| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2795039 | Cytokine | 2009 | 8 Pages |
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 °C), normothermia (37 °C), and hypothermia (34 °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 °C-HP group and were lowest in 34 °C-HP group. Furthermore, sustained high plasma levels of IL-6 were observed only in 39 °C-HP group. In contrast, plasma levels of anti-inflammatory cytokine, IL-10 at 1 h were highest in 34 °C-HP group, and lowest in 39 °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.
