Cellular basis for the monophasic action potential. Which electrode is the recording electrode?

BACKGROUND The cellular basis for the monophasic action potential (MAP) has long been a matter of debate. At the center of the controversy is the issue as to which of the two electrodes is the recording electrode and which is the indifferent electrode. The present study is designed to address this issue. METHODS Transmembrane action potentials (TAPs) and either intramural MAPs or contact (Franz-like) MAPs were recorded from adjacent sites in canine arterially perfused ventricular wedge preparations. Intramural MAPs were recorded using thin wire electrodes referenced to a KCl electrode. RESULTS Local cooling or injection of ATX-II into the region subtending the inactivating (contact or KCl) electrode did not affect the MAP. Similar maneuvers at the site of the noninactivating electrode always prolonged the MAP. The intramural MAP always prolonged in proportion to the TAP, whereas the contact MAP did not, often displaying apparent early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs) due to its much wider field of view, which captured activity from the region of prolonged repolarization as well as the remote normal regions. CONCLUSIONS Our results suggest that (1) it is not the contact or MAP electrode that records the MAP, but rather the noninactivating "indifferent" electrode and (2) intramural MAPs provide more accurate recordings of local activity. The data provide compelling evidence in support of the hypothesis that the MAP represents the extracellular potential difference between active and inactive sites within the heart rather than injury currents flowing at the boundary of the active and inactive zone under the inactivating electrode.

[1]  R. Barr,et al.  Current flow patterns in two-dimensional anisotropic bisyncytia with normal and extreme conductivities. , 1984, Biophysical journal.

[2]  R. Plonsey,et al.  A mathematical evaluation of the core conductor model. , 1966, Biophysical journal.

[3]  M. Gardberg,et al.  Monophasic Curve Analysis and the Ventricular Gradient in the Electrogram of Strips of Turtle Ventricle , 1959, Circulation Research.

[4]  B. Surawicz,et al.  Comparison of cardiac monophasic action potentials recorded by intracellular and suction electrodes. , 1959, The American journal of physiology.

[5]  D. Garcia-Dorado,et al.  Cardiovascular Research , 1966 .

[6]  C. Antzelevitch,et al.  Transmural Heterogeneity of Ventricular Repolarization Under Baseline and Long QT Conditions in the Canine Heart In Vivo: Torsades de Pointes Develops with Halothane but not Pentobarbital Anesthesia , 2000, Journal of cardiovascular electrophysiology.

[7]  M R Franz,et al.  Current status of monophasic action potential recording: theories, measurements and interpretations. , 1999, Cardiovascular research.

[8]  M R Franz,et al.  Long-term recording of monophasic action potentials from human endocardium. , 1983, The American journal of cardiology.

[9]  C Antzelevitch,et al.  Cellular basis for the electrocardiographic J wave. , 1996, Circulation.

[10]  J. Burdon-Sanderson On the Time‐Relations of the Excitatory Process in the Ventricle of the Heart of the Frog , 1880 .

[11]  W Craelius,et al.  QTU Prolongation and Polymorphic Ventricular Tachyarrhythmias Due to Bradycardia‐Dependent Early: Afterdepolarizations Afterdepolarizations and Ventricular Arrhythmias , 1988, Circulation research.

[12]  M R Franz,et al.  Method and theory of monophasic action potential recording. , 1991, Progress in cardiovascular diseases.

[13]  R. Plonsey Action potential sources and their volume conductor fields , 1977, Proceedings of the IEEE.

[14]  Gan-XinYan,et al.  Cellular Basis for the Electrocardiographic J Wave , 1996 .

[15]  David B. Geselowitz,et al.  A bidomain model for anisotropic cardiac muscle , 2006, Annals of Biomedical Engineering.

[16]  J. Spear,et al.  Cesium chloride-induced long QT syndrome: demonstration of afterdepolarizations and triggered activity in vivo. , 1985, Circulation.