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- W2034381030 abstract "The slowly activating delayed-rectifier potassium current, IKs, is a major outward current responsible for the repolarization of the cardiac action potential (AP). Dysfunction of this channel can lead to AP prolongation, resulting in the long QT syndrome. We hypothesized that anesthetic-induced AP prolongation is caused by inhibition of IKs, in addition to the inhibition of IKr (rapidly activating delayed-rectifier potassium channel current), a condition often found in drug-induced AP prolongation. The whole-cell patch clamp technique was used to study the effects of isoflurane on IKs and IKr recorded from guinea pig single ventricular myocytes. The effect of protein kinase C on IKs inhibition by isoflurane was also investigated. Isoflurane inhibited IKs in a concentration- and temperature-dependent manner. The inhibitory effects of isoflurane at clinically relevant concentrations of 0.3 and 0.6 mM were greater at 22°C than at 36°C. Voltage-dependent activation of IKs was not affected at these concentrations. IKs deactivation kinetics were accelerated by isoflurane at 22°C but not at 36°C. Isoflurane inhibition of IKs was significantly greater than that of IKr. Protein kinase C activation enhanced IKs but did not suppress the inhibitory effect of isoflurane. Our results suggest that IKs inhibition is one of the mechanisms underlying anesthetic-induced AP and QT prolongation. Because most of the ion channel studies on anesthetic effects are conducted at room temperature, the temperature-dependent effect on IKs confirms the importance of anesthetic experiments conducted at physiological temperature." @default.
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- W2034381030 date "2003-05-01" @default.
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- W2034381030 title "The Effects of Isoflurane on the Cardiac Slowly Activating Delayed-Rectifier Potassium Channel in Guinea Pig Ventricular Myocytes" @default.
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- W2034381030 doi "https://doi.org/10.1213/01.ane.0000057604.56578.77" @default.
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