1994 Fiscal Year Final Research Report Summary
Cell protection of allopurinol during ischemia-reperfusion in the lung.
| Project/Area Number |
05671258
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Anesthesiology/Resuscitation studies
|
|---|
| Research Institution | MIE UNIVERSITY |
|---|
Principal Investigator |
OKUDA Masahiro Mie Univ.Hospital Lecturer, 医学部・付属病院, 講師 (90204130)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAKAI Yasushi Mie Univ.Hospital Assistant, 医学部・付属病院, 助手 (00227729)
|
|---|
| Project Period (FY) |
1993 – 1994
|
| Keywords | Lung / Ischemia-Reperfusion Injury / Free Rdical / Xanthine Oxidase |
|---|
| Research Abstract |
Tangstate enriched diet for 3-4 weeks depleted the lung XD and XO by 80%. Using isolated perfused lungs of these rats, 90 minutes ischemia and reperfusion were performed. The lungs of XO deficient rats were protected from ischemia reperfusion injury as compared with the lungs of normal rats. Allopurinol, XO inhibitor was also effective to protect the lungs from ischemia-reperfusion. Therefore it is clear that XO mediates ischemia-reperfusion injury in the lung. In another experiment, SOD and catalase, oxygen radical scavenger, also protected the lungs from 60 minutes ischemia and reperfusion, which indicates that oxygen radicals involves in lung ischemia-reperfusion injury. On the other hand, we found that XD to XO conversion was not occurred by 90 minutes ischemia. Moreover, continuous ventilation during ischemia with 100 N2 decreased ischemia-reperfusion lung injury. These results suggest that XO is unlikely to be a main source of oxygen radical after reperfusion.
Recent reports demonstrated that the main source of oxygen radicals after ischemia-reperfusion was polymorphonuclear leukocyte (PMN) and tissue fixed macrophage. In addition, Terada reported that tungstate diet prevent leukocyte accumulation in the lung after intestinal ischemia. Therefore, XD and XO may contribute to PMN activation during ischemia-reperfusion.
|
