Enflurane depression of myocardial slow action potentials

Area of Science:

• Cardiovascular Physiology
• Anesthesiology
• Cellular Electrophysiology

Background:

• Anesthetic agents like enflurane can impact cardiac function.
• Understanding the specific electrophysiological and contractile effects is crucial for patient safety.

Purpose of the Study:

• To investigate the effects of enflurane on myocardial electrophysiology and contractility.
• To determine the concentration-dependent effects of enflurane on normal and slow action potentials (APs) and muscle contractions.

Main Methods:

• Simultaneous measurement of action potentials and contractions in guinea-pig papillary muscle.
• Administration of enflurane at varying concentrations (1-6%) in a controlled perfusate.
• Induction of slow APs using isoproterenol and/or theophylline in partially depolarized muscle preparations.

Main Results:

• Normal AP maximum rate of rise (+Vmax) and amplitude were unaffected, but duration decreased at >=3% enflurane.
• Slow AP +Vmax significantly declined with enflurane concentrations of 2% (to 90%), 3% (to 80%), and 4% (to 74%).
• Cardiac contractility decreased significantly, with 4% enflurane reducing fast AP-driven contractions to 20% and slow AP-driven contractions to 35% of control.

Conclusions:

• Enflurane concentrations of 2% and above inhibit slow (Na+-Ca++) channels responsible for slow APs.
• This inhibition of slow channels likely contributes to the negative inotropic effects observed with enflurane.
• The study highlights enflurane's specific impact on cardiac electrophysiology and contractility, particularly concerning slow channel function.