<p>(A–D) <i>Hif1a<sup>f/f</sup></i> SurfactantCre+ mice or littermate controls (SurfactantCre+) matched in age, weight, and gender were exposed to ventilator-induced lung injury (VILI; pressure-controlled mechanical ventilation at an inspiratory pressure of 45 mbar with an inspired oxygen concentration of 100%, exposure time 120 min). <sup>13</sup>C glucose was administered i.p. 30 min prior to the experimental procedure. Determination of <sup>13</sup>C glucose and <sup>13</sup>C carbohydrates during VILI was performed using liquid chromatography–tandem mass spectrometry (LC-MS). Glut 1 transcript level was determined by real-time RT-PCR relative to house-keeping gene beta-actin and expressed as fold induction relative to sham-operated controls (mean ± SD, <i>n</i> = 3). (A) <sup>13</sup>C glucose. (B) Glut-1 transcript levels. (C) <sup>13</sup>C fructose 1,6 bisphosphate. (D) <sup>13</sup>C lactate. (E–H) To examine the functional role of glycolysis, wild-type mice treated with the glycolysis inhibitor 2-deoxy-D-glucose (200 mg/kg dose, i.p.) 30 min prior to the experimental procedure, and subsequently exposed to VILI (see above). Albumin concentration in the bronchoalveolar fluid (E) by enzyme-linked immunosorbent assay (ELISA), pulmonary gas exchange (F) by the ratio of the arterial partial pressure of oxygen (PaO2) to the fraction of inspired oxygen (FiO2), and MPO activity by using a murine ELISA from lung tissue (G) or IL-6 levels (H) in lung tissue homogenates using a mouse enzyme-linked immunosorbent assay (ELISA). Results are presented as mean ± s.d. (<i>n</i> = 6). (I and J) Mechanical ventilation was instituted and SurfactantCre+ controls or <i>Hif1a<sup>f/f</sup></i> SurfactantCre+ mice with and without 2-DG treatment were exposed to VILI (pressure-controlled mechanical ventilation at an inspiratory pressure of 35 mbar with an inspired oxygen concentration of 100%) until a cardiac standstill was observed in the surface electrocardiogram (<i>p</i><0.05, <i>n</i> = 6).</p
