Effects of sugammadex and rocuronium on electro-mechanical activity of cardiac myocytes

Sugammadex reverses the effects of steroidal neuromuscular-blocking agents, such as rocuronium, by encapsulating these agents. Its cardiovascular adverse effects include QTc prolongation, hypotension, bradycardia, atrioventricular block, atrial fibrillation, and asystole. Additionally, rocuronium has cardiac side effects, such as bradycardia, hypotension, cardiac arrest, circulatory collapse, and ventricular fibrillation. Herein, we investigated the effects of sugammadex, rocuronium, and combined rocuronium + sugammadex on cardiac electrophysiological parameters.

In vitro experiments were performed using ventricular myocytes obtained from male Wistar rats. Myocyte contraction and relaxation responses were recorded along with action potential (AP), and L-type calcium (ICaL) and potassium channel currents (Ito, Iss, and IK1).

Sugammadex caused dose-dependent decreases in myocyte contraction and relaxation responses. Rocuronium had no effect in this respect, whereas its co-administration with sugammadex led to decreased contraction responses. Sugammadex prolonged the AP repolarization phase, whereas rocuronium prolonged all AP phases. Co-administration of sugammadex and rocuronium did not significantly affect AP parameters. Sugammadex suppressed the peak ICaL value, while rocuronium caused an even greater decrease. Co-administration of these drugs further decreased the current-voltage characteristics of the ICaL. However, no significant effects were observed on the potassium currents.

Separate or combined administration of sugammadex and rocuronium had various effects on myocyte contractility, AP, and ICaL, which could cause significant changes leading to adverse cardiac events. Further experimental and clinical studies are required to understand the clinical consequences of the modulatory effects of these drugs on cardiac electrophysiological parameters.