Several clinical and experimental studies have shown that lung injury occurs shortly after brain damage. The responsible mechanisms involve neurogenic pulmonary edema, inflammation, the harmful action of neurotransmitters, or autonomic system dysfunction. Mechanical ventilation, an essential component of life support in brain-damaged patients (BD), may be an additional traumatic factor to the already injured or susceptible to injury lungs of these patients thus worsening lung injury, in case that non lung protective ventilator settings are applied. Measurement of respiratory mechanics in BD patients, as well as assessment of their evolution during mechanical ventilation, may lead to preclinical lung injury detection early enough, allowing thus the selection of the appropriate ventilator settings to avoid ventilator-induced lung injury. The aim of this review is to explore the mechanical properties of the respiratory system in BD patients along with the underlying mechanisms, and to translate the evidence of animal and clinical studies into therapeutic implications regarding the mechanical ventilation of these critically ill patients.
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http://dx.doi.org/10.5492/wjccm.v5.i1.65 | DOI Listing |
Acta Bioeng Biomech
June 2024
2Daping Hospital, Army Medical Center, Chongqing, China.
: This study explores how thoracic orientation affects lung pressure and injury outcomes from shock waves, building on earlier research that suggested human posture impacts injury severity. : A layered finite element model of the chest was constructed based on the Chinese Visual Human Dataset (CVH), including the rib and intercostal muscle layers. The dynamic response of the chest under 12 different angle-oriented shock waves under incident pressures of 200 kPa and 500 kPa was calculated.
View Article and Find Full Text PDFEnviron Toxicol
January 2025
Department of Biochemistry, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey.
Sepsis remains the leading cause of multiple-organ injury due to endotoxemia. Astaxanthin (ASTA), widely used in marine aquaculture, has an extraordinary potential for antioxidant and anti-inflammatory activity. Purinergic receptor (e.
View Article and Find Full Text PDFFEBS Lett
January 2025
Department of Microbiology and Immunology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Tissue fibrosis is a progressive pathological process with excessive deposition of extracellular matrix proteins (ECM). Myofibroblasts, identified by alpha-smooth muscle actin (αSMA) expression, play an important role in tissue fibrosis by producing ECM. Here, we found that the Wnt antagonist Dickkopf1 (DKK1) induced gene expressions associated with inflammation and fibrosis in lung fibroblasts.
View Article and Find Full Text PDFLife Metab
February 2025
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200438, China.
Abdominal aortic aneurysm (AAA) is strongly correlated with obesity, partially due to the abnormal expansion of abdominal perivascular adipose tissue (PVAT). Cell death-inducing DNA fragmentation factor-like effector C (CIDEC), also known as fat-specific protein 27 (FSP27) in rodents, is specifically expressed in adipose tissue where it mediates lipid droplet fusion and adipose tissue expansion. Whether and how CIDEC/FSP27 plays a role in AAA pathology remains elusive.
View Article and Find Full Text PDFJ Intensive Med
January 2025
Department of Critical Care Medicine, The Eighth Medical Center of Chinese PLA General Hospital, Beijing, China.
Background: The roles of the Pink1/Parkin pathway and mitophagy in lung injury during heat stroke remain unclear. In this study, we investigated the role of Pink1/Parkin-mediated mitophagy in acute lung injury (ALI) in rats with exertional heat stroke (EHS).
Methods: Sixty Sprague Dawley rats were randomly divided into control (CON), control + Parkin overexpression (CON + Parkin), EHS, and EHS + Parkin overexpression (EHS + Parkin) groups.
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