Klockgether-Radke A P, Pawlowski P, Neumann P, Hellige G
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Department of Anaesthesiological Research, Göttingen, Germany.
Eur J Anaesthesiol. 2005 Feb;22(2):135-9. doi: 10.1017/s0265021505000256.
Hypotension, especially in elderly and hypovolaemic patients, is frequently associated with intravenous midazolam administration. The mechanisms are not completely understood. This study was designed to investigate the mechanisms involved in the relaxing effect of midazolam on coronary arteries.
The substance was studied in isolated porcine coronary artery rings precontracted by either potassium chloride or prostaglandin F2alpha.
Midazolam caused vasodilatation in a concentration-dependent manner. Relaxation was more pronounced in prostaglandin F2alpha precontracted segments than in those treated with potassium chloride (P < 0.001). Vasodilatation was unaffected by Nomega-nitro-L-arginine, indomethacin and glibenclamide. Tetraethylammonium chloride, an inhibitor of the BK(Ca) K+ channel (a high conductance Ca(2+)-sensitive K+ channel), dose dependently attenuated the vasodilating effect of midazolam (P < 0.01).
Hyperpolarization of the smooth muscle cell in the vessel wall, elicited by the activation the BK(Ca) K+ channel, may contribute to the vasorelaxing effect of midazolam.
低血压，尤其是在老年和低血容量患者中，常与静脉注射咪达唑仑有关。其机制尚未完全明确。本研究旨在探究咪达唑仑对冠状动脉舒张作用的相关机制。
在由氯化钾或前列腺素F2α预收缩的离体猪冠状动脉环中研究该物质。
咪达唑仑呈浓度依赖性地引起血管舒张。在前列腺素F2α预收缩的节段中舒张作用比用氯化钾处理的节段更明显（P < 0.001）。血管舒张不受Nω-硝基-L-精氨酸、吲哚美辛和格列本脲的影响。氯化四乙铵，一种BK（Ca）钾通道（一种高电导钙敏感钾通道）的抑制剂，剂量依赖性地减弱咪达唑仑的血管舒张作用（P < 0.01）。
血管壁平滑肌细胞的超极化，由BK（Ca）钾通道的激活引发，可能有助于咪达唑仑的血管舒张作用。
