Klockgether-Radke A P, Schulze H, Neumann P, Hellige G
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Department of Anesthesiological Research, Göttingen, Germany.
Eur J Anaesthesiol. 2004 Mar;21(3):226-30. doi: 10.1017/s0265021504003126.
Propofol may cause undesirable hypotension due to vasodilation. The underlying mechanisms are not completely understood. We investigated the mechanisms by which propofol relaxes vascular segments.
We studied the effect of propofol on isolated porcine coronary artery rings precontracted with potassium chloride or prostaglandin F2alpha.
Propofol, in a concentration-dependent manner, relaxed all segments at concentrations of 5 microg mL(-1) and above. This relaxation was unaltered in the presence of N(omega)-nitro-L-arginine, indomethacin, diltiazem and glibenclamide. Tetraethylammonium chloride, an inhibitor of the BK(Ca) K+ channel (a high conductance Ca2+-sensitive K+ channel), dose-dependently attenuated the vasodilating effect of propofol (P < 0.001).
Our results suggests that the activation of the BK(Ca) channel may contribute to the vasodilating effect of propofol, hereby causing hyperpolarization of the smooth muscle membrane and reduction of smooth muscle tone.
丙泊酚可能因血管舒张而导致不良性低血压。其潜在机制尚未完全明确。我们研究了丙泊酚使血管段舒张的机制。
我们研究了丙泊酚对用氯化钾或前列腺素F2α预收缩的离体猪冠状动脉环的作用。
丙泊酚在5微克/毫升及以上浓度时，以浓度依赖方式使所有血管段舒张。在存在N（ω）-硝基-L-精氨酸、吲哚美辛、地尔硫卓和格列本脲的情况下，这种舒张作用未改变。氯化四乙铵是大电导钙敏感钾通道（BK（Ca）钾通道）的抑制剂，它剂量依赖性地减弱丙泊酚的血管舒张作用（P < 0.001）。
我们的结果表明，BK（Ca）通道的激活可能有助于丙泊酚的血管舒张作用，从而导致平滑肌膜超极化并降低平滑肌张力。
