Electrophysiologic Mechanisms of Sevoflurane on Prolongation of the QT Interval: K+ Currents in Rat Ventricular Myocytes / 대한마취과학회지

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).

Electrophysiologic Effect of Desflurane on the Prolongation of Action Potential Duration in Ventricular Myocytes / 대한마취과학회지

BACKGROUND: Desflurane has been reported to prolong the QTc. Several ionic currents that contribute to the prolongation of the action potential (AP) duration were investigated using guinea pig (GP) and rat ventricular myocytes. METHODS: The normal APs were measured in isolated GP papillary muscles at 37 degrees C. Ventricular myocytes were obtained from GP and rat hearts. Both the delayed outward K+ current (I(K)) and the inward rectifier K+ current (I(KI)) were assessed using a voltage ramp protocol. A more detailed study on the I(K) was performed. The ICa, L was measured. In the rat ventricular myocytes, the transient outward K+ current (I(to)) was obtained. All the patch clamp experiments were carried out at room temperature. The values are presented as mean +/- SD. RESULTS: 0.91 mM desflurane significantly prolonged the APD in the GP ventricular myocytes. Using a linear voltage ramp protocol, the I(KI) at -130 mV and the peak outward I(KI) at -60 to -50 mV were not found to be significantly reduced by 0.78 and 1.23 mM desflurane, respectively. However, the peak outward I(K) at +60 mV was significantly reduced to 63 +/- 19% and 58 +/- 12% of the baseline by 0.78 and 1.23 mM desflurane, respectively. At a membrane potential of +60 mV, 0.78 and 1.23 mM desflurane reduced the Ito to 80 +/- 8% and 68 +/- 7%, respectively. A concentration-dependent reduction in the ICa, L was observed. CONCLUSIONS: The prolongation of the APD induced by clinically relevant concentrations of desflurane in GP and rat ventricular myocytes is most likely the result of I(K) and I(to) suppression.

Significance of Brain Protection and Neurophysiological Monitoring in Carotid Endarterectomy

We present our results of carotid endarterectomy performed in 12 patients(bilateral in 2 patients) under prospective brain protection-monitoring protocol during the past two years. The protocol consists of induced hypertension, mild hypothermia, and pentothal burst suppression under bipolar two-channel compressed spectral array(CSA) monitoring. Eleven of the 12 patients recovered without any new deficit from the surgery, and this result was expected as their CSA monitoring showed no significant changes. One patient had multiple untreated aneurysms, and therefore, hypertension was not applied. This patient developed significant postoperative neurological deficits correlated well with the CSA changes. One of the major advantages of CSA monitoring is that dosage of thiopental sodium for burst suppression, that varied greatly from 1,016mg to 3,220mg, could be titrated on each patient based upon the CSA findings. Another important benefit of our brain protection-monitoring protocol is that unnecessary shunting procedure could be avoided. In conclusion, brain protection under CSA monitoring could prevent dangerous ischemic insults from circulatory disruption on already vulnerable ischemic hemisphere in patients requiring carotid endarterectomy.

The Realization of Early Diagnostic System for Cerebral Ischemia Using Compressed Spectral Array(CSA)

The trials to detect the cerebral ischemia during the brain surgery have been continued since last three decades. The intraoperative Xenon isotope cerebral blood flow(CBF) measurement and EEG monitoring were proven to be useful techniques for this purpose. But these techniques have several drawbacks and are not easily applicable in most institutions. Authors, therefore, developed a intraoperative cerebral ischemia monitoring system which applied the digital electroencephalography(EEG) and compressed spectral array(CSA) technique. Technical details of our system and the examples of clinical applications are described.