scholarly journals Effects of Volatile Anesthetics on Atrial and AV Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart 

1998 ◽  
Vol 89 (2) ◽  
pp. 434-442 ◽  
Author(s):  
Pekka M. J. Raatikainen ◽  
Mark F. Trankina ◽  
Timothy E. Morey ◽  
Donn M. Dennis
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Action Potential Duration ◽  
Volatile Anesthetics ◽  
Monophasic Action Potential ◽  
Computer Assisted ◽  
Conduction Time ◽  
Av Node ◽  
Refractory Periods ◽  
Supraventricular Tachycardias

Background Knowledge of the anesthetic effects on atrial and atrioventricular (AV) nodal electrophysiologic properties is fundamental to understand the modulatory role of anesthetics on the pathogenesis of supraventricular tachycardias, and to individualize the perioperative management of patients with supraventricular tachycardias or AV nodal conduction disturbances. Therefore the authors studied the effects of three commonly used volatile anesthetics on the electrophysiologic properties of the atrium and AV node. Methods The concentration-dependent electrophysiologic effects of halothane, isoflurane, and desflurane (0-2 minimum alveolar concentration [MAC]) were studied in guinea pig Langendorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action potential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulation protocol. The concentrations of anesthetics in the gas phase were monitored by an infrared gas analyzer. Results Volatile anesthetics caused markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conduction the most, whereas desflurane caused the greatest shortening of atrial monophasic action potential duration. Halothane had no significant effect on atrial refractoriness, whereas at 2 MAC desflurane significantly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1+/-13.5% and 13.2+/-14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics to prolong AV nodal conduction time and AV nodal ERP was halothane > desflurane > isoflurane. Conclusion The different electrophysiologic effects of volatile anesthetics in the atrium and AV node suggest that these agents may modulate atrial dysrhythmogenesis in distinctly different ways.

Dual effects of external magnesium on action potential duration in guinea pig ventricular myocytes

1995 ◽  
Vol 268 (6) ◽  
pp. H2321-H2328 ◽  
Author(s):  
S. Zhang ◽  
T. Sawanobori ◽  
H. Adaniya ◽  
Y. Hirano ◽  
M. Hiraoka
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Decay Time ◽  
Action Potential Duration ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Membrane Surface ◽  
Surface Charges ◽  
Whole Cell Patch Clamp ◽  
K Current

Effects of extracellular magnesium (Mg2+) on action potential duration (APD) and underlying membrane currents in guinea pig ventricular myocytes were studied by using the whole cell patch-clamp method. Increasing external Mg2+ concentration [Mg2+]o) from 0.5 to 3 mM produced a prolongation of APD at 90% repolarization (APD90), whereas 5 and 10 mM Mg2+ shortened it. [Mg2+]o, at 3 mM or higher, suppressed the delayed outward K+ current and the inward rectifier K+ current. Increases in [Mg2+]o depressed the peak amplitude and delayed the decay time course of the Ca2+ current (ICa), the latter effect is probably due to the decrease in Ca(2+)-induced inactivation. Thus 3 mM Mg2+ suppressed the peak ICa but increased the late ICa amplitude at the end of a 200-ms depolarization pulse, whereas 10 mM Mg2+ suppressed both components. Application of 10 mM Mg2+ shifted the voltage-dependent activation and inactivation by approximately 10 mV to more positive voltage due to screening the membrane surface charges. Application of manganese (1-5 mM) also caused dual effects on APD90, similar to those of Mg2+, and suppressed the peak ICa with slowed decay. These results suggest that the dual effects of Mg2+ on APD in guinea pig ventricular myocytes can be, at least in part, explained by its action on ICa with slowed decay time course in addition to suppressive effects on K+ currents.

