillate to determine whether heart failure rats responded to ␤-adrenoceptor stimulation. Alveolar fluid clearance in heart failure rats was increased by 194% after terbutaline stimulation compared with a 153% increase by terbutaline in control rats. To determine the mechanisms responsible for this accelerated alveolar fluid clearance, we measured ion transporter expression (ENaC, Na-KATPase, CFTR). No significant upregulation was observed for these ion transporters in the heart failure rats. Lung morphology showed significant alveolar epithelial type II cell hyperplasia in heart failure rats. Thus, alveolar epithelial type II cell hyperplasia is the likely explanation for the increased terbutaline-stimulated alveolar fluid clearance in heart failure rats. These data provide evidence for previously unrecognized mechanisms that can protect against or hasten resolution of alveolar edema in heart failure. albumin; terbutaline APPROXIMATELY FIVE MILLION Americans are living with heart failure, with 400,000 new cases diagnosed annually (18). A major clinical problem in heart failure is the development of pulmonary venous (and consequently, pulmonary capillary) hypertension, which ultimately may lead to pulmonary edema and impaired blood oxygenation. Recent studies have demonstrated that excess pulmonary edema fluid is cleared from the alveoli secondary to active transepithelial Na transport (14, 31). The alveolar epithelium plays a critical role during pulmonary edema recovery by actively absorbing Na (14, 31). ␤-adrenoceptor and dopamine receptor agonists increase Na transport and thus hasten the resolution of pulmonary edema (2, 6, 31). These observations have important clinical significance because they suggest that ␤-adrenoceptor-or dopamine receptor-agonist therapy might help patients to recover more rapidly from pulmonary edema (2, 16).Lungs of heart failure patients undergo extensive remodeling (18,25,26), resulting in architectural changes such as pulmonary artery and vein wall thickening, pulmonary arteriole muscularization, and capillary endothelial and alveolar epithelial basement membrane thickening (18). Collectively, such remodeling results in increased alveolocapillary barrier thickness, correlating with reduced microvascular fluid and protein permeabilities (11,20,45). In addition to the aforementioned changes, alveolar epithelial type II cell proliferation may occur in these lungs (25,26). Hence, the hypot...

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Ultrastructure of the alveolar‐capillary wall in mitral stenosis

Cited by 79 publications

References 13 publications

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

Mediastinal Lymphadenopathy in Patients Undergoing Cardiac Transplant Evaluation

β-Adrenoceptor stimulation of alveolar fluid clearance is increased in rats with heart failure

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