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Bronchoalveolar Lavage in Inhalation Lung Toxicity
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
K. Randall Young, Herbert Y. Reynolds
In contrast to the well-recognized adverse clinical effects of very high inspired oxygen tensions, conventional clinical wisdom has deemed lower concentrations (21-50% FiO2) to be safe. Griffith and colleagues (1986) performed baseline and follow-up BAL and [99mTc] DTPA clearance studies on normal individuals before and after exposure to normal “therapeutic” oxygen concentrations. They observed that permeability of the blood-air barrier, as judged by BAL albumin concentration, was increased after breathing concentrations of oxygen of 30% or higher for a mean duration of 45 hr. Lung clearance of the isotope was significantly increased in the group who breathed 50% oxygen, and in these individuals there was a trend toward an increased percentage of BAL neutrophils. In none of the individuals was there bronchoscopic evidence of lung inflammation or biochemical evidence of lung tissue injury as judged by BAL concentrations of LDH, alkaline phosphatase, potassium, or several eicosanoids. These findings suggest that even concentrations of oxygen widely considered to be "safe" have the potential for causing subtle but potentially important alterations in lung structure.
Immersion and drowning
Published in Jason Payne-James, Richard Jones, Simpson's Forensic Medicine, 2019
Jason Payne-James, Richard Jones
Seawater is generally three times more hyperosmolar than blood plasma, and following inhalation the hyperosmotic seawater can result in serious effects to the lung and alveoli. These effects may be predominantly categorised into insufficiency of pulmonary surfactant, blood–air barrier disruption, inflammation, oxidative stress, autophagy and apoptosis. Aspiration of fresh or sea water therefore leads to systemic hypoxaemia causing myocardial depression, reflex pulmonary vasoconstriction and altered pulmonary capillary permeability, contributing to pulmonary oedema. There is an inverse relationship between survival and the volume of aspirated fluid but even small quantities (i.e., as little as 30 mL) can cause arterial hypoxaemia.
Pulmonary Lymph and Lymphatics
Published in Waldemar L. Olszewski, Lymph Stasis: Pathophysiology, Diagnosis and Treatment, 2019
A basement membrane separates the pulmonary capillary endothelial cells from the interstitial space. The basement membrane of the alveolar capillaries and the basement membrane of the alveolar epithelial cells join to form a single unit where the blood-air barrier is thinnest. Pericytes or flattened interstitial cells may play a role in the passage of fluids through the vessel walls. They are not seen in the areas where the basement membranes are joined.12 The endothelium may be discontinuous with intercellular gaps, as seen in the viscera (e.g., liver and kidney) or continuous with tight intercellular junctions, as seen in muscle capillaries.13,14 Pulmonary capillaries tend to have a continuous endothelium and appear to be more permeable than muscular capillaries.2,14–16
Pulmonary delivery of resveratrol-β-cyclodextrin inclusion complexes for the prevention of zinc chloride smoke-induced acute lung injury
Published in Drug Delivery, 2022
Wanmei Wang, Yan Liu, Pan Pan, Yueqi Huang, Ting Chen, Tianyu Yuan, Yulong Ma, Guang Han, Jiahuan Li, Yiguang Jin, Fei Xie
Lung tissue damage would directly weaken respiratory ability, although no specific investigations had been done on the effect of ZnCl2 smoke exposure on the respiratory function indices of mice. It was reported that ZnCl2 smoke exposure damaged the bronchi, alveoli, and blood–air barrier (Xie et al., 2019). In this study, we found that ZnCl2 smoke exposure reduced the lung volume, increased the airway resistance, and reduced the TV, PEF and EF50. Both RES-β-CD and BUD modified the levels of TV, PEF, and EF50, of which RES-β-CD was better than BUD. The normal physical activity of animals needs good pulmonary function and high SpO2. RES-β-CD could enhance the physical activity of the ALI mice by attenuating lung injury and increasing SpO2.
Stabilization of Nrf2 leading to HO-1 activation protects against zinc oxide nanoparticles-induced endothelial cell death
Published in Nanotoxicology, 2021
Longbin Zhang, Liyong Zou, Xuejun Jiang, Shuqun Cheng, Jun Zhang, Xia Qin, Zhexue Qin, Chengzhi Chen, Zhen Zou
Endothelial cells form a one-cell-thick walled layer called the endothelium that lines the whole vascular system from the heart to the smallest capillary and regulates the passage of endogenous/exogenous materials and immune cells into and out of the bloodstream. These endothelial cells are recognized as major participants in inflammatory reactions (Pober and Sessa 2007). In particular, pulmonary microvascular endothelial cells and alveolar epithelial cells compose the blood-air barrier, which is the most important physiological structure for efficient pulmonary gas exchange. Disruption of the blood-air barrier is the fundamental pathophysiological characteristics of acute lung injury (Matthay, Ware, and Zimmerman 2012). Revealing the mechanisms underlying ZnONPs-induced endothelial cells damage will contribute to a better understanding of ZnONPs-induced lung injury and associated cardiovascular diseases (Wu et al. 2019). Therefore, we investigated whether ZnONPs induced the activation of Nrf2 in endothelial cells and mouse blood vessels and explored the antioxidative mechanisms activated in the context of ZnONPs treatment in vitro and in vivo.
Biochemical and immunological aspects of COVID-19 infection and therapeutical intervention of oral low dose cytokine therapy: a systematic review
Published in Immunopharmacology and Immunotoxicology, 2021
Ratheesh M, Sheethal S, Svenia P. Jose, Sony Rajan, Sulumol Thomas, Tariq Jagmag, Jayesh Tilwani
The pathogenesis is still unclear and in most of the patients, the virus is found infecting the lungs, thereby causing respiratory diseases. Studies have reported that the pathophysiology of ARDS caused by COVID-19 is due to the disruption of the blood-air barrier in the alveolar sacs. As a result, the plasma enters the air sacs and causes a sudden increase in immune reaction and also attracts inflammatory cells such as monocytes and neutrophils, resulting in the excessive infiltration of inflammatory cells into the lungs and causing damage to the lungs. This damage is the result of viral attack along with the overexpression of immune cells [5]. Even though it is a protective mechanism to destroy the invading virus, it has a deleterious end-result on the body. Some other under recognized conditions of COVID-19 infections such as secondary haemophagocytic lymphohistiocytosis, hyper-inflammatory syndrome with hyper-cytokinaemia, lead to multiple organ failure associated with hyper-ferritinaemia [6]. Thus, based on the reports and studies conducted so far, the dangerous impact of this virus is due to immune dysfunction [5].