Abstract

Objective To investigate the effect of dexmedetomidine pretreatment on the expression of caspase-12 in lung tissues undergoing one-lung ventilation(OLV)in rats. Methods Thirty male Sprague-Dawley rats, aged 6–8 weeks, weighing 180–220 g, were randomly allocated into 3 groups(n=10 each)using a random number table: two-lung ventilation(TLV)group, OLV group and dexmedetomidine group(Dex group). Bilateral lungs were ventilated for 2 h in group TLV.In OLV and Dex groups, unilateral lung was ventilated for 1.5 h followed by 0.5 h TLV.In group Dex, dexmedetomidine was infused intravenously at a rate of 3.0 μg·kg–1·h–1 over 60 min starting from 60 min prior to OLV.The equal volume of normal saline was given instead of dexmedetomidine in OLV and TLV groups.Peak airway pressure(Ppeak)and mean airway pressure(Paw)were recorded at 45 min of OLV and 15 min of TLV in OLV and Dex groups, and at 15 min of TLV in group TLV.The rats were then sacrificed, and left lungs were removed for microscopic examination of the pathologic changes(using HE staining)and the ultrastructure of lung tissues(with transmission electron microscope)and for determination of wet to dry lung weight ratio(W/D ratio), cell apoptosis in lung tissues(by TUNEL), caspase-12 mRNA expression(using real-time reverse transcriptase-polymerase chain reaction), and caspase-12 expression(by Western blot). Results Ppeak and Paw were significantly lower at 15 min of TLV than at 45 min of OLV in OLV and Dex groups(P<0.05). Compared to group TLV, W/D ratio and AI were significantly increased, and the expression of caspase-12 protein and mRNA was up-regulated in OLV and Dex groups(P<0.01). Compared to group OLV, W/D ratio and AI were significantly decreased, and the expression of caspase-12 protein and mRNA was down-regulated in group Dex(P<0.01). The pathologic changes of lung tissues were significantly alleviated in group Dex as compared with group OLV. Conclusion The mechanism by which dexmedetomidine pretreatment alleviates acute lung injury caused by OLV is associated with down-regulated expression of caspase-12 and inhibited cell apoptosis in rats. Key words: Dexmedetomidine; Respiration, artificial; Respiratory distress syndrome, adult; Caspase 12

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