2,3-Butanedione monoxime (BDM) decreases sarcoplasmic reticulum Ca content by stimulating Ca release in isolated rat ventricular myocytes

1998 ◽  
Vol 436 (5) ◽  
pp. 776-781 ◽  
Author(s):  
W. Adams ◽  
A. W. Trafford ◽  
D. A. Eisner
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Butanedione Monoxime ◽  
Isolated Rat

Antagonistic Actions of Halothane and Sevoflurane on Spontaneous Ca2+Release in Rat Ventricular Myocytes

2006 ◽  
Vol 105 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Mark D. Graham ◽  
Philip M. Hopkins ◽  
Simon M. Harrison
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Positive Inotropic Effect ◽  
Ventricular Myocytes ◽  
Inotropic Effect ◽  
Release Process ◽  
Rat Ventricular Myocytes ◽  
Fura 2 ◽  
Threefold Increase ◽  
Subcellular Target ◽  
Isolated Rat

Background Halothane has been reported to sensitize Ca(2+) release from the sarcoplasmic reticulum (SR), which is thought to contribute to its initial positive inotropic effect. However, little is known about whether isoflurane or sevoflurane affect the SR Ca(2+) release process, which may contribute to the inotropic profile of these anesthetics. Methods Mild Ca(2+) overload was induced in isolated rat ventricular myocytes by increase of extracellular Ca(2+) to 2 mM. The resultant Ca(2+) transients due to spontaneous Ca(2+) release from the SR were detected optically (fura-2). Cells were exposed to 0.6 mM anesthetic for a period of 4 min, and the frequency and amplitude of spontaneous Ca(2+) transients were measured. Results Halothane caused a temporary threefold increase in frequency and decreased the amplitude (to 54% of control) of spontaneous Ca(2+) transients. Removal of halothane inhibited spontaneous Ca release before it returned to control. In contrast, sevoflurane initially inhibited frequency of Ca(2+) release (to 10% of control), whereas its removal induced a burst of spontaneous Ca(2+) release. Isoflurane had no significant effect on either frequency or amplitude of spontaneous Ca(2+) release on application or removal. Sevoflurane was able to ameliorate the effects of halothane on the frequency and amplitude of spontaneous Ca(2+) release both on application and wash-off. Conclusions Application of halothane and removal of sevoflurane sensitize the SR Ca(2+) release process (and vice versa on removal). Sevoflurane reversed the effects of halothane, suggesting they may act at the same subcellular target on the SR.

Effects of the Ca2+ sensitizer EMD 57033 on intracellular Ca2+ in rat ventricular myocytes: relevance to arrhythmogenesis during positive inotropy

2000 ◽  
Vol 99 (6) ◽  
pp. 547-554 ◽  
Author(s):  
Makoto KAWAI ◽  
John A. LEE ◽  
Clive H. ORCHARD
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Rise Time ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Troponin C ◽  
Intact Cells ◽  
Positive Inotropy ◽  
Rat Ventricular Myocytes ◽  
Cross Bridge ◽  
Butanedione Monoxime

We have investigated the effects of the calcium-sensitizing inotropic agent EMD 57033 on Ca2+ handling in intact and skinned rat ventricular myocytes. Intracellular Ca2+ was monitored using fura 2. Myocytes were saponin-skinned, allowing study of sarcoplasmic reticulum (SR) function. In intact myocytes EMD 57033 (1–10 µmol/l) produced a concentration-dependent decrease in the amplitude of the Ca2+ transient and prolonged its declining phase, but had no effect on the rise time. In skinned myocytes, the amplitude of spontaneous Ca2+ release from the SR was decreased by EMD 57033 (5 and 10 µmol/l), although this agent had no significant effect on the frequency of spontaneous Ca2+ release. In the presence of the cross-bridge inhibitor 2,3-butanedione monoxime (5 mmol/l), or in a low bathing Ca2+ concentration (1 mmol/l), EMD 57033 (10 µmol/l) had smaller effects on both the amplitude and time course of the Ca2+ transient in intact cells than in the absence of 2,3-butanedione monoxime or in the presence of 2 and 5 mmol/l Ca2+ respectively. These data suggest that the effects of EMD 57033 on Ca2+ are due to changes in Ca2+ binding to troponin C, secondary to cross-bridge formation. Thus, during positive inotropy, EMD 57033 is unlikely to provoke arrhythmias due to effects on SR Ca2+ handling. In intact cells, its effects on Ca2+ handling would be expected to protect against arrhythmias.

Estimation of myofibrillar responsiveness to Ca 2+ in isolated rat ventricular myocytes

1998 ◽  
Vol 436 (5) ◽  
pp. 639-645 ◽  
Author(s):  
K. Hongo ◽  
Yoichiro Kusakari ◽  
Masato Konishi ◽  
Satoshi Kurihara ◽  
Seibu Mochizuki
Keyword(s):  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Isolated Rat

Effect of partial blockade of the Na+/Ca2+-exchanger on Ca2+ handling in isolated rat ventricular myocytes

2007 ◽  
Vol 576 (1-3) ◽  
pp. 1-6 ◽  
Author(s):  
Károly Acsai ◽  
Attila Kun ◽  
Attila S Farkas ◽  
Ferenc Fülöp ◽  
Norbert Nagy ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Partial Blockade ◽  
Isolated Rat
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