scholarly journals Ionic Mechanisms Underlying Action Potential Prolongation by Focal Cerebral Ischemia in Rat Ventricular Myocytes

2009 ◽  
Vol 23 (4-6) ◽  
pp. 305-316 ◽  
Author(s):  
Ling Wang ◽  
Lihua Sun ◽  
Yanli Zhang ◽  
Huiwei Wu ◽  
Chao Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Focal Cerebral Ischemia ◽  
Rat Ventricular Myocytes ◽  
Ionic Mechanisms ◽  
Action Potential Prolongation

Electrophysiologic Mechanism Underlying Action Potential Prolongation by Sevoflurane in Rat Ventricular Myocytes

2007 ◽  
Vol 107 (1) ◽  
pp. 67-74 ◽  
Author(s):  
Jee Eun Chae ◽  
Duck Sun Ahn ◽  
Myung Hee Kim ◽  
Carl Lynch ◽  
Wyun Kon Park
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Inward Rectifier ◽  
Rat Ventricular Myocytes ◽  
Steady State Inactivation ◽  
K Current ◽  
Action Potential Prolongation ◽  
Sustained Outward Current

Abstract Background: Despite prolongation of the QTc interval in humans during sevoflurane anesthesia, little is known about the mechanisms that underlie these actions. In rat ventricular myocytes, the effect of sevoflurane on action potential duration and underlying electrophysiologic mechanisms were investigated. Methods: The action potential was measured by using a current clamp technique. The transient outward K+ current was recorded during depolarizing steps from −80 mV, followed by brief depolarization to −40 mV and then depolarization up to +60 mV. The voltage dependence of steady state inactivation was determined by using a standard double-pulse protocol. The sustained outward current was obtained by addition of 5 mm 4-aminopyridine. The inward rectifier K+ current was recorded from a holding potential of −40 mV before their membrane potential was changed from −130 to 0 mV. Sevoflurane actions on L-type Ca2+ current were also obtained. Results: Sevoflurane prolonged action potential duration, whereas the amplitude and resting membrane potential remained unchanged. The peak transient outward K+ current at +60 mV was reduced by 18 ± 2% (P < 0.05) and 24 ± 2% (P < 0.05) by 0.35 and 0.7 mm sevoflurane, respectively. Sevoflurane had no effect on the sustained outward current. Whereas 0.7 mm sevoflurane did not shift the steady state inactivation curve, it accelerated the current inactivation (P < 0.05). The inward rectifier K+ current at −130 mV was little altered by 0.7 mm sevoflurane. L-type Ca2+ current was reduced by 28 ± 3% (P < 0.05) and 33 ± 1% (P < 0.05) by 0.35 and 0.7 mm sevoflurane, respectively. Conclusions: Action potential prolongation by clinically relevant concentrations of sevoflurane is due to the suppression of transient outward K+ current in rat ventricular myocytes.

Droperidol Inhibits Intracellular Ca2+, Myofilament Ca2+Sensitivity, and Contraction in Rat Ventricular Myocytes

2005 ◽  
Vol 102 (6) ◽  
pp. 1165-1173 ◽  
Author(s):  
Toshiya Shiga ◽  
Sandro Yong ◽  
Joseph Carino ◽  
Paul A. Murray ◽  
Derek S. Damron
Keyword(s):  
Nitric Oxide ◽  
Action Potential ◽  
Action Potential Duration ◽  
Ventricular Myocytes ◽  
Nitric Oxide Production ◽  
Cellular Mechanisms ◽  
Rat Ventricular Myocytes ◽  
Oxide Production ◽  
Perfused Hearts ◽  
Ca Sensitivity

