| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
|
|---|
| Research Abstract |
Surgical stress results in the response of the neuroendocrine system and the release of mediators. Macrophages at the wound are known to be activated firstly, and produce cytokines such as tumor necrosis factor and interleukins. Cytokines further activate polymorphonuclear neutrophil (PMN), lymphocyte and fibroblast. The serum concentration of IL-6 which correlates with duration of operation and blood loss, is considered to reflect the magnitude of surgical stress. Superoxide (0_2^-) generated from activated PMNs prevents infection by killing bacteria and also causes the membrane damage by lipid peroxidation. On the other hand, serum concentration of superoxide dismutase (SOD) which neutralizes 0_2^- as antioxidant, increases after surgery.
In the patients who develop multiple organ failure (MOF), serum concentrations of cytokines, SOD and lipid peroxides are significantly higher than those of non-MOF patients.
These results suggest that the postoperative complications result from the inadequate host response, and that the oxidative stress by free radicals may play an important role in the development of organ failure following surgical stress.
|
