2002 Fiscal Year Final Research Report Summary
Partial liquid ventilation as an anti-inflammatory treatment in ARDS
| Project/Area Number |
12671454
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Tokyo Medical & Dental University |
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Principal Investigator |
NAKAZAWA Koichi Tokyo Medical & Dental University, Anesthesiology, Associate Professor, 大学院・医歯学総合研究科, 助教授 (10207756)
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| Co-Investigator(Kenkyū-buntansha) |
MAKITA Koshi MAKITA,Koshi, 大学院・医歯学総合研究科, 教授 (20199657)
YOKOYAMA Kuninori YOKOYAMA,Kuninori, 大学院・医歯学総合研究科, 助手 (00014176)
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| Project Period (FY) |
2000 – 2002
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| Keywords | ARDS / Perflubron / Liquid ventilation / Partial liquid ventilation / Endotoxemia |
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| Research Abstract |
To determine whether partial liquid ventilation (PLV) modified lung inflammatory response, we analyzed blood cytokine levels and cytokine mRNA expression in the lungs, using a rat model of endotoxemia. Thirty-six rats were allocated into one of four groups. The first group received conventional gas ventilation (CV group), the second group received 10 ml/kg perflubron intratracheally in combination with mechanical gas ventilation (PLV group), the third group received 20mg/kg Escherichia coli lipopolyssacharide (LPS) intravenously in combination with mechanical gas ventilation (LPS group), and the fourth group received PLV and LPS (PLAT+LPS group). Blood levels of TNF-α, IL-1β, IL-6, IL-10, INF-γ and IL-1 receptor antagonist were significantly increased in LPS and PLV+LPS groups. mRNA expression of pro-and anti-inflammatory cytokines in the lung tissue was also significantly increased in these groups. mRNA expression of IL-6 in PLV+LPS group was significantly increased in comparison with LPS group. Other cytokine mRNA expression including IL-10 and IL-1β was also potentiated in PLV+LPS group, however this was not significant. Our results suggest that PLV does not protect the lungs against inflammation in systemic endotoxemia in rats
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