Electrophysiologic Mechanisms of Sevoflurane on Prolongation of the QT Interval: K+ Currents in Rat Ventricular Myocytes.
10.4097/kjae.2006.50.4.454
- Author:
Jee Eun CHAE
1
;
Chong Hoon KIM
;
Kyung Tae MIN
;
Wyun Kon PARK
Author Information
1. Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul, Korea. wkp7ark@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
action potential;
inwardly rectifying K+ current;
rat;
sevoflurane;
transient outward K+ current;
ventricular myocytes
- MeSH:
Action Potentials;
Animals;
Heart;
Membrane Potentials;
Muscle Cells*;
Rats*
- From:Korean Journal of Anesthesiology
2006;50(4):454-462
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Whereas sevoflurane (SEVO) has been reported to prolong the QT interval, little has been known on the electrophysiologic effects of SEVO which contributes to the prolongation of action potential (AP) duration. METHODS: The ventricular myocytes were obtained from enzymatically treated rat hearts. The standard whole cell voltage-clamp methods were used. The AP was measured using current clamp technique. As a repolarizing K+ current, the transient outward K+ current (I(to)), the sustained outward K+ current (I(sus)), and the inwardly rectifying K+ current (I(kI)) were measured. The L-type Ca2+ current (I(Ca), L) was also obtained. After the baseline measurements, the myocytes were exposed to 1.7 and 3.4% SEVO. SEVO concentrations in Tyrode superfusate at room temperature were 0.35 and 0.7 mM for 1.7 and 3.4% SEVO, respectively. Results are mean +/- SEM. RESULTS: SEVO prolonged the AP duration, while the amplitude and the resting membrane potential remained unchanged. At membrane potential of +60 mV, peak I(to) was significantly reduced by 18 +/- 2 and 24 +/- 2% by 0.35 and 0.7 mM SEVO, respectively. 0.7 mM SEVO did not shift the steady-state inactivation curve. Isus was unaffected by 0.7 mM SEVO. The I(kI) at -130 mV was little altered by 0.7 mM SEVO. I(Ca), L was significantly reduced by 28 +/- 3 and 33 +/- 1% by 0.35 and 0.7 mM SEVO, respectively. CONCLUSIONS: Prolongation of AP duration by SEVO in rat ventricular myocytes is likely to be caused by a reduction of I(to). Resting membrane potential was unaffected by SEVO, which seems to be related to no alteration of I(kI).
