Dexmedetomidine inhibits 5-HT-induced intrapulmonary artery vasoconstriction

NONG Lidan; DENG Chunyu; KUANG Sujuan; ZHANG Guangyan; CUI Jianxiu

doi:10.3969/j.issn.1673-4254.2014.03.03

Abstract：Objective To investigate the effect of dexmedetomidine on 5- HT- induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms. Methods Lung tissue was obtained from patients undergoing surgery for lung carcinoma. Intrapulmonary arteries were dissected and cut into rings, which were mounted in a Multi Myograph system to determine the effect of dexmedetomidine (0.3-3 nmol/L) on 5-HT-induced vasoconstractions. The influences of the endothelium removal and various drugs including L-NAME, yohimbine and indomethacin were tested on the effects of dexmedetomidine. Results Dexmedetomidine (0.1-100 nmol/L) did not obviously affect the resting tension of endothelium-intact human intrapulmonary arteries. 5- HT induced concentration- dependent contraction in endothelium- intact intrapulmonary arteries[pD2:6.11 ± 0.05, Emax:(102.10 ± 1.96)%]. In the rings with intact endothelium, dexmedetomidine (0.3-3 nmol/L) significantly attenuated the Emax and pD2 of 5-HT-induced vasoconstriction[pD2:5.94±0.03, Emax:(79.96±1.31)%]. 5-HT also induced concentration-dependent contraction in endothelium-denuded intrapulmonary arteries [pD2: 6.10 ± 0.07, Emax:(107.40 ± 3.20)%]. Dexmedetomidine produced no significant effects on the rings with denuded endothelium. The effects of dexmedetomidine on 5-HT-induced vasoconstriction was suppressed by L-NAME and yohimbine, but not by indomethacin. Conclusion Dexmedetomidine can inhibit 5-HT-induced vasoconstriction of isolated human intrapulmonary arteries probably throughα2-adrenergic acceptor and NO released from the endothelium.