The effects of chemical subendocardial ablation on the activation rate gradient during ventricular fibrillation. Cha, Yong-Mei, Takumi Uchida, Paul L. Wolf, Barry B. Peters, Michael C. Fishbein, Hrayr S. Karagueuzian, and Peng-Sheng Chen. Division of Cardiology, Department of Medicine (Y.-M.C., B.B.P.) and the Department of Pathology (P.L.W.), the UCSD and the Veterans Affairs Medical Centers, San Diego, and the Department of Pathology (M.C.F) and the Division of Cardiology, Department of Medicine (H.S.K and P.-S.C), Cedars-Sinai Medical Center and UCLA School of Medicine, Los Angeles, California
APStracts 2:0226H, 1995.
The mechanism by which an endocardial-epicardial activation rate gradient develops after one or two minutes of sustained ventricular fibrillation is unknown. We recorded from electrodes on the epicardium and from hook electrodes in the endocardium in 3 open -chest control dogs during prolonged ventricular fibrillation. The same recordings were also made in 7 dogs after right ventricular subendocardial ablation with Lugol's solution, and in 3 dogs after substituting air for the cavitary blood. The effects of these interventions, i.e., Lugol's ablation (N=2) and the exposure to air (N=2) on the subendocardial Purkinje fiber transmembrane action potential properties were also evaluated in vitro using microelectrode recording techniques. The in vivo studies showed a significant endocardial-epicardial rate gradient in the control dogs and in dogs that had air substituting for the cavitary blood. In comparison, in dogs that underwent chemical subendocardial ablation, the activation cycle lengths for the endocardium and the epicardium were not significantly different. The in vitro studies showed that subendocardial Purkinje fiber action potentials could still be recorded for up to 10 min of exposure to air. In comparison, in the tissues subjected to chemical ablation, no transmembrane action potentials could be recorded from either the Purkinje fibers or the superficial ventricular muscle cells. We conclude that the development of an endocardial-epicardial activation rate gradient during prolonged ventricular fibrillation depends on the presence of intact subendocardial Purkinje fibers and ventricular myocytes. The retained cavitary blood is not responsible for the development of the rate gradient. 

Received 22 August 1994; accepted in final form 24 May 1995.
APS Manuscript Number H757-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  8 June 1995.