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. 1998 Nov 3;98(18):1921-7.
doi: 10.1161/01.cir.98.18.1921.

Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations

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Characteristics and distribution of M cells in arterially perfused canine left ventricular wedge preparations

G X Yan et al. Circulation. .

Abstract

Background: Much of the characterization of the M cell to date has been accomplished using isolated tissues and cells. This study uses an arterially perfused wedge preparation to examine the characteristics and distribution of M cells within the anterior wall of the canine left ventricle under more physiological conditions.

Methods and results: Floating microelectrodes were used to record transmembrane action potentials simultaneously from epicardial, M region, and endocardial or subendocardial Purkinje sites in isolated arterially perfused canine left ventricular wedge preparations. A transmural ECG was recorded concurrently. M cells with the longest action potentials were found in the deep subendocardium in wedge preparations isolated from the anterior wall of the left ventricle. Fairly smooth transitions in action potential duration (APD) were observed except in the region between epicardium and deep subepicardium. Tissue resistivity increased 2.8-fold in this region and much more modestly in the deep subendocardium. Dispersion of APD90 across the left ventricular wall averaged 51+/-19 and 64+/-25 ms at basic cycle lengths of 1000 and 2000 ms, respectively, whereas transmural dispersion of repolarization time was smaller (34+/-18 and 45+/-25 ms), owing to the endocardial to epicardial activation sequence.

Conclusions: We conclude that the qualitative differences between the 3 ventricular cell types previously described in isolated tissues and cells are maintained in intact canine left ventricular wall preparations in which the myocardial cells are electrically well coupled. As anticipated, differences in APD are quantitatively smaller because of electrotonic interactions among the 3 cell types. Our data indicate that transmural dispersion of repolarization is the result of intrinsic differences in APD of cells spanning the ventricular wall as well as a heterogeneous distribution of tissue resistivity across the wall.

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