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Galantamine protects against hydrochloric acid aspirationinduced acute respiratory distress syndrome in rabbits
Abstract
Purpose: To study the effect of galantamine on anti-inflammatory responses in acid aspiration-induced acute respiratory syndrome (ARDS), and the underlying mechanism.
Methods: Six groups of male rabbits (156), i.e., control group, ARDS group, galantamine + ARDS (GAL) group, galantamine + ARDS + methyllycaconitine (MLA) group, galantamine + ARDS + vagotomy (Vag) group, and galantamine + ARDS + atropine sulfate (ATS) group. ARDS model was produced by acid aspiration. After 4 h, TNF-α, IL-6 and IL-1β were assayed in lung tissue, while corticosterone levels were determined in blood. Histopathological lesions and wet-to-dry (W/D) weight ratio of lung tissue (n = 10) were assessed. After 12 h, HMGB1 protein and corticosterone levels were determined in lung tissue and blood, respectively. Mortality rate was determined after 72 h.
Results: Acid aspiration-induced ARDS induced disorganization of lung structure, and elevated TNF-α, IL-6, IL-1β, and HMGB1activities, and lung W/D weight ratio. The acid-induced ARDS, as well as increases in W/D weight ratio, pro-inflammatory cytokines and lung lesions were significantly decreased by galantamine pretreatment. Methyllycaconitin, vagotomy and atropine sulfate abolished the galantamine-induced suppression of acute inflammatory response, pathological changes in lungs, and W/D weight ratio. However, serum corticosterone levels were not significantly altered in each group.
Conclusion: Galantamine reduces inflammation in acid aspiration-induced ARDS by the cholinergic anti-inflammatory pathway.
Keywords: Galantamine, Hydrochloric acid, Aspiration-induced, Respiratory distress syndrome, Methyllycaconitin, Vagotomy, Atropine sulfate
