Low-molecular-weight heparin reduces hyperoxia-augmented ventilator-induced lung injury via serine/threonine kinase-protein kinase B

Table 2 Physiologic conditions at the beginning and end of ventilation

	Nonventilated Room air	Nonventilated Hyperoxia	V_T 30 ml/kg Room air	V_T 30 ml/kg Hyperoxia
PH	7.40 ± 0.05	7.37 ± 0.01	7.35 ± 0.04	7.34 ± 0.02
PaO2 (mmHg)	98.6 ± 0.3	423.5 ± 4.3	86.9 ± 0.7	399.7 ± 3.6
PaCO2 (mmHg)	39.1 ± 0.2	39.6 ± 0.7	37.3 ± 1.2	43.4 ± 1.5
MAP (mmHg)
Start	85.5 ± 1.2	85.9 ± 1.9	84.8 ± 1.5	84.5 ± 2.4
End	85.1 ± 0.6	84.9 ± 0.8	77.5 ± 3.0	77.3 ± 2.3
PIP (mmHg)
Start			24.3 ± 1.2	24.9 ± 1.3
End			27.7 ± 1.0	28.2 ± 1.3

Arterial blood gases and mean arterial pressure were obtained from nonventilated mice and mice ventilated at a tidal volume of 30 ml/kg for 8 hours (n = 10 per group). MAP = mean arterial pressure; PIP = peak inspiratory pressure; V_T = tidal volume. The physiological data of control groups were similar during the experiment and were used as the beginning data of mechanical ventilation. Because no differences were observed among hyperoxia with enoxaparin, without enoxaparin, and Akt deficient groups, the data were combined.

ISSN: 1465-993X