Differences in the Changing Trends of Monophasic Action Potential Duration and Effective Refractory Period of the Ventricular Myocardium After Myocardial Infarction in Vivo

Abstract

growing body of evidence suggests that heterogeneity of electrophysiological characteristics is an important property of the ventricular myocardium. 1,2 Importantly, a subpopulation of cells, called midmyocardial cells (M cells), have been described in the ventricular wall of the guinea pig, 3 canine 1 and human. 2 The M cells display a longer action potential duration (APD) and a steeper dependence of APD on rate than epicardial or endocardial cells. This electrophysiological difference between M cells and the other cell types is the main source of the heterogeneity observed in the normal heart.Transmural and regional heterogeneities in the electrical properties of cardiac cells contribute to the normal function of the heart. They are susceptible to many pathological factors, such as ischemia, hypertrophy, or heart failure, and any significant alternation in these electrical heterogeneities can lead to the development of life-threatening cardiac arrhythmias and sudden death. The heterogeneity of the ventricular electrical properties is reflected in aspects such as APD, effective refractory period (ERP) and conduction velocity, and is more marked in vitro than in the intact heart. 4 In the setting of ischemia, hypertrophy, or heart failure, the altered electrophysiological heterogeneity of the Circulation Journal Vol.68, December 2004ventricle may have significance in the development of ventricular arrhythmias, but the dynamic variations of the electrophysiological characteristics of the ventricle under pathological conditions are poorly understood.Myocardial infarction (MI) can create abnormal electrophysiological substrates that trigger ventricular arrhythmias and at different stages of MI, the mechanism underlying the ventricular arrhythmias vary. The study by Anyukhovsky et al suggested that myocardial injury may in fact permit dispersion of repolarization to be manifested transmurally in vivo, and in the setting of Ca 2+ overload the transmural electrophysiological dispersion of ventricle wall may be further exaggerated. 4 Consequently, the aims of the present study were twofold. First, to investigate the effects of MI on transmural electrophysiological characteristics in the rabbit heart in vivo and second, to compare the changing trends of the monophasic APD (MAPD) and ERP of the endocardial, M and epicardial cells after MI in vivo. Methods Animal PreparationForty New Zealand white rabbits, including both male and female, weighing 2-2.5 kg, were randomized into either a sham operation (SO) group (n=10) or MI group (n=30). All rabbits were anesthetized with sodium pentobarbital (30 mg/kg iv). Additional smaller doses were given as needed to maintain deep anesthesia. Under controlled ventilation, a thoracotomy through a left parasternal inciCirc J 2004; 68: 1205 -1209 (Received March 22, 2004; revised manuscript received August 26, 2004; accepted August 30, 2004

Differences in the Aging-Associated Trends of the Monophasic Action Potential Duration and Effective Refractory Period of the Right and Left Atria of the Rat

“…In the present experiment we used a glass microelectrode as the recording electrode because research 8,19 has shown that it reflects the AP of the cardiac myocyte, and compared with the results from the recording electrode used in our previous study, 17 MAPs were easily obtained using the glass microelectrode and their amplitude was much higher. The MAP duration obtained by the 2 types of recording electrodes were identical.…”

“…16 The bipolar stimulation electrode and the reference electrode were made of teflon-coated stainless steel wire, the distal tip of which was 0.5 mm long and nacked. 17 MAPs were obtained from the epicardium of the right and left atria. The stimulation electrode was fixed to the epicardial surface of the right ventricle, and the reference electrode to the root of the pulmonary artery.…”

Effect of Nifekalant, a Class III Anti-Arrhythmic Agent, on Ca2+ Waves in Rat Intact Trabeculae

“…18,19 Moreover, such tachyarrhythmias may occur in digitalis intoxication and cardiac hypertrophy by the triggered mechanism caused by Ca 2+ overload. 20 In these cases, it is possible that nifekalant may be pro-arrhythmic if the patient is sensitive to this effect, because nifekalant can increase the amplitude of DADs as shown in Fig 5. In contrast, it has been reported that nifekalant can prolong the myocardial refractory period, 4,[6][7][8][9]41 suggesting that nifekalant exerts a suppressive action against re-entrant arrhythmias, 7,9 although the prolongation of repolarization can be associated with pro-arrhythmic actions inducing torsades de pointes tachycardia or ventricular fibrillation because of early afterdepolarizations. 42 Therefore, when we use nifekalant and other class III anti-arrhythmic agents to treat patients with tachyarrhythmias, we should pay careful attention to the basic mechanisms underlying the arrhythmias.…”

Effects of ramipril on ventricular arrhythmia after myocardial infarction in rabbits

“…[12] MAPs of the epicardium, midmyocardium and endocardium at MI area in the left ventricle were recorded. In order to guarantee two different recordings at the same point, the distal point at 10 mm to the fi rst diagonal branch of the LAD artery was taken as the reference point, and the point at 3 mm to its right left as the recording point.…”