1994 Fiscal Year Final Research Report Summary
LIPID PEROXIDATION AFTER ESOPHAGECTOMY
| Project/Area Number |
05671094
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Digestive surgery
|
|---|
| Research Institution | NIPPON MEDICAL SCHOOL |
|---|
Principal Investigator |
SASAJIMA Koji NIPPON MEDICAL SCHOOL FIRST DEPARTMENT OF SURGERY ASSOCIATE PROFESSOR, 医学部, 助教授 (80158930)
|
|---|
| Project Period (FY) |
1993 – 1994
|
| Keywords | ESOPGAGEAL CANCER / SURGICAL STRESS / TISSUE INJURY / FREE RADICALS / NEUTROPHIL / SUPEROXIDE / CYTOKINE |
|---|
| 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.
|
