Measurement variability of right atrial and ventricular monophasic action potential and refractory period measurements in the standing non-sedated horse

To investigate the possibility of transmural recording of repolarization through the ventricular wall, KCl monophasic action potential (MAP) electrodes positioned along plunge needles were developed and tested. The MAP electrode consists of a silver wire surrounded by agarose gel containing KCl, which slowly eluted into the adjacent tissue to depolarize it. In six dogs, a plunge needle containing three KCl MAP electrodes was inserted into the left ventricle to simultaneously record from the subepicardium, midwall, and subendocardium. In six pigs, eight plunge needles containing three KCl MAP electrodes and two plunge needles containing similar electrodes except for the absence of KCl were inserted into the ventricles. In three guinea pig papillary muscles, a KCl electrode was used to record MAPs along with two microelectrodes for recording transmembrane potentials. Transmural MAP recordings could be made for >1 h in dogs and >2 h in pigs with a significant decrease in MAP amplitude over time but without a significant change in MAP duration. With the electrodes without KCl in pigs, the injury potentials subsided in <30 min. When the pacing rate was changed to alter the action potential duration and refractory period in dogs, the MAP duration correlated with the local effective refractory period ( r = 0.94). The time course of the MAP duration recorded with a KCl MAP electrode in guinea pig papillary muscles corresponded well with that of the transmembrane potential recorded with an adjacent microelectrode. It is possible to record transmural repolarization of the ventricles with KCl MAP electrodes on plunge needles. The MAP is caused by the KCl rather than being a nonspecific injury potential.

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The Recording of the Human Right Atrial Monophasic Action Potential

Cardiac Pacing ◽

10.1007/978-3-642-66356-7_9 ◽

1976 ◽

pp. 80-83

Author(s):

T. Pop ◽

D. Fleischmann ◽

S. Effert

Keyword(s):

Action Potential ◽

Monophasic Action Potential ◽

Right Atrial ◽

Human Right

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Acute and Chronic Effects of Sotalol and Atenolol on Monophasic Action Potential Duration and Effective Refractory Period

Clinical Science ◽

10.1042/cs070005p ◽

1986 ◽

Vol 70 (s13) ◽

pp. 5P-5P

Author(s):

BPJ Way ◽

JC Forfar ◽

SM Cobbe

Keyword(s):

Action Potential ◽

Action Potential Duration ◽

Refractory Period ◽

Effective Refractory Period ◽

Monophasic Action Potential ◽

Chronic Effects ◽

Acute And Chronic Effects

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Dose-Dependent Effects of Ranolazine on Reentrant Ventricular Arrhythmias Induced After Subacute Myocardial Infarction in Rabbits

Journal of Cardiovascular Pharmacology and Therapeutics ◽

10.1177/1074248419858113 ◽

2019 ◽

Vol 25 (1) ◽

pp. 65-71 ◽

Cited By ~ 1

Author(s):

Vassileios Moschovidis ◽

Vassileios Simopoulos ◽

Soultana Stravela ◽

Konstantina Dipla ◽

Apostolia Hatziefthimiou ◽

...

Keyword(s):

Myocardial Infarction ◽

Ventricular Tachycardia ◽

Action Potential ◽

Refractory Period ◽

Ventricular Arrhythmias ◽

Cycle Length ◽

Sustained Ventricular Tachycardia ◽

Effective Refractory Period ◽

Monophasic Action Potential ◽

Coronary Artery Ligation

Ranolazine has been found to prevent ventricular arrhythmias (VAs) during acute myocardial infarction (AMI). This study aimed to investigate its efficacy on VAs induced several days post-MI. For this purpose, 13 anesthetized rabbits underwent coronary artery ligation. Ten of these animals that survived AMI were reanesthetized 3 to 7 days later for electrophysiologic testing. An endocardial monophasic action potential combination catheter was placed in the right ventricle for simultaneous pacing and recording. Monophasic action potential duration, ventricular effective refractory period (VERP), and VAs induced by programmed stimulation were assessed. Measurements were performed during control pacing, and following an intravenous infusion of either a low-dose ranolazine (2.4 mg/kg, R1) or a higher dose ranolazine (4.8 mg/kg cumulative dose, R2). During control stimulation, 2 animals developed primary ventricular fibrillation (VF), 6 sustained ventricular tachycardia (sVT), and 2 nonsustained VT (nsVT). R1 did not prevent the appearance of VAs in any of the experiments; in contrast, it aggravated nsVT into sVT and complicated sVT termination in 2 of 6 animals. Sustained ventricular tachycardia cycle length and VERP were only slightly decreased after R1 (112 ± 5 vs 110 ± 6 ms and 101 ± 11 vs 98 ± 10 ms, respectively). R2 suppressed inducibility of control nsVT, VF, and sVT in 2 animals. In 4 animals with still inducible sVT, R2 significantly prolonged VT cycle length by 150 ± 23 ms ( P < .01), and VERP by 120 ± 7 ms ( P < .001) versus control. In conclusion, R2 exerted antiarrhythmic efficacy against subacute-MI VAs, whereas R1 rather aggravated than prevented these arrhythmias. Ventricular effective refractory period prolongation could partially explain the antiarrhythmic action of R2 in this rabbit model.

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