Calcium-dependent slow action potentials in potassium-depolarized guinea-pig ventricular myocardium enhanced by barium ions

1980 ◽  
Vol 315 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Tsuguhisa Ehara ◽  
Minoru Inazawa
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Ventricular Myocardium ◽  
Barium Ions ◽  
Calcium Dependent ◽  
Slow Action Potentials

Effect of temperature on isoprenaline- and barium-induced slow action potentials in guinea-pig ventricular strips

1986 ◽  
Vol 17 (5) ◽  
pp. 559-563 ◽  
Author(s):  
Stefano Manzini ◽  
Massimo Parlani ◽  
Elena Martucci ◽  
Carlo Alberto Maggi ◽  
Alberto Meli
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Effect Of Temperature ◽  
Slow Action Potentials

scholarly journals Myocardial Depressant Effects of Sevoflurane

1996 ◽  
Vol 84 (5) ◽  
pp. 1166-1176 ◽  
Author(s):  
Wyun Kon Park ◽  
Joseph J. Pancrazio ◽  
Chang Kook Suh ◽  
Carl III Lynch
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Action Potential ◽  
Papillary Muscle ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Peak Force ◽  
Rapid Cooling ◽  
K Current ◽  
Slow Action Potentials

Background The effects of anesthetic concentrations of sevoflurane were studied in isolated myocardial tissue to delineate the mechanisms by which cardiac function is altered. Methods Isometric force of isolated guinea pig ventricular papillary muscle was studied at 37 degrees C in normal and 26 mM K+ Tyrode's solution at various stimulation rates. Normal and slow action potentials were evaluated using conventional microelectrodes. Effects of sevoflurane on sarcoplasmic reticulum function in situ were also evaluated by its effect on rapid cooling contractures, which are known to activate Ca2+ release from the sarcoplasmic reticulum, and on concentrations of rat papillary muscle. Finally, Ca2+ and K+ currents of isolated guinea pig ventricular myocytes were examined using the whole-cell patch clamp technique. Results Sevoflurane equivalent to 1.4% and 2.8% depressed guinea pig myocardial contractions to approximately 85 and approximately 65% of control, respectively, although the maximum rate of force development at 2 or 3 Hz and force in rat myocardium after rest showed less depression. In the partially depolarized, beta-adrenergically stimulated myocardium, sevoflurane selectively depressed late peak force without changing early peak force, whereas it virtually abolished rapid cooling contractures. Sevoflurane did not alter the peak amplitude or maximum depolarization rate of normal and slow action potentials, but action potential duration was significantly prolonged. In isolated guinea pig myocytes at room temperature, 0.7 mM sevoflurane (equivalent to 3.4%) depressed peak Ca2+ current by approximately 25% and increased the apparent rate of inactivation. The delayed outward K+ current was markedly depressed, but the inwardly rectifying K+ current was only slightly affected by 0.35 mM sevoflurane. Conclusions These results suggest that the direct myocardial depressant effects of sevoflurane are similar to those previously described for isoflurane. The rapid initial release of Ca2+ from the sarcoplasmic reticulum is not markedly decreased, although certain release pathway, specifically those induced by rapid cooling, appear to be depressed. Contractile depression may be partly related to the depression of Ca2+ influx through the cardiac membrane. The major electrophysiologic effect of sevoflurane seems to be a depression of the delayed outward K+ current, which appears to underlie the increased action potential duration.

Sign in / Sign up

Export Citation Format

Share Document