Roles of nitric oxide, malondialdehyde, and fibronectin in an experimental peripheral nerve ischemia-reperfusion model.

Although there are many studies of the neuropathology of the ischemic degeneration of peripheral nerves, the pathogenesis is not well-understood. The roles of several biomolecules on this process were previously reported. An adhesion molecule, fibronectin, which is applied locally (as a conduit material), is very effective in nerve recovery. This study was carried out to evaluate the roles of fibronectin, lipid peroxidation, and nitric oxide (NO) in an experimental model of peripheral nerves. Ischemia and reperfusion injury of sciatic nerves was rendered by clamping the femoral artery and vein. Rats were divided into nine groups. Ischemia and reperfusion were not applied to group 1. In group 2, only ischemia was performed, but reperfusion was not accomplished. For groups 3-9, 1, 2, and 24 h and 1, 2, 3, and 4 weeks of reperfusion were applied following 3 h of ischemia. Then NO, malondialdehyde (MDA), and fibronectin levels were observed in serum samples of rats. Colorimetric and nephelometric assays were used for determination of the levels of these parameters. In this study, all biochemical parameters were found to be increased in the ischemia groups when compared with the control group 1 (P < 0.05). A significant difference was observed between study groups with respect to MDA, NO, and fibronectin levels (P < 0.05). Also, some correlations were established between biochemical parameters in the same group, depending on the varying reperfusion time (r > 0.50). Ischemia causes some important changes in biochemical parameters, and depending on the reperfusion time, nerve injury continues for a while. In our study, we observed that serum levels of MDA decreased in the periods when NO and fibronectin simultaneously increased. Such increases may contribute to neural recovery, and there may be interactions among them.