کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2760096 | 1150166 | 2011 | 6 صفحه PDF | دانلود رایگان |

ObjectiveTo investigate the effects of JM-1232(-) on norepinephrine (10−6 mol/L)- and high K+ (40 mmol/L)-induced contractions in isolated human gastroepiploic arteries (GEA), and to compare them with the effects of midazolam and propofol. In addition, to investigate whether the benzodiazepine-receptor antagonist, flumazenil, or μ-opioid-receptor antagonist, naloxone, influenced the vascular effects of JM-1232(-).DesignAn in vitro experimental study.SettingUniversity laboratory.ParticipantsGEA segments were used from 69 patients undergoing coronary artery bypass graft surgery.Measurements and Main ResultsJM-1232(-) produced dose-dependent relaxation effects in the rings. Although these effects of JM-1232(-) were greater than those of midazolam and propofol at high concentrations (10−5-10−4 mol/L), there were no significantly different relaxation effects at the clinical concentrations of 3 × 10−6 mol/L JM-1232(-), 3 × 10−6 mol/L midazolam, and 1 × 10−5 mol/L propofol. In addition, all these effects were independent of the presence of a functional endothelium. Vasorelaxation induced by JM-1232(-) on norepinephrine-preconstricted GEA was inhibited by flumazenil, but not by naloxone.ConclusionsThese results indicate that JM-1232(-) dose-dependently relaxes smooth muscle in human GEA, this effect being independent of the endothelium. Within the ranges of plasma concentrations achieved in clinical practice, JM-1232(-) had similar vasorelaxation effects to midazolam and propofol. JM-1232(-)-induced vasorelaxation was inhibited by flumazenil, indicating that JM-1232(-)-induced vasorelaxation occurred via peripheral benzodiazepine receptor activation in the GEA.
Journal: Journal of Cardiothoracic and Vascular Anesthesia - Volume 25, Issue 1, February 2011, Pages 72–77