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Role of heme oxygenase-1/carbon monoxide system in pulmonary ischemia-reperfusion injury

^a Department of Pathophysiology, Wenzhou Medical College, Wenzhou 325035, Zhejiang, China
^b Department of Anesthesiology, First Affiliated Hospital of Wenzhou Medical College, Wenzhou 325003, Zhejiang, China

*Corresponding author. Tel.: +86-577-88069459; fax: +86-577-88383956.

E-mail address: wzlinlina{at}tom.com (L. Lin).

The aim of this study is to investigate the effect of heme oxygenase-1 (HO-1)/carbon monoxide (CO) system in pulmonary ischemia-reperfusion injury (PIRI) in rabbits. The rabbits were randomly assigned to three groups (n=10, in each): control group (C), PIR group (I-R), PIR+Hemin group (H) and PIR+zinc protoporphyrin IX (ZnPP) group (Z). There were changes to several parameters which included plasma carboxyhemoglobin (COHb), wet to dry ratio of lung tissue weight (W/D), the injured alveoli rate (IAR) and the HO-1 enzymatic activity. Immunohistochemistry and in situ hybridization for HO-1 was detected in lung. The electron microscopic observation for lung tissue injury was done after PIRI. The plasma content of COHb increased by reperfusion was strengthened by hemin but weakened by ZnPP. The HO-1 activity in lung tissue was upregulated by PIRI, further enhanced by hemin and abolished by ZnPP. Except for the C group, HO-1 was upregulated in all other groups in the pulmonary endothelial cells, some pulmonary vascular smooth muscle cells, extima of vessels and epithelial cells of airway. The injury parameters were highest in the Z group, the second was in the IR group, then the H group and the C group. HO-1/CO system was activated and may be one of the protective signal pathway during PIRI in rabbits.

Key Words: Ischemia-reperfusion injury; Lung; Heme oxygenase-1; Carbon monoxide