Lidocaine attenuates hyperoxic lung injury in rabbits

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Abstract
Background:High concentrations of oxygen acute lung injury. Neutrophils are thought to play a pivotal role in the pathogenesis of this lung injury through the release of oxygen radicals, neutral proteases, and lysosomal enzymes. Lidocaine has been shown to inhibit neutrophil function. We examined whether intravenous pretreatment with lidocaine attenuated acute lung injury induced by hyperoxia.Method:Twenty‐seven anaesthetized male rabitts were allocated to receive one of three treatments (n = 9 for each group): ventilation with 100% oxygen for 36 h with and without lidocaine treatment, and ventilation with air for 36 h without lidocaine. In the lidocaine‐treated group, a single intravenous lidocaine 2 mg/kg was administered immediately after the initiation of exposure to 100% oxygen;Results:Pure oxygen for 36 h caused no significant changes in haemodynamics, lung mechanics, or PaO2/FiO2ratio. However, hyperoxia significantly increased the lung W/D weight ratio, the influx of neutrophils into the lung, and BALF concentrations of C3a, C5a, TNF‐α, IL‐1β, and albumin. Lidocaine attenuated these increases (W/D ratio: 5.7vs5.1, %PMN: 19.2%vs1.6%, C3a: 62 ng/dlvs14 ng/dl, C5a: 7.9 ng/dlvs4.1 ng/dl, TNF‐α: 25 fmol/mlvs2.8 fmol/ml, IL‐1β: 36 fmol/mlvs2.2 fmol/ml, and albumin: 9.5 mg/dlvs2.8 mg/dl, all:P6cpmvs2.3×106cpm,Pvs4,PConclusion:These findings suggest that intravenous lidocaine has a prophylatic effect on initial hyperoxic lung injury (pulmonary vascular permeability, histopathological, and biochemical BALF changes) in rabbits. The effects of lidocaine on more severe lung injury (decreased oxygenation) caused by hyperoxia for 72 h deserve further study.