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利多卡因静脉输注增加健康小鼠机械通气时血浆抗炎细胞因子IL-10
Original Article
Lidocaine increases the anti-inflammatory cytokine IL-10 following mechanical ventilation in healthy mice
S. VAN DER WAL1,*, M. VANEKER1, M. STEEGERS1, B. VAN BERKUM1, M. KOX2, J. VAN DER LAAK3, J. VAN DER HOEVEN2, K. VISSERS1 andG. J. SCHEFFER1
Article first published online: 14 OCT 2014
DOI: 10.1111/aas.12417
Background
Mechanical ventilation (MV) induces an inflammatory response that may result in (acute) lung injury. Lidocaine, an amide local anesthetic, has anti-inflammatory properties in vitro and in vivo, possibly due to an attenuation of pro-inflammatory cytokines, intracellular adhesion molecule-1 (ICAM-1), and reduction of neutrophils influx. We hypothesized an attenuation of MV-induced inflammatory response with intravenously administered lidocaine.
Methods
Lidocaine (Lido) (2, 4, and 8 mg/kg/h) was intravenously administered during 4 h of MV with a tidal volume of 8 ml/kg, positive end expiratory pressure 1,5 cmH2O and FiO2 0.4. We used one ventilated control (CON) group receiving vehicle. After MV, mice were euthanized, and lungs and blood were immediately harvested, and cytokine levels and ICAM-1 levels were measured in plasma and lung homogenates. Pulmonary neutrophils influx was determined in LEDER-stained slices of lungs. Anesthetic need was determined by painful hind paw stimulation.
Results
Lidocaine-treated animals (Lido 2, 4 and 8 mg/kg/h) showed higher interleukin (IL)-10 plasma levels compared to control animals. Lidocaine treatment with 8 mg/kg/h (Lido 8) resulted in higher IL-10 in lung homogenates. No differences were observed in pro-inflammatory cytokines, ICAM-1, and pulmonary influx between the different ventilated groups.
Conclusions
Intravenously administered lidocaine increases levels of plasma IL-10 with infusion from 2, 4, and 8 mg/kg/h and pulmonary levels of IL-10 with 8 mg/kg/h in a murine mechanical ventilation model. Intravenously administered lidocaine appears to reduce anesthetic need in mice.
http://onlinelibrary.wiley.com/doi/10.1111/aas.12417/abstract
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