Background Droperidol has recently been associated with cardiac arrhythmias and sudden cardiac death. Changes in action potential duration seem to be the cause of the arrhythmic behavior, which can lead to alterations in intracellular free Ca concentration ([Ca]i). Because [Ca]i and myofilament Ca sensitivity are key regulators of myocardial contractility, the authors' objective was to identify whether droperidol alters [Ca]i or myofilament Ca sensitivity in rat ventricular myocytes and to identify the cellular mechanisms responsible for these effects. Methods Freshly isolated rat ventricular myocytes were obtained from adult rat hearts. Myocyte shortening, [Ca]i, nitric oxide production, intracellular pH, and action potentials were monitored in cardiomyocytes exposed to droperidol. Langendorff perfused hearts were used to assess overall cardiac function. Results Droperidol (0.03-1 mum) caused concentration-dependent decreases in peak [Ca]i and shortening. Droperidol inhibited 35 mm KCl-induced increase in [Ca]i, with little direct effect on sarcoplasmic reticulum Ca stores. Droperidol had no effect on action potential duration but caused a rightward shift in the concentration-response curve to extracellular Ca for shortening, with no concomitant effect on peak [Ca]i. Droperidol decreased pHi and increased nitric oxide production. Droperidol exerted a negative inotropic effect in Langendorff perfused hearts. Conclusion These data demonstrate that droperidol decreases cardiomyocyte function, which is mediated by a decrease in [Ca]i and a decrease in myofilament Ca sensitivity. The decrease in [Ca]i is mediated by decreased sarcolemmal Ca influx. The decrease in myofilament Ca sensitivity is likely mediated by a decrease in pHi and an increase in nitric oxide production.

Mesenteric Lymph From Rats With Thermal Injury Prolongs the Action Potential and Increases Ca2+ Transient in Rat Ventricular Myocytes

Shock ◽  
2003 ◽  
Vol 20 (5) ◽  
pp. 458-464 ◽  
Author(s):  
Atsuko Yatani ◽  
Da-Zhong Xu ◽  
Song-Jung Kim ◽  
Stephen F. Vatner ◽  
Edwin A. Deitch
Keyword(s):  
Action Potential ◽  
Thermal Injury ◽  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Mesenteric Lymph

Changes of action potential and L-type calcium channel current of Sprague–Dawley rat ventricular myocytes by different amlodipine isomers

2008 ◽  
Vol 86 (9) ◽  
pp. 620-625 ◽  
Author(s):  
Ru-xing Wang ◽  
Wen-ping Jiang
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Channel Blockers ◽  
Sprague Dawley ◽  
Patch Clamp Technique ◽  
Rat Ventricular Myocytes ◽  
Channel Current ◽  
Steady State Inactivation

To investigate the effects of S- and R-amlodipine (Aml) on action potential (AP) and L-type calcium channel current (ICa-L), the whole-cell patch-clamp technique was used on rat ventricular myocytes to record AP, ICa-L, peak currents, steady-state activation currents, steady-state inactivation currents, and recovery currents from inactivation with S-Aml and R-Aml at various concentrations. Increasing concentrations of S-Aml gradually shortened AP durations (APDs). At concentrations of 0.1, 0.5, 1, 5, and 10 μmol/L, S-Aml blocked 1.5% ± 0.2%, 25.4% ± 5.3%, 65.2% ± 7.3%, 78.4% ± 8.1%, and 94.2% ± 5.0% of ICa-L, respectively (p < 0.05), and the half-inhibited concentration was 0.62 ± 0.12 µmol/L. Current–voltage curves were shifted upward; steady-state activation and inactivation curves were shifted to the left. At these concentrations of S-Aml, the half-activation voltages were –16.01 ± 1.65, –17.61 ± 1.60, –20.17 ± 1.46, –21.87 ± 1.69, and –24.09 ± 1.87 mV, respectively, and the slope factors were increased (p < 0.05). The half-inactivation voltages were –27.16 ± 4.48, –28.69 ± 4.52, –31.19 ± 4.17, –32.63 ± 4.34, and –35.16 ± 4.46 mV, respectively, and the slope factors were increased (p < 0.05). The recovery times from inactivation of S-Aml were prolonged (p < 0.05). In contrast, R-Aml had no effect on AP and ICa-L (p > 0.05) at the concentrations tested. Thus, only S-Aml has calcium channel blockade activity, whereas R-Aml has none of the pharmacologic actions associated with calcium channel blockers.

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