| Project/Area Number |
17591629
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Anesthesiology/Resuscitation studies
|
|---|
| Research Institution | Kobe University |
|---|
Principal Investigator |
NISHINA Kahoru Kobe University, University Hospital, Assistant Professor, 医学部附属病院, 講師 (20311780)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MIKAWA Katsuya Kobe University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (40229662)
|
|---|
| Project Period (FY) |
2005 – 2006
|
| Project Status |
Completed (Fiscal Year 2006)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
|---|
| Keywords | acute lung injury / ventilation / alveolar epitheium / cytokine / fluorocarbon / neutrophil / shear stress |
|---|
| Research Abstract |
The aim of our study was to explore mechanism of ventilator-induced lung injury and seek its therapy. Acute lung injury was induced by high tidal volume ventilation (15 mL/kg) in rabbits (Injury Group). In Non-injury Group, the lungs were mechanically ventilated by standard volume (8 mL/kg). In Injury Group, oxygenation and lung compliance were decreased 2 hrs after the start of ventilation. Furthermore, plasma cytokine (IL-6) level was increased. Light microscopic examination showed that high tidal volume ventilation caused lung edema and infiltration of neutrophils into alveolar spaces. Intratracheal administration of fluorocarbon to the injured lungs attenuated aggravation of oxygenation, lung compliance, and histological damage, but failed to inhibit cytokine production. The second study used cultured alveolar epithelial type II cells (AEC-II). Shear stress for 2 hrs did not change conformation of AEC-II (A549), but increased expression of IL-6 and MCP-1 mRNA. Treatment of fluorocarbon inhibited shear stress-induced mRNA expression of the inflammatory cytokines. Our studies suggest that fluorocarbon improved oxygenation and pathological changes in in-vivo lung injury model, and attenuation of inflammation with fluorocarbon did not play an important role in the mechanism of improvement.
|
