• Yasumasa Morita, Shigeto Oda, Tomohito Sadahiro, Masataka Nakamura, Taku Oshima, Shunsuke Otani, and Hiroyuki Hirasawa.
• Department of Emergency and Critical Care Medicine, Chiba University Graduate School of Medicine, 1-8-1 Inohana, Chuou, Chiba, Japan. qyj13214@nifty.com
• Cytokine. 2009 Jul 1;47(1):48-55.

Background And PurposeInjurious 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.MethodsAfter performing anesthesia, tracheostomy, and catheter insertion, rats were ventilated with 17cmH(2)O of PIP in the low-pressure (LP) group or 35cmH(2)O 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 6h.ResultsPlasma levels of pro-inflammatory cytokines, TNF-a and IL-6 at 1h 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 1h were highest in 34 degrees C-HP group, and lowest in 39 degrees C-HP group.ConclusionThe 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.

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