Abstract: AIM: To investigate the relationship between apoptosis and pulmonary ischemia-reperfusion injury in rabbits and the intervention of tertram ethylpyrazine. METHODS: An in situ ischemia-reperfusion lung injury rabbit model was established in vivo. Apoptotic cells were explored by the terminal deoxynucleotidyl transferase-mediate dUTP nick-end labelling (TUNEL) technique. The index of quantitative assessment of histologic lung (IQA) was detected by Murata' s way. The correlation was analyzed between the apoptosis and IQA of pulmonary ischemia- reperfusion injury. RESULTS: Obvious apoptosis of pneumocytes occurred at reperfusion 1, 3, and 5 h after 1 h ischem ia-reperfusion lung injury, and the peak was on 3h after reperfusion. The apoptotic cells decreased in TMP groups compared with IR groups. The values of IQA in IR group were significantly higher than those in TMP group (P <0.01). There was a significant positive correlation between the apoptosis index and IQA (r = 0.718, P < 0.01). CONCLUSION: The apoptosis may significantly contribute to ischemia-reperfusion pulmonary injury and the tertram ethylpyrazine can protect PIRI by anti- apoptosis of pneumocytes.

Key words: pulmonary ischemia-reperfusion injury, the index of quantitative assessment of histologic lung (IQA), apoptosis, tertram ethylpyrazine