Effect of ketamine on pneumocyte apoptosis and expression of caspase-3 mRNA after lung ischemia/reperfusion injury in rabbits

Objective To investigate the effect of ketamine on pneumocyte apoptosis and expression of caspase-3 mRNA after lung ischemia/ reperfusion injury in rabbits. Methods Ninety Rabbits used for unilateral lung ischemia/reperfusion model were randomly divided into three groups(thirty rabbits in each group): control group(C group), ischemia/reperfusion group(I/R group) and ketamine group(KET group). 30 rabbits in each group were averagely divided at 1h, 3h, 5h after reperfusion. The activity of superoxide dismutase(SOD), concentration of malondialdehyde(MDA), con-tent of tumor necrosis factor-alpha(TNF-α) and change of apoptosis index(AI) at each groups were measured respectively in different groups. TUNEL staining and in situ hybridization were used to detect pneumocyte apoptosis and expression of Caspase-3 mRNA; Image analysis was also performed. Results The activity of SOD was significantly lower in I/R group than in C group(P0.01) at the same time point; while the content of MDA, TNF-αand AI were obviously higher in I/R group than in C group(P0.01). Compared with I/R group, the level of SOD was higher, however, MDA, TNF-α and AI were lower at different degree(P0.01 or P0.05) in KET group at the same time point. TUNEL-positive cells were mainly located in alveolar epithelial cell and vascular endothelial cell, the expression of Caspase-3 mRNA were mainly located in vascular endothelial cell after the lung reper-fusion. The expression of caspase-3 mRNA in the I/R groups was significantly increased compared with that of C groups at each time point. Mean-while, pneumocyte apoptosis was also enhanced. Whereas both of them were sharply decreased after ketamine was used. Conclusion Ketamine could inhibit the pneumocyte apoptosis during pulmonary ischemia/reperfusion injury by reducing contents of MDA, TNF- α, increasing the activity of SOD, and decreasing expression of caspase-3mRNA, thus alleviated injury on pulmonary tissue of reperfusion injuried rabbits.