首页> 外文期刊>Anesthesia and Analgesia: Journal of the International Anesthesia Research Society >The electrophysiological effects of racemic ketamine and etomidate in an in vitro model of 'border zone' between normal and ischemic/reperfused guinea pig myocardium.
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The electrophysiological effects of racemic ketamine and etomidate in an in vitro model of 'border zone' between normal and ischemic/reperfused guinea pig myocardium.

机译:外消旋氯胺酮和依托咪酯在正常和缺血/再灌注豚鼠心肌之间“边界区”体外模型中的电生理作用。

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BACKGROUND: Etomidate and ketamine are used during induction of anesthesia in high-risk patients. However, their effects on action potential (AP) variables and ischemia/reperfusion-induced arrhythmias and conduction blocks are unknown. METHODS: Guinea pig right ventricular muscle strips were mounted in a 5-mL double chamber bath with the strips separated into two zones by an impermeable latex membrane. One-half (normal zone) was exposed to normal perfusate while the other half (altered zone) was exposed to hypoxia, hyperkalemia, acidosis, and lack of glucose. AP variables were recorded continuously in the normal and altered zones. Spontaneous arrhythmias and conduction blocks were noted. Etomidate (10(-7), 10(-6), and 10(-5) M) and ketamine (10(-6), 10(-5), and 10(-4) M) were superfused into the bath throughout the experiment and the electrophysiologic effects compared with the control group. RESULTS: We found that under control conditions, etomidate and ketamine did not modify resting membrane potential, maximal upstroke velocity, AP amplitude, or AP duration at 90% of repolarization (APD90). Ketamine (10(-4) M), but not weaker concentrations and none of the concentration of etomidate, reversed the ischemia-induced shortening of APD90 and APD dispersion. Etomidate and ketamine did not modify the occurrence of conduction block during simulated ischemia. In contrast, ketamine (25% at 10(-6) M, 13% at 10(-5) M, and 13% at 10(-4) M vs 90% in the control group, P < 0.05) but not etomidate (38% at 10(-7) M, 63% at 10(-6) M, and 63% at 10(-5) M vs 90% in the control group, NS) decreased the incidence of reperfusion-induced spontaneous arrhythmias. CONCLUSIONS: In guinea pig myocardium, our data suggest that ketamine, in clinically relevant concentrations, decreases ischemia-induced AP shortening and spontaneous reperfusion-induced ventricular arrhythmias. Further study is required to precisely determine the effect of etomidate on reperfusion-induced arrhythmias.
机译:背景:依托咪酯和氯胺酮用于高危患者的麻醉诱导中。但是,它们对动作电位(AP)变量和缺血/再灌注引起的心律不齐和传导阻滞的影响尚不清楚。方法:将豚鼠右心室肌条安装在5 mL双室浴中,并用不可渗透的乳胶膜将其分成两个区域。一半(正常区域)暴露于正常灌流液中,另一半(改变区域)暴露于缺氧,高钾血症,酸中毒和缺乏葡萄糖。在正常和变化区域连续记录AP变量。注意到自发性心律不齐和传导阻滞。将依托咪酯(10(-7),10(-6)和10(-5)M)和氯胺酮(10(-6),10(-5)和10(-4)M)熔入浴中在整个实验过程中,电生理效应与对照组相比。结果:我们发现,在对照条件下,依托咪酯和氯胺酮在90%的复极化(APD90)下不会改变静息膜电位,最大上冲程速度,AP振幅或AP持续时间。氯胺酮(10(-4)M),但浓度并不弱,且依托咪酯的浓度均无,可逆转缺血诱导的APD90和APD分散缩短。依托咪酯和氯胺酮不会改变模拟缺血期间传导阻滞的发生。相反,氯胺酮(在10(-6)M时为25%,在10(-5)M时为13%,在10(-4)M时为13%,而对照组为90%,P <0.05),但不是依托咪酯(在10(-7)M时38%,在10(-6)M时63%,在10(-5)M时63%与对照组的90%,NS)降低了再灌注引起的自发性心律失常的发生率。结论:在豚鼠心肌中,我们的数据表明,氯胺酮在临床上相关的浓度可降低局部缺血引起的AP缩短和自发性再灌注引起的室性心律失常。需要进一步研究以精确确定依托咪酯对再灌注引起的心律不齐的影响。

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