Action potential duration and force-frequency relationship in isolated rabbit, guinea pig and rat cardiac muscle

1996 ◽  
Vol 166 (2) ◽  
pp. 150-155 ◽  
Author(s):  
P. Szigligeti ◽  
C. Pankucsi ◽  
T. B�ny�sz ◽  
A. Varr� ◽  
P. P. N�n�si
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potential Duration ◽  
Force Frequency ◽  
Frequency Relationship

Effect of sotalol, aprindine and the combination aprindine—sotalol on monophasic action potential duration

1986 ◽  
Vol 7 (1) ◽  
pp. 47-53 ◽  
Author(s):  
R. STROOBANDT ◽  
J. BRACHMANN ◽  
H. KESTELOOT ◽  
W. KÜBLER ◽  
J. SENGES
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Monophasic Action Potential

Excitability and electrical response of ischemic heart muscle

1960 ◽  
Vol 198 (6) ◽  
pp. 1143-1147 ◽  
Author(s):  
Chandler McC. Brooks ◽  
Jerome L. Gilbert ◽  
Martin E. Greenspan ◽  
Gertrude Lange ◽  
Hector M. Mazzella
Keyword(s):  
Action Potential ◽  
Blood Supply ◽  
Heart Muscle ◽  
Action Potentials ◽  
Electrical Response ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Monophasic Action Potential ◽  
Ventricular Muscle ◽  
Refractory Periods

Measurements were made of the changes in the monophasic action potential, excitability, durations of the refractory periods and conduction times in an area of left ventricular muscle during the development of ischemia subsequent to ligation of the ramus descendens anterior. The degree and duration of the ischemia produced varied greatly and effects were related thereto. It was found that action potentials shortened as did the refractory periods; thresholds fell momentarily and then rose progressively as tissue responsiveness failed due to continuing ischemia. Latency of responses increased, the action potentials decreased in amplitude and alternation occurred before the tissue became completely unresponsive. Early re-establishment of a blood supply caused a reversal of the abnormalities. The significance of these changes to the origin of arrhythmias is discussed.

Hypoxia-induced activation of KATP channels limits energy depletion in the guinea pig heart

1995 ◽  
Vol 269 (2) ◽  
pp. H734-H742 ◽  
Author(s):  
U. K. Decking ◽  
T. Reffelmann ◽  
J. Schrader ◽  
H. Kammermeier
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Monophasic Action Potential ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
Guinea Pig Heart

The functional role of ATP-dependent potassium (KATP) in hypoxic cardiac failure was investigated in isolated guinea pig hearts with glibenclamide and rimalkalim as inhibitor and activator, respectively. Monophasic action potential duration at 90% of repolarization (MAP50), left ventricular function, and cardiac energy status (31P nuclear magnetic resonance spectroscopy) were measured during normotoxic (95% O2) and hypoxic (20% O2) perfusion. In normoxic hearts, 1 microM glibenclamide did not affect MAP50, left ventricular function, and coronary flow (n = 4). In contrast, rimalkalim rapidly shortened MAP50 and left ventricular pressure (LVP) in a dose-dependent fashion (e.g., by 60.2 +/- 3.5 and 80.8 +/- 8.2%, respectively, with 0.6 microM rimalkalim). This latter effect was reversed by 1 microM (glibenclamide (n = 4). With hypoxic perfusion, a reduction in LVP was observed, along with a shortening of the action potential (MAP90; 202 +/- 13 vs. 164 +/- 9 ms) and an increase in coronary flow. Glibenclamide (1 microM) reversed the MAP90 shortening and the increase in coronary flow. In addition, glibenclamide increased LVP transiently (n = 4). When coronary flow of hypoxic hearts was kept constant, however, glibenclamide elicited a sustained positive inotropic effect (n = 7). After glibenclamide, an increase in LVP from 54 +/- 4 to 64 +/- 3 mmHg was observed, along with a reduction in the free energy change of ATP hydrolysis from -54.5 +/- 1.9 to -52.9 +/- 0.2 nJ/mol and a further increase in the coronary venous adenosine from 269 +/- 48 to 1,680 +/- 670 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

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