Abstract

The influence of transient circulatory arrest on oxidant status during the healing of a tibial fracture was investigated in rats by the use of a hindlimb tourniquet technique. One of the most reliable indicators for cytological damage is lipid peroxidation, which can be demonstrated by malondialdehyde (MDA) levels. Fifty-eight Wistar rats were used in this study. To determine the basal MDA levels of bone, 10 rats not exposed to ischemia were killed by an overdose of ether. The remaining 48 rats were randomly divided into two groups (control and ischemia). The control and ischemia groups were then randomly divided into 4 groups of 6 rats each. In 48 rats, the left tibia was fractured and fixed intramedullarly. In the ischemic group, complete acute transient ischemia for 4.5 h was imposed after the fracture. In the control group, no other intervention except the fracture was done. Rats from the control and ischemic groups were killed on days 3, 7, 14, and 28, and MDA levels were determined in tibial bone and callus tissue. The MDA levels of the control and ischemic groups were compared with basal MDA levels in the bone of 10 rats. There was an apparent difference between the basal and control group MDA levels on days 3 and 7 (p < 0.01), between the basal and ischemic group MDA levels on days 3, 7, and 14 (p < 0.01). In addition, the ischemic group showed a statistically significant increase in MDA levels on days 3, 7 and 14 compared with the control group (p < 0.01). We conclude that complete acute transient ischemia affects the oxidant status during fracture healing. This effect especially occurs during the ischemic period, inflammation, and callus formation of fracture healing.

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