Effect of CORM-3 on blood transfusion-related acute lung injury in rats with traumatic brain injury / 中华麻醉学杂志

ABSTRACT

Objective:To evaluate the effect of carbon monoxide-releasing molecule-3 (CORM-3) on blood transfusion-related acute lung injury in rats with traumatic brain injury (TBI).Methods:Seventy-two clean-grade healthy adult male Sprague-Dawley rats, weighing 300-350 g, were divided into 4 groups ( n=18 each) using the random number table method: sham operation group (group S), TBI group (T group), TBI plus 10 ml/kg plasma transfusion group (TP group), and TBI plus 10 ml/kg plasma transfusion plus CORM-3 group (TPC group). TBI was induced by dropping a 20-g weight from 20 cm height falling freely in anesthetized rats.Plasma 10 ml/kg was infused via the femoral vein after TBI in TP and TPC groups.The rats were sacrificed at 24 h after plasma transfusion, and lung tissues were obtained for determination of wet/dry weight (W/D) ratio, cell apoptosis, and expression of caspase-3, Bid, Bim and Puma (by Western blot). The lung injury score was calculated using the results of HE staining.Lung ultrasonography was performed for assessment of sonographic score, and the apoptosis rate was calculated by the TUNEL staining method. Results:Compared with S group, the W/D ratio, lung injury score, sonographic score and apoptosis rate were significantly increased, and the expression of activated caspase-3, Bid, Bim and Puma was up-regulated in the other three groups ( P<0.05). Compared with T group, the W/D ratio, lung injury score, sonographic score and apoptosis rate were significantly increased, and the expression of activated caspase-3, Bid, Bim and Puma was up-regulated in TP group ( P<0.05). Compared with TP group, the W/D ratio, lung injury score, sonographic score and apoptosis rate were significantly decreased, and the expression of activated caspase-3, Bid, Bim and Puma was down-regulated in TPC group ( P<0.05). Conclusion:CORM-3 can reduce acute lung injury related to blood transfusion in rats with TBI, and the mechanism may be related to inhibiting cell apoptosis in lung tissues.