Intravenous lidocaine attenuates acute lung injury induced by hydrochloric acid aspiration in rabbits

Background: Neutrophils play a crucial role in the pathogenesis of acid-induced acute lung injury. Lidocaine inhibits the function of neutrophils. This study aimed to determine whether lidocaine attenuates acute lung injury induced by hydrochloric acid (HC1) instillation. Methods: In study 1, rabbits were divided into four groups (n = 7 each). Lung injury was induced by intratracheal HC1 (0.1 N, 3 ml/kg) in two groups. The other two groups received saline intratracheally. Lidocaine given intravenously (2 mg/kg bolus + 2 mg.kg(-1).h(-1) infusion) was started 10 min before intratracheal instillation in one HC1 and one saline group, and saline Teas given intravenously in the other two groups. In study 2, rabbits (four groups of seven animals each) received HC1 (0.1 N, 3 ml/kg) intratracheally. Treatment with intravenous lidocaine was started 10 min before, 10 min after, or 30 min after acid instillation, or saline was given intravenously 10 min before instillation. Results: In study 1, HC1 caused deterioration of the partial pressure of oxygen (Pa-O2), lung leukosequestration, decreased lung compliance, and increased the lung met-to-dry weight ratio and albumin, interleukin-6 (IL-6), and IL-8 levels in bronchoalveolar lavage fluid. Lidocaine pretreatment attenuated these changes. Hydrochloric acid increased superoxide anion production by neutrophils and caused morphologic lung damage, both of which were lessened by lidocaine. In study 2, lidocaine given 10 min after acid instillation was as effective as pretreatment in Pa-O2 lung mechanics, and histologic examination. However, Pa-O2 changes in lidocaine 30 min after injury were similar to those in saline given intravenously. Conclusions: Intravenous lidocaine started before and immediately after acid instillation attenuated the acute lung injury, in part by inhibiting the sequestration and activation of neutrophils.