Glass Microelectrode Studies on Intramural Papillary Muscle Cells

Abstract

Although the electrophysiological properties of intramural ventricular myocardial cells are important to an understanding of cardiac excitation and conduction, they have not been well defined. The paucity of information stems from limitations on the depth of penetration by glass microelectrodes and from difficulties in perfusing the deep layers. Therefore, a tissue slicing technique that satisfactorily exposes all the layers of a papillary muscle specimen from the endocardium to the epicardium was developed for electrophysiological examination. Glass microelectrodes were then used to explore these slice preparations to define the electrophysiological characteristics of intramural cells in the normal dog. Transmembrane potentials recorded from subendocardial and deep myocardial cells in the papillary muscle slices were comparable to those recorded from standard preparations. Similarities included action potential duration and configuration, relationships among resting potential, action potential configuration, and extracellular potassium concentration, and dependency of action potential duration on cycle length. However, the average magnitudes of measured electrophysiological characteristics were consistently greater in the subsurface cells tested in papillary muscle slices than they were in the surface cells tested in the standard preparations, i.e., resting potential was 2-4 mv more negative, action potential amplitude was 7-9 mv larger, and maximum rate of voltage change (maximum dV/dt) was 40-140 v/sec larger. Deep myocardial tissues also exhibited enhanced responsiveness (the curve relating activation potential to maximum dV/dt of the response shifted up and to the left), cell populations with large maximum dV/dt, and estimated conduction velocities in excess of three times those in the surface cell layers. These findings provide a reasonable explanation for (I) discrepancies between previously reported values for ventricular conduction velocity. (2) rapid impulse spread to the papillary muscle tip. and (3) bidirectional activation of the papillary muscle and large trabeculae. They also suggest the possibility of functional pathways that facilitate rapid activation of the deep myocardial lavers. KEY WORDS intramural cells papillary muscle slice intramural conduction intramyocardial cells electrophysiology• The electrical properties of endocardial and epicardial surface cells from the hearts of various mammalian species have been extensively charac- This work was supported in part by Grant 681875 from the Americsn Heart Association, by Grants A72-6 and C72-7 from the Chicago Heart Association, by the Reingold Estate, and by U. S. Public Health Service Training Grant TO-1-GM00162-14 from the National Institutes of Health.The original work was carried out in partial fulfillment of the requirements for a Ph.D. in Pharmacology by L. Solberg. Dr. Solberg was a J. B. Kahn. Jr. Fellow in Pharmacology and Dr. Singer is an Established Investigator of the American Heart Association.Please terized using intracel...

Effects of quinidine on action potentials and ionic currents in isolated canine ventricular myocytes.

“…First, it is possible that we are studying different cell types, one that occurs in the surface of the myocardium for intact preparations and another that is isolated from deep in the ventricular wall. 37 Second, the presence of restricted intercellular spaces endows multicellular preparations with certain inhomogeneities due to accumulation and depletion of extracellular ions to which isolated myocytes are largely not as susceptible. It is possible, therefore, that the decrease in K + conductance that occurs with quinidine causes a decrease in cleft K + accumulation, which has further direct effects on K + conductances.…”

Regional alterations of repolarizing K+ currents among the left ventricular free wall of rats with ascending aortic stenosis

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During normal cardiac cycles, the wave of excitation travels from endocardial to epicardial regions. Due to the shorter action potential duration (APD) in epicardial myocytes (Solberg et al 1974), they repolarize earlier and thus repolarization of the ventricle travels in the opposite direction from epicardial to endocardial regions. These differences in APD are responsible for the fact that in the normal heart the main vector of the T_wave in the electrocardiogram (ECG) points in the same direction as the main vector of the QRS complex (Cohen et al 1976;Franz et al 1987).Recently, studies investigating the regional distribution of ionic currents underlying the ventricular action potential (AP) in normal hearts have identified inhomogeneities in the distribution of repolarizing currents among the ventricular wall, which could account for the gradient in APD.

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“…During normal cardiac cycles, the wave of excitation travels from endocardial to epicardial regions. Due to the shorter action potential duration (APD) in epicardial myocytes (Solberg et al 1974), they repolarize earlier and thus repolarization of the ventricle travels in the opposite direction from epicardial to endocardial regions. These differences in APD are responsible for the fact that in the normal heart the main vector of the T‐wave in the electrocardiogram (ECG) points in the same direction as the main vector of the QRS complex (Cohen et al 1976; Franz et al 1987).…”

d-Sotalol Induces Marked Action Potential Prolongation and Early Afterdepolarizations in M but Not Epicardial or Endocardial Cells of the Canine Ventricle

“…Action potentials with relatively long APDs have been first observed in the deep layers of papillary muscles of the canine ventricle (29) and in myocytes isolated from the rat ventricle (30). In the canine ventricle, M cells have been described and characterized in the deep subepicardial and midmyocardial layers of the free wall (23,28), deep subendocardial layers of the septum and papillary muscles (24), ventricular myocytes (31,32), and recently in arterially perfused wedge preparations (33,34), as well as in the canine heart in vivo (35)(36)(37)(38).…”