Objective The mechanism of Verapamil in reversing alterations of cellular electrophysiology underlying ventricular arrhythmia in dogs with multiple organ dysfunction syndrome (MODS) was not reported and their relationship to arrhythmogenesis was likely very limited.
Methods 12 dogs, of weight 8.67±0.75 kg, were divided into two groups: control group (n=6) and MODS group (n=6). MODS lasting for 72 h was induced. Ventricular myocytes were enzymatically isolated. Early afterdepolarizations (EAD), action potential durations (APD) and L-type calcium currents were assessed before and after Verapamil perfusion.
Results Sinus arrhythmias in all MODS dogs (100%; 6 of 6, n=6) and premature ventricular beats in 4 MODS dogs (66%; 4 of 6, n=6) were recorded, while no arrhythmias were found in control animals. The prolongation of APD associated with decreased L-type Ca2+ currents and frequent provocation of EAD were the typical electrophysiological alterations in myocytes of MODS dogs. The AP prolongation was shortened, L-type calcium currents was decreased, EAD was suppressed by using Verapamil (100 μmol/l) in ventricular myocytes of MODS dogs (66%; 4 of 6, n=6). EAD could be induced after elusion of Verapamil.
Conclusions The cellular electrophysiology changes within 72 h in the heart of MODS dogs were APD prolongation, markedly decreased L-type Ca2+ currents as well as frequently provoked EAD. Verapamil appears to be an effective agent in reversing the alternations of cellular electrophysiology in the early stage of MODS.
- multiple organ dysfunction syndrome (MODS)
- action potential duration (APD)
- early afterdepolarizations (EAD)