期刊
CYTOKINE
卷 47, 期 1, 页码 48-55出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2009.04.004
关键词
Ventilator-induced lung injury; Cytokine; Hypothermia; Normothermia; Hyperthermia
资金
- Japan Society for the Promotion of Science [16390514, 19390457]
- Grants-in-Aid for Scientific Research [16390514, 19390457] Funding Source: KAKEN
Background and purpose: Injurious ventilation with high peak inspiratory pressure (PIP) is known to cause systemic inflammatory response through cytokine production. This study was performed to examine whether body temperature could regulate cytokine production in ventilator-induced lung injury (VILI) model. Methods: After performing anesthesia, tracheostomy, and catheter insertion, rats were ventilated with 17 cm, H2O of PIP in the low-pressure (LP) group or 35 cm H2O in the high-pressure (HP) group. Then, each group was divided into three subgroups; hyperthermia (39 degrees C), normothermia (37 degrees C), and hypothermia (34 degrees C) group. Six groups were observed for 6 h. Results: Plasma levels of pro-inflammatory cytokines, TNF-a and IL-6 at 1 h after the start of observation were highest in 39 degrees C-HP group and were lowest in 34 degrees C-HP group. Furthermore, sustained high plasma levels of IL-6 were observed only in 39 degrees C-HP group. In contrast, plasma levels of anti-inflammatory cytokine, IL-10 at 1 h were highest in 34 degrees C-HP group, and lowest in 39 degrees C-HP group. Conclusion: The body temperature significantly affects cytokine production in a model of VILI. Body temperature control may be a potentially effective therapeutic modality to regulate cytokine production in VILI. (C) 2009 Elsevier Ltd. All rights reserved.
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