Abstract:

Objective: To observe the effects of ischemic postconditioning (I-postC) on the lung injury after limb ischemia reperfusion(LIR) in the rats, and to investigate the protective effect and the possible mechanisms.Methods: 24 Wistar rats were randomly divided into control group, ischemia-reperfusion group(IR group) and I-postC group(n=8).Referring to routine method in our department, the model rats which underwent 4 h ischemia and 4 h reperfusion of hind limbs were made.In control group, the rubber band around the limb was loose and the blood flow was not blocked.In I-postC group, before reperfusion, ischemia 5 min and reperfusion 5 min were performed in the rats, repeated for 3 times and then perfusion 4 h was taken, The blood and lung tissue from every rat were taken accurately.The percentages of CD18 positive cells in peripheral blood, the levels of soluble intercellular adhesion molecule-1(sICAM-1)and P-selectin in plasma, the myeloperoxidase (MPO) activities in lung tissue, the levels of intercellular adhesion molecule-1 (ICAM-1) and P-selectin in lung tissue of the rats in various groups were detected.The partial pressure of oxygen (PaO₂) and partial pressure of carbon dioxide (PaCO₂) were measured.The morphological changes of lung tissue under light and electron microscopes were observed.Results: Compared with control group, the percentage of CD18 positive cells and the levels of sICAM-1 and P-selectin of the rats in IR groups were increased(P<0.01);PaO₂ and PaCO₂ were decreased significantly;the MPO activity in lung tissue was also significantly increased(P<0.01).The HE staining results showed lung interstitial vascular dilation, congestion, PMN infiltration, the increased gap blood vessel, alveolar septal thickening, alveolar exudation, bronchial epithelial cell shedding and necrosis of the rats in IR group.Compared with IR group, the values of biochemical indicators mentioned above were decreased obviously(P<0.01);PaO₂ and PaCO₂ were increased significantly(P<0.01); the activities of inflammatory factors in plasma and lung tissue were decreased (P<0.01); the pathological changes of lung damage were improved significantly.Conclusion: I-postC can reduce the lung injury after LIR in the rats, and the mechanism may be related to inhibiting the inflammatory reaction.

Key words: ischemic postconditioning, inflammatory reaction, reperfusion injury, lung tissue, limb, rats, Wistar