Dexmedetomidine inhibits 5-HT-induced intrapulmonary artery vasoconstriction.
- Author:
Lidan NONG
1
,
2
;
Chunyu DENG
;
Sujuan KUANG
;
Guangyan ZHANG
;
Jianxiu CUI
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Dexmedetomidine; pharmacology; Female; Humans; In Vitro Techniques; Male; Middle Aged; Pulmonary Artery; drug effects; Serotonin; pharmacology; Vasoconstriction; drug effects
- From: Journal of Southern Medical University 2014;34(3):303-307
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of dexmedetomidine on 5-HT-induced constrictions of isolated human intrapulmonary arteries and explore the mechanisms.
METHODSLung 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 vasoconstrictions. The influences of the endothelium removal and various drugs including L-NAME, yohimbine and indomethacin were tested on the effects of dexmedetomidine.
RESULTSDexmedetomidine (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.
CONCLUSIONDexmedetomidine can inhibit 5-HT-induced vasoconstriction of isolated human intrapulmonary arteries probably through α2-adrenergic acceptor and NO released from the endothelium.