Ventricular arrhythmias are commonly observed in patients with acute coronary occlusion and ischemia. The purpose of the present study is to determine ischemic electrophysiological effects and their role in ischemia-induced arrhythmia. Optical mapping of the membrane potential with voltage-sensitