In a rat model of haemorrhagic shock, Ang-1 reduced vascular leakage, and it inhibited microvascular endothelial cell apoptosis in vitro and in vivo [107, 138] . In this model, Ang-1promoted cell survival was partly controlled through integrin adhesion [139] . It has been suggested that EC apoptosis in haemorrhagic shock contributes to endothelial hyperpermeability [140] [141] [142] . Apoptosis is one of the reactions to MODSrelated injury as demonstrated in hypoxia/reperfusion [143] .