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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Mucosal Immunol. 2012 Nov 28;6(4):762–775. doi: 10.1038/mi.2012.114

Figure 5.

Figure 5

Phenotypic characterization of Muc5ac−/− mice during ventilator-induced lung injury (VILI). (a–f) Muc5ac−/− mice or corresponding littermate controls matched in age, sex, and weight (Muc5a+/+) were mechanically ventilated (inspiratory pressure (Pinsp) 45 mbar, inspired oxygen fraction (FiO2) 1.0, positive-end expiratory pressure 3 mbar). (a) Arterial blood samples were collected at indicated time points and analyzed for oxygen partial pressure (PaO2) by a bedside blood gas analyzer. Ratio of PaO2 and FiO2 was calculated. Data are shown as mean ± s.d. (n = 6 per group). (b) Bronchoalveolar lavage (BAL) fluid was collected at the indicated time points and was analyzed for albumin content. Data are shown as mean ± s.d. (n = 6 per group). (c) At indicated time points, lungs were excised, patted dry, and weighed. Then lungs were dried for 48 h, and lung water content (mg lung water per mg dry tissue) was determined. Data are shown as mean ± s.d. (d) Muc5ac−/− or corresponding littermate controls were mechanically ventilated as described above. Lungs were fixed in situ and stained with hematoxylin and eosin (H&E). (original magnification x 40; n = 4). (e) For quantification of tissue damage due to mechanical ventilation, a histological score for VILI was assessed in Muc5ac+/+ and Muc5ac−/− mice based on H&E stainings. Results are displayed as median ± s.d. (n = 5). (f) Muc5ac−/− or corresponding littermate controls were mechanically ventilated as described above until a cardiac standstill was observed in the surface electrocardiogram. (n = 5).

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