Protective effects of dexmedetomidine on blunt chest trauma–induced pulmonary contusion in rats

Abstract

Dexmedetomidine is a new and highly selective α2-adrenoreceptor agonist with potent anti-inflammatory capacity. This study explored the effects of dexmedetomidine on regulating hemodynamics, the plasma tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) levels, immunohistochemical localization of nuclear factor κB (NF-κB) from blunt chest trauma-induced pulmonary contusion in rats. Fifty Sprague-Dawley rats were randomly assigned into five equal groups (n = 10) as follows: uninjured control group, uninjured plus dexmedetomidine group, injured group, injured plus dexmedetomidine group, injured plus dexmedetomidine plus yohimbine (IDY), an α2-adrenergic receptor antagonist, group. Dexmedetomidine was infused continuously through the left femoral vein cannula at the rate of 5.0 µg/kg per hour after blunt chest trauma 30 minutes in uninjured plus dexmedetomidine group, injured plus dexmedetomidine group, and IDY group. Animals in the IDY group received 0.2-mg/kg yohimbine immediately after the administration of dexmedetomidine. The right femoral artery was cannulated to monitor mean arterial pressure and heart rate and to draw blood samples. The plasma TNF-α and IL-1β levels were measured using enzyme-linked immunosorbent assays. The lung tissue NF-κB expression was determined by immunohistochemistry. Bilateral blunt chest trauma produced progressive hypotension and a prolonged descent in heart rate. The plasma TNF-α and IL-1β levels as well as the NF-κB activation of lung significantly increased after blunt chest trauma challenge alone. Dexmedetomidine not only significantly modified hemodynamics and relieved the infiltration of inflammatory cells into alveolar spaces but also inhibited the plasma TNF-α and IL-1β production as well as the lung NF-κB activation (p < 0.05, respectively). Yohimbine treatment significantly reversed the effects of dexmedetomidine (p < 0.05). The administration of dexmedetomidine has beneficial effects on pulmonary contusion from blunt chest trauma in rats. The mechanisms were likely to inhibit the NF-κB activation via α2-adrenergic receptors and attenuate the proinflammatory cytokine responses.