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Background: We aimed to demonstrate the positive effects of the serine protease inhibitor aprotinin on neural ischemia-reperfusion injury and apoptosis in a rat model. Methods: There were 18 rats divided into 3 groups: group A (sham, n = 6), group B (ischemia-reperfusion, n = 6), and group C (ischemia-reperfusion + aprotinin, n = 6). The systolic blood pressure of the group B and C rats was decreased to 40% to 50% of the normal level by taking blood from the femoral vein to develop hemorrhagic shock. The blood was retained and given to the remaining group B and C rats for reperfusion 20 minutes after the procedure. In group B, isotonic solution and, in group C, aprotinin was administered to the rats 5 minutes before reperfusion. After the rats were killed, the brain tissue samples were fixed for histopathologic examination. Brain tissue superoxide dismutase, malondialdehyde, and tissue myeloperoxidase level and apoptotic cell analyses were performed in all groups. Results: Superoxide dismutase level decreased from group A to group B and increased from group B to group C (p < 0.05). Malondialdehyde and myeloperoxidase levels and apoptotic cells increased from group A to group B and decreased from group B to group C (p < 0.05). Conclusion: The results suggest that the systemic use of aprotinin in ischemic neural tissue prevents reperfusion injury and also protects the morphologic, functional, and biochemical integrity of the neural tissue.

The aim of this study was to investigate whether enhanced stimulation voltage could be a predictor of the extent of injury in acute compressive peripheral nerve trauma.The femoral nerves were exposed on both sides, in 11 anesthetized rabbits. Supramaximal stimulation voltage was used to produce a maximal-amplitude compound muscle action potential (CMAP) from the quadriceps femoris muscle. Afterward, the left femoral nerve was clipped for 1 minute, and the right femoral nerve for 5 minutes to produce an acute compressive injury. Immediately after removal of the clip, the proximal and distal sides of the clippage site were stimulated by gradually increased voltage until CMAPs were obtained. The same procedure was repeated at the 30th and 60th minutes. The ratio of the CMAP amplitudes obtained from proximal and distal stimulation was measured to establish a classification.The stimulation voltages and amplitudes of the CMAPs before clippage were similar with the after-clippage values obtained from distal stimulation (p0.05), but the after-clippage values obtained from proximal stimulation were different in both sides (p0.05). Doubled stimulation voltage was enough to obtain CMAPs on the left side, but eightfold the initial level was required on the right side. The amplitude ratios recovered to preinjury levels in all of the subjects on the left side, but only two showed recovery on the right side (p0.001). Histopathologically, there was axonal compression without discontinuity on the left side, whereas the fibers were dispersed on the right side.Stimulation voltage was found to discriminate the severity of the lesion in experimental peripheral nerve injury. Proximal to distal amplitude ratio seems to be a prognostic factor when the injury is less severe.

Six patients received 1 g and six other patients received 2 g of cefoperazone and sulbactam 15 minutes before lumbar disc surgery. Liquid chromatographic analysis of disc tissue revealed that only patients receiving the 2-g dose had mean tissue levels above the minimum inhibitory concentration for Staphylococcus aureus and epidermidis.