Pulmonary Vascular Congestion: A Mechanism for Distal Lung Unit Dysfunction in Obesity.

PLoS One

André Cournand Pulmonary Physiology Laboratory, Division of Pulmonary, Critical Care and Sleep, Bellevue Hospital/New York University School of Medicine, New York, NY, United States of America.

Published: August 2016

Rationale: Obesity is characterized by increased systemic and pulmonary blood volumes (pulmonary vascular congestion). Concomitant abnormal alveolar membrane diffusion suggests subclinical interstitial edema. In this setting, functional abnormalities should encompass the entire distal lung including the airways.

Objectives: We hypothesize that in obesity: 1) pulmonary vascular congestion will affect the distal lung unit with concordant alveolar membrane and distal airway abnormalities; and 2) the degree of pulmonary congestion and membrane dysfunction will relate to the cardiac response.

Methods: 54 non-smoking obese subjects underwent spirometry, impulse oscillometry (IOS), diffusion capacity (DLCO) with partition into membrane diffusion (DM) and capillary blood volume (VC), and cardiac MRI (n = 24). Alveolar-capillary membrane efficiency was assessed by calculation of DM/VC.

Measurements And Main Results: Mean age was 45±12 years; mean BMI was 44.8±7 kg/m2. Vital capacity was 88±13% predicted with reduction in functional residual capacity (58±12% predicted). Despite normal DLCO (98±18% predicted), VC was elevated (135±31% predicted) while DM averaged 94±22% predicted. DM/VC varied from 0.4 to 1.4 with high values reflecting recruitment of alveolar membrane and low values indicating alveolar membrane dysfunction. The most abnormal IOS (R5 and X5) occurred in subjects with lowest DM/VC (r2 = 0.31, p<0.001; r2 = 0.34, p<0.001). Cardiac output and index (cardiac output / body surface area) were directly related to DM/VC (r2 = 0.41, p<0.001; r2 = 0.19, p = 0.03). Subjects with lower DM/VC demonstrated a cardiac output that remained in the normal range despite presence of obesity.

Conclusions: Global dysfunction of the distal lung (alveolar membrane and distal airway) is associated with pulmonary vascular congestion and failure to achieve the high output state of obesity. Pulmonary vascular congestion and consequent fluid transudation and/or alterations in the structure of the alveolar capillary membrane may be considered often unrecognized causes of airway dysfunction in obesity.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4817979PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0152769PLOS

Publication Analysis

Top Keywords

alveolar membrane
16
pulmonary vascular
12
vascular congestion
12
distal lung
12
lung unit
8
membrane diffusion
8
membrane dysfunction
8
membrane
7
pulmonary
5
predicted
5

Similar Publications

Pre-extraction alveolar buccal bone overbuilding: a preclinical investigation.

Oral Maxillofac Surg

December 2024

Department of Oral Implantology, Osaka Dental University, 8-1 Kuzuhahanazonocho, Hirakata, 573-1121, Osaka, Japan.

Background: The pre-extraction overbuilding procedure was designed aiming to mitigate buccal bone resorption following tooth extraction. The objective of this study was to compare the efficacy of pre-extraction and juxta-extraction buccal overbuilding treatments in preserving buccal bone volume following tooth extraction.

Material And Methods: At the test sites (pre-extraction sites), an alveolar crest overbuilding was performed on the buccal aspect of the distal root of the fourth premolar using a xenograft covered with a collagen membrane.

View Article and Find Full Text PDF

KRAS was long deemed undruggable until the discovery of the switch-II pocket facilitated the development of specific KRAS inhibitors. Despite their introduction into clinical practice, resistance mechanisms can limit their effectiveness. Initially, tumors rely on mutant KRAS, but as they progress, they may shift to alternative pathways, resulting in intrinsic resistance.

View Article and Find Full Text PDF

Endothelial CD38-induced endothelial-to-mesenchymal transition is a pivotal driver in pulmonary fibrosis.

Cell Mol Life Sci

December 2024

National Engineering Research Center for Bioengineering Drugs and the Technologies, Institute of Translational Medicine, Jiangxi Medical College, Nanchang University, Nanchang, 330031, China.

Idiopathic pulmonary fibrosis (IPF) is a prevalent interstitial lung disease with high mortality. CD38 is a main enzyme for intracellular nicotinamide adenine dinucleotide (NAD) degradation in mammals. It has been reported that CD38 participated in pulmonary fibrosis through promoting alveolar epithelial cells senescence.

View Article and Find Full Text PDF

[FER-1 inhibits methylglyoxal-induced ferroptosis in mouse alveolar macrophages ].

Nan Fang Yi Ke Da Xue Xue Bao

December 2024

Department of Histology and Embryology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi 830000, China.

Objectives: To investigate the inhibitory effect of FER-1 on methylglyoxal-induced ferroptosis in cultured mouse alveolar macrophages.

Methods: MH-S cells derived from mouse alveolar macrophages treated with 90 μg/mL methylglyoxal, 10 μmol/mL FER-1MG+FER-1, or both were examined for intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and ferrous ion (Fe) levels and changes in mitochondrial membrane potential. Western blotting was performed to detect the protein expression levels of glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthase 4 (ACSL4).

View Article and Find Full Text PDF

Objective: To investigate the protective effect of lycopene on lung oxidative damage induced by atmospheric fine particulate matter(PM_(2.5)) in rats.

Methods: Sixty 7-week-old male Sprague-Dawley rats were randomly divided into six groups: normal control group, PM_(2.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!