Effect of lidocaine on expression of high mobility group box 1 protein mRNA during lidocaine-induced attenuation of pulmonary vascular endothelial dysfunction in septic rats / 中华麻醉学杂志

ABSTRACT

Objective:To evaluate the effect of lidocaine on the expression of high-mobility group box 1 protein (HMGB1) mRNA during lidocaine-induced attenuation of pulmonary vascular endothelial dysfunction in septic rats.Methods:Thirty clean-grade healthy male Sprague-Dawley rats, aged 8-12 weeks, weighing 250-300 g, were divided into 3 groups ( n=10 each) by the random number table method: sham operation group (S group), sepsis group (C group) and lidocaine group (L group). Sepsis model was developed by cecal ligation and puncture in anesthetized animals.In group S, only surgery was performed without ligation.In group L, lidocaine 10 mg/kg was injected into the tail vein immediately after model preparation, followed by 10 mg·kg -1·h -1 infusion for 3 h. Groups S and C received the equal volume of normal saline instead.At 24 h after model preparation, rats were sacrificed and blood samples were collected from the inferior vena cava, and lung tissues were harvested.Serum tumor necrosis factor-alpha (TNF-α) and syndecan-1 levels were measured by enzyme-linked immunosorbent assay, HMGB1 mRNA expression in lung tissues was detected using quantitative real-time polymerase chain reaction, wet/dry lung weight ratio was measured, and pulmonary vascular endothelial structure was observed with a transmission electron microscope. Results:Compared with group S, the serum TNF-α and syndecan-1 concentrations and wet/dry lung weight ratio were significantly increased, and the expression of HMGB1 mRNA in lung tissues was up-regulated in C and L groups ( P<0.05). Compared with group C, the serum TNF-α and syndecan-1 concentrations and wet/dry lung weight ratio were significantly decreased, and the expression of HMGB1 mRNA in lung tissues was down-regulated in group L ( P<0.05). The results of transmission electron microscope showed that the pulmonary vascular endothelium was intact and continuous, and the structure was dense in group S; the pulmonary vascular endothelium was discontinuous, and the structure was significantly loose in group C; the pulmonary vascular endothelium was basically intact, and the structure was slightly loose in group L. Conclusions:Lidocaine may reduce pulmonary vascular endothelial dysfunction in septic rats by inhibition of HMGB1 mRNA expression.