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Possible Mechanisms of Relaxing Effect of Ketamine on Isolated Rat Aorta

Ketamine在離體大白鼠主動脈之血管作用可能的機轉

摘要


本實驗是以離體老鼠主動脈環,完整內皮和去除內皮兩種型式,先以phenylephrine(alpha-1 agonist)10^(-6) M,或高鉀溶液75 mM誘發收縮,累加ketamine(10^(-6)-10^(-3) M)舒張之,做出劑量-反應曲線,發現ketamine對於完整內皮之血管舒張作用,比去除內皮型式高。其劑量-反應曲線呈有意義之右移,顯示ketamine之直接血管張作用,部份與內皮有關。可能是經由endothelium-derived relaxing factor(EDRF)的釋放,此有待進一步探討。ketamine對於血管平滑肌之舒張作用的轉機,能抑制phenylephrine誘發之receptor-mediated鈣離子內流和sarcoplasmic reticulum釋放鈣離子,而且phasic phase比tonic phase抑制大。Ketamine也能抑制高鉀溶液誘發之voltage-dependent鈣離子內流,而且fast phase比slow phase抑制大。我們的結論是ketamine之直接血管舒張作用部份與內皮有關。其可能作用機轉包括鈣離子內流和EDRF之釋放。

並列摘要


The influence of endothelium on the vasodilating effect of ketamine and its possible mechanisms of action on intracellular calcium concentrations were investigated. Experiments were carried out using isolated rat aortic rings in vitro, preconstructed with phenylphrine (an alpha-1 adrenoceptor agonist) and high concentration of potassium. We found that the vasodilating effect of ketamine was greater in aortic reings with intact endothelium than in denuded endothelium preparations in a dose-dependent manner. This indicated that the relaxation effect of ketamine is partially endothelium-dependent in rat aorta. Ketamine (pre-treatment, 10^(-4) M) significantly inhibited the fast phase of contraction induced by phenylephrine (10^(-5) M). Ketamine (pre-tratment, 10^(-4) M) also signicantly inhibited both the fast and slow phases of contraction produced by high concentration of potassium (75 mM). We concluded that the vasodilating effect of ketamine is partially endothelium-dependent and that mechanisms of this effect may involve inhibition of calcium influx and release of an endothelium-derived relaxing factor.

並列關鍵字

Ketamine Endothelium Phenylephrine High potassium Rat aorta

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