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

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.

[1]  M. Rosen,et al.  The M cell. , 1999, Journal of cardiovascular electrophysiology.

[2]  C Antzelevitch,et al.  Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome. , 1998, Circulation.

[3]  M. Rosen,et al.  Effects of quinidine on repolarization in canine epicardium, midmyocardium, and endocardium: II. In vivo study. , 1997, Circulation.

[4]  C Antzelevitch.  Are M cells present in the ventricular myocardium of the pig? A question of maturity. , 1997, Cardiovascular research.

[5]  CharlesAntzelevitch,et al.  Sodium Channel Block With Mexiletine Is Effective in Reducing Dispersion of Repolarization and Preventing Torsade de Pointes in LQT2 and LQT3 Models of the Long-QT Syndrome , 1997 .

[6]  A. Rodríguez-Sinovas,et al.  Lack of evidence of M-cells in porcine left ventricular myocardium. , 1997, Cardiovascular research.

[7]  C. Antzelevitch,et al.  Electrophysiological Characteristics of the M Cell , 1997 .

[8]  C. Cryer,et al.  The heart's fibre alignment assessed by comparing two digitizing systems. Methodological investigation into the inclination angle towards wall thickness. , 1997, Technology and health care : official journal of the European Society for Engineering and Medicine.

[9]  C Antzelevitch,et al.  Cellular and ionic mechanisms underlying erythromycin-induced long QT intervals and torsade de pointes. , 1996, Journal of the American College of Cardiology.

[10]  M. Rosen,et al.  Regional differences in electrophysiological properties of epicardium, midmyocardium, and endocardium. In vitro and in vivo correlations. , 1996, Circulation.

[11]  M Restivo,et al.  The electrophysiological mechanism of ventricular arrhythmias in the long QT syndrome. Tridimensional mapping of activation and recovery patterns. , 1996, Circulation research.

[12]  C. Antzelevitch,et al.  Evidence for the Presence of M Cells in the Guinea Pig Ventricle , 1996, Journal of cardiovascular electrophysiology.

[13]  J. Brachmann,et al.  Electrophysiological properties of individual muscle layers in the in vivo canine heart , 1996 .

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

[15]  F. Charpentier,et al.  Electrophysiologic characteristics of cells spanning the left ventricular wall of human heart: evidence for presence of M cells. , 1995, Journal of the American College of Cardiology.

[16]  CharlesAntzelevitch,et al.  Characteristics of the Delayed Rectifier Current (IKr and IKs) in Canine Ventricular Epicardial, Midmyocardial, and Endocardial Myocytes , 1995 .

[17]  C. Antzelevitch,et al.  Characteristics of the delayed rectifier current (IKr and IKs) in canine ventricular epicardial, midmyocardial, and endocardial myocytes. A weaker IKs contributes to the longer action potential of the M cell. , 1995, Circulation research.

[18]  J. Stewart.  Manual of Histological Techniques and Their Diagnostic Application , 1995 .

[19]  C Antzelevitch,et al.  Role of M cells in acquired long QT syndrome, U waves, and torsade de pointes. , 1995, Journal of electrocardiology.

[20]  C Antzelevitch,et al.  Distribution of M Cells in the Canine Ventricle , 1994, Journal of cardiovascular electrophysiology.

[21]  H. C. Cook,et al.  Manual of Histological Techniques and Their Diagnostic Application , 1994 .

[22]  C. Antzelevitch,et al.  Differences in the Electrophysiological Response of Canine Ventricular Epicardium and Endocardium to Ischemia Role of the Transient Outward Current , 1993, Circulation.

[23]  C Antzelevitch,et al.  Ionic bases for electrophysiological distinctions among epicardial, midmyocardial, and endocardial myocytes from the free wall of the canine left ventricle. , 1993, Circulation research.

[24]  G. Gintant,et al.  Heterogeneity within the ventricular wall. Electrophysiology and pharmacology of epicardial, endocardial, and M cells. , 1991, Circulation research.

[25]  C Antzelevitch,et al.  A subpopulation of cells with unique electrophysiological properties in the deep subepicardium of the canine ventricle. The M cell. , 1991, Circulation research.

[26]  P. Kuo,et al.  Cardiac Electrophysiology: From Cell to Bedside , 1991 .

[27]  W. Cascio,et al.  Passive electrical properties, mechanical activity, and extracellular potassium in arterially perfused and ischemic rabbit ventricular muscle. Effects of calcium entry blockade or hypocalcemia. , 1990, Circulation research.

[28]  R. Lux,et al.  Correlation between in vivo transmembrane action potential durations and activation-recovery intervals from electrograms. Effects of interventions that alter repolarization time. , 1990, Circulation.

[29]  B M Steinhaus,et al.  Estimating Cardiac Transmembrane Activation and Recovery Times From Unipolar and Bipolar Extracellular Electrograms: A Simulation Study , 1989, Circulation research.

[30]  J. A. Abildskov,et al.  Estimation of ventricular transmembrane action potential durations and repolarization times from unipolar electrograms , 1981 .

[31]  Dd. Streeter,et al.  Gross morphology and fiber geometry of the heart , 1979 .

[32]  K Millar,et al.  The sequence of normal ventricular recovery. , 1972, American heart journal.

[33]  J. Ross,et al.  Fiber Orientation in the Canine Left Ventricle during Diastole and Systole , 1969, Circulation research.

[34]  D. Durrer,et al.  Spread of activation in the left ventricular wall of the dog. IV. Two and three dimensional analysis. , 1955, American heart journal.