Figure 1.
Assessments of durations of mechanical systole (a), QT interval (b) and electromechanical window (c) during steady-state pacing and extrasystolic stimulation in perfused guinea-pig heart.
Basal representative recordings of left ventricular (LV) developed pressure (Pres), volume-conducted ECG, and LV epicardial monophasic action potentials (MAP) are shown. The dashed lines on the MAP trace in this figure, and Figures 3 and 4 indicate the moments of regular stimulus (S1) and premature stimulus (S2) application.
Figure 2.
Representative episodes of monomorphic ventricular tachycardia (VT) recorded during hypokalemic perfusion in spontaneously beating guinea-pig and rabbit heart preparations.
In each panel, simultaneous recordings of left ventricular (LV) developed pressure (Pres), volume-conducted ECG, and LV and right ventricular (RV) epicardial monophasic action potentials (MAP) are shown.
Figure 3.
Representative episodes of torsade de pointes induced by programmed ventricular stimulation in hypokalemic guinea-pig and rabbit heart preparations.
Panels A and B are arranged as described in the legend for Figure 2.
Table 1.
Basal and hypokalemic QT intervals, Q-Pend intervals, and electromechanical window values determined during steady-state pacing and extrasystolic stimulations in guinea-pig and rabbit hearts.
Figure 4.
Representative left ventricular (LV) and right ventricular (RV) epicardial monophasic action potential (MAP) recordings obtained during programmed ventricular stimulation in basal conditions and following hypokalemic perfusion in guinea-pig and rabbit heart preparations.
In each set of recordings, the numbers above the MAP trace indicate action potential duration (APD90) (ms), and the numbers under the MAP trace indicate the activation time values (ms) measured in regular beats (the second MAP in each trace) and extrasystolic beats (the fourth MAP in each trace). In basal recordings (panels A and B), note a greater action potential duration at RV compared to LV epicardium, and an increase in activation time along with APD90 shortening in S2-evoked beats as compared to preceding regular beats. Also note that hypokalemia (panels C and D) prolongs action potential duration, and increases the LV-to-RV difference in activation time, indicating conduction slowing.
Figure 5.
Effects of hypokalemia on the local repolarization time and its components, the activation time and action potential duration (APD90), determined at distinct left ventricular (LV) and right ventricular (RV) epicardial recording sites during steady-state pacing (S1) and extrasystolic stimulation (S2) in guinea-pig heart preparations.
The measurements were taken from three LV recording sites (site 1 is the lateral LV wall, site 2 is the anterior LV wall, and site 3 is the posterior LV wall) and three RV recording sites (site 1 is the posterior RV wall, site 2 is the anterior RV wall, and site 3 is the lateral RV wall), while implementing the programmed stimulation protocol shown in Figure 4. *P<0.05 vs. corresponding basal value.
Figure 6.
Effects of hypokalemia on the local repolarization time and its components, the activation time and action potential duration (APD90), determined at distinct left ventricular (LV) and right ventricular (RV) epicardial recording sites during steady-state pacing (S1) and extrasystolic stimulation (S2) in rabbit heart preparations.
The location of individual epicardial recording sites in LV and RV chamber is indicated in the legend for Figure 5. *P<0.05 vs. corresponding basal value.