Effect of dexmedetomidine on cell apoptosis during lung ischemia-reperfusion injury in a rat model of cardiopulmonary bypass

Abstract

Objective To evaluate the effect of dexmedetomidine on cell apoptosis during lung ischemia-reperfusion (I/R) injury in a rat model of cardiopulmonary bypass (CPB). Methods Ninety-six SPF healthy adult male Sprague-Dawley rats, weighing 350-500 g, were divided into 4 groups (n=24 each) using a random number table method: sham operation group(group S), CPB group(group C), CPB plus left lung I/R group (group IR), and CPB plus left lung I/R plus dexmedetomidine group (group D). The chest was only opened, and the rats underwent no CPB in group S. Only the CPB model was established in group C. The model of left lung I/R injury was established based on the CPB model in group IR.In group D, the model of CPB plus left pulmonary I/R injury was established, dexmedetomidine was intravenously infused in a dose of 3 μg/kg through the tail vein, followed by a continuous infusion of 1.5 μg·kg-1·h-1 until the end of surgery.Eight rats were selected in each group before operation (T0), at 10 min after opening the left hilum (T1), and at the end of operation (T2), the left lung tissues were taken for examination of pathological changes (with a light microscope) which were scored and for determination of cell apoptosis, and immunohistochemistry score (IHS) was assessed.The apoptosis index was calculated. Results Compared with group S, the pathological changes of lung tissues, IHS and apoptosis index were significantly increased at T1, 2 in the other three groups (P<0.05). Compared with group C, the pathological changes of lung tissues, IHS and apoptosis index were significantly increased at T1, 2 in IR and D groups (P<0.05). Compared with group IR, the pathological changes of lung tissues, IHS and apoptosis index were significantly decreased at T2 in group D (P<0.05). Conclusion The mechanism by which dexmedetomidine reduces lung I/R injury during CPB is related to inhibiting cell apoptosis in rats. Key words: Dexmedetomidine; Extracorporeal circulation; Lung; Reperfusion injury; Apoptosis