Lung dysfunction is common in critical illness, and evidence of Ang/Tie involvement has been found in animal models. In a rat model of acute respiratory distress syndrome, Ang-1 reduces permeability and inflammation, whereas Tie2 deficiency increases damage [21] . In an experimental model of asthma, Ang-1 mRNA was decreased, and Ang-1 supplementation decreased alveolar leakage and NF-κB-dependent inflammation [22] . In hypoxia-induced pulmonary hypertension in rats, decreased activity of the Tie2 pathway contributed to right ventricular load, and this effect was antagonized by Ang-1 [23]. On the other hand, a causative role for Ang-1 in pulmonary hypertension has also been suggested [24] . In hyperoxic lung injury, Ang-2 is involved in lung permeability and inflammation [25] .