Table 1.
Parameters of systemic hemodynamics, lung mechanics, pulmonary gas exchange, metabolism, and acid-base.
Parameters of systemic hemodynamics, lung mechanics, pulmonary gas exchange, metabolism, and acid-base status in mice without (Non-CS) and with (CS) cigarette smoke exposure over three to four weeks prior to blunt chest trauma and after four hours mechanical ventilation with air (FiO2 0.21) or 100% O2 (FiO2 1.0) (n = 8 in each group). All data are median (quartiles).
Table 2.
Plasma and lung tissue cytokine and chemokine concentrations.
Plasma (in pg·mL-1) and lung tissue (in pg·mgprotein-1) cytokine and chemokine concentrations at the end of the four-hours observation period (n = 8 in each group) obtained from mice without (Non-CS) and with (CS) cigarette smoke exposure over 3–4 weeks prior to blunt chest trauma and mechanical ventilation with air (FiO2 0.21) or 100% O2 (FiO2 1.0). All data are median (quartiles).
Table 3.
Parameters of lung histopathology.
Parameters of lung histopathology at the end of the four-hours observation period (n = 8 in each group) obtained from mice without (Non-CS) and with (CS) cigarette smoke exposure over 3–4 weeks prior to blunt chest trauma and mechanical ventilation with air (FiO2 0.21) or 100% O2 (FiO2 1.0) (n = 8 in each group). Parameters were scored as 0 (normal lung histology without pathological findings), 0.5 (minor histological injury), 1 (moderate and patchy histological injury), 1.5 (major histological injury < 25% of the lung involved), and 2 (major histological injury 25–50% of the lung involved). All data are median (quartiles).
Fig 1.
Typical examples of the histopathological items scored.
Upper panel: Lung region with little histopathological abnormalities, i.e. no dystelectasis/ atelectasis, normal thickness of alveolar membranes, and little lymphocyte immigration. Dotted arrows show some degree of protein debris in the airspaces. Lower panel: Lung region with major histological injury (alveolar membrane thickening and lymphocyte immigration grade 1.5 each). Solid arrows show alveolar smokers’ macrophages within the airways.
Fig 2.
Results of the immune blotting for HO-1.
Original western blots and quantitative analysis of lung tissue expression of HO-1 from mice without (open boxplots; n = 8 each) and with (hatched boxplots; n = 7 each) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) together with two blots each (right part of blot panel) from control animals that did not undergo cigarette smoke exposure, anaesthesia, chest trauma, and surgery. All data are median (quartiles, range) as fold increase over values from control animals; § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 3.
Results of the immune blotting for activated caspase-3.
Original western blots and quantitative analysis of lung tissue expression of activated caspase-3 from mice without (open boxplots; n = 8 each) and with (hatched boxplots; n = 7 each) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) together with two blots each (right part of blot panel) from control animals that did not undergo cigarette smoke exposure, anaesthesia, chest trauma, and surgery. All data are median (quartiles, range) as fold increase over values from control animals; § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 4.
Results of the EMSA for NF-κ activation.
Original gel shifts and quantitative analysis of lung tissue expression of NF-κB activation from mice without (open boxplots; n = 8 each) and with (hatched boxplots; n = 7 each) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) together with two blots each (right part of blot panel) from control animals that did not undergo cigarette smoke exposure, anaesthesia, chest trauma, and surgery. All data are median (quartiles, range) as fold increase over values from control animals; § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 5.
Results of the immune blotting for HIF-1α.
Original western blots and quantitative analysis of lung tissue expression of HIF-1α expression from mice without (open boxplots; n = 8 each) and with (hatched boxplots; n = 7 each) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) together with two blots each (right part of blot panel) from control animals that did not undergo cigarette smoke exposure, anaesthesia, chest trauma, and surgery. All data are median (quartiles, range) as fold increase over values from control animals; § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 6.
Results of the immunohistochemistry for nitrotyrosine.
Typical examples (upper panel) and quantitative analysis (lower panel) of immunohistochemistry for lung tissue nitrotyrosine formation from mice without (dotted boxplots) and with (hatched boxplots) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) (n = 8 in each group). All data median (quartiles, range), § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 7.
Results of the immunohistochemistry for P2X7.
Typical examples (upper panel) and quantitative analysis (lower panel) of immunohistochemistry for lung tissue expression of the purinergic receptor P2X7 from mice without (dotted boxplots) and with (hatched boxplots) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) (n = 8 in each group). All data median (quartiles, range), § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).
Fig 8.
Results of the immunohistochemistry for P2X4.
Typical examples (upper panel) and quantitative analysis (lower panel) of immunohistochemistry for lung tissue expression of the purinergic receptor P2X4 from mice without (dotted boxplots) and with (hatched boxplots) cigarette smoke exposure prior to blunt chest trauma and mechanically ventilated with air (white boxplots) and 100% O2 (grey boxplots) (n = 8 in each group). All data median (quartiles, range), § p < 0.05 vs. corresponding cigarette smoke exposure group, $ p < 0.05 vs. corresponding air ventilation group (Kruskall-Wallis analysis of variance on ranks with post-hoc Dunn’s test for multiple comparisons).