dinoprost and Acute-Lung-Injury

The acute ozone induced lung injury model has been widely used to explore injury and repair processes induced by oxidant overload. The current study evaluated acute ozone exposure effects on prostaglandin F

Topics: Acute Lung Injury; Animals; Biomarkers; Dinoprost; Inflammation; Oxidative Stress; Ozone; Rats

Sex-specific differences in pulmonary morbidity in humans are well documented. Hyperoxia contributes to lung injury in experimental animals and humans. The mechanisms responsible for sex differences in the susceptibility towards hyperoxic lung injury remain largely unknown. In this investigation, we tested the hypothesis that mice will display sex-specific differences in hyperoxic lung injury. Eight week-old male and female mice (C57BL/6J) were exposed to 72 h of hyperoxia (FiO2>0.95). After exposure to hyperoxia, lung injury, levels of 8-iso-prostaglandin F2 alpha (8-iso-PGF 2α) (LC-MS/MS), apoptosis (TUNEL) and inflammatory markers (suspension bead array) were determined. Cytochrome P450 (CYP)1A expression in the lung was assessed using immunohistochemistry and western blotting. After exposure to hyperoxia, males showed greater lung injury, neutrophil infiltration and apoptosis, compared to air-breathing controls than females. Pulmonary 8-iso-PGF 2α levels were higher in males than females after hyperoxia exposure. Sexually dimorphic increases in levels of IL-6 (F>M) and VEGF (M>F) in the lungs were also observed. CYP1A1 expression in the lung was higher in female mice compared to males under hyperoxic conditions. Overall, our results support the hypothesis that male mice are more susceptible than females to hyperoxic lung injury and that differences in inflammatory and oxidative stress markers contribute to these sex-specific dimorphic effects. In conclusion, this paper describes the establishment of an animal model that shows sex differences in hyperoxic lung injury in a temporal manner and thus has important implications for lung diseases mediated by hyperoxia in humans.

Topics: Acute Lung Injury; Animals; Apoptosis; Biomarkers; Blotting, Western; Dinoprost; Female; Humans; Hyperoxia; Immunohistochemistry; In Situ Nick-End Labeling; Lung Injury; Male; Mice; Mice, Inbred C57BL; Neutrophil Infiltration; Oxidative Stress; Sex Characteristics

Acute lung injury contributes to the mortality of patients after lung resection and one-lung ventilation (OLV). The objective of this study was to characterise the effect of lung resection and OLV on proposed biomarkers of lung injury in exhaled breath condensate (EBC) and plasma.. In adults undergoing lung resection, EBC was collected before and at 30-min intervals during OLV. Inflammatory mediators were assayed in plasma samples taken preoperatively, immediately postoperatively and 24 h postoperatively.. EBC pH decreased from 6.51 ± 0.43 preoperatively, to 6.17 ± 0.78 and 6.09 ± 0.83 at 30 and 60 min, respectively (mean ± SD, P = 0.034, n = 20). Plasma concentrations of the receptor for advanced glycation end-products, von Willebrand factor and interleukin-6 increased comparing preoperative and postoperative samples (all P < 0.001, n = 30). By contrast, levels of Krebs von den Lungen-6 and surfactant protein-D decreased (P < 0.001, n=30), and correlated inversely with the extent of lung resected.. Lung resection and OLV was associated with a rapid reduction in EBC pH and differential changes in plasma biomarkers of lung injury. Further investigation of EBC pH as a marker of ventilator-induced lung injury is warranted.

Topics: Acute Lung Injury; Adult; Aged; Aged, 80 and over; Biomarkers; Breath Tests; Dinoprost; Female; Humans; Hydrogen Peroxide; Interleukin-6; Leukotriene B4; Lung; Male; Middle Aged; Mucin-1; Pulmonary Surfactant-Associated Protein D; Receptor for Advanced Glycation End Products; Receptors, Immunologic; Ventilator-Induced Lung Injury; von Willebrand Factor; Young Adult