Effects of 2,3‐Butanedione Monoxime on Atrial—Atrioventricular Nodal Conduction in Isolated Rabbit Heart

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Abstract
2,3-Butanedione monoxime (BDM) has been found to reversibly block cardiac contraction, without blocking electrical conduction. This study characterizes the dose-dependent effects of BDM on the conduction through the atrioventricular node (AVN) of rabbit heart. Thirteen isolated atrial-AVN preparations were used in control, during and after exposure to 5, 10, and 20 mM BDM. Anterograde and retrograde pacing protocols were used to obtain the Wenckebach cycle length, effective and functional refractory periods of the AVN, index of AVN conduction delay (the area under the AVN conduction curve), as well as index of intra-atrial conduction delay between the AVN inputs. Compared to control, 5 and 10 mM BDM produced either shortening or no effect on all of the above parameters except a slight (6% and 14%, respectively) increase in the intra-atrial delay. At 20 mM, BDM produced a further increase in the intra-atrial delay (up to 50%) as well as in the retrograde AVN conduction delay (up to 16%), while the characteristics of the anterograde conduction were still improved. The effects of perfusion with BDM on these parameters were reversible after washout. Aside from its known effect as an electromechanical uncoupler, BDM reversibly altered some of the electrical responses of the AVN. Most of these alterations, however, did not impede but rather improved AVN conduction. Since a dose of 10 mM is sufficient to fully eliminate undesirable motion, BDM should be considered a safe and valuable tool in AVN studies in vitro requiring a mechanically quiescent preparation.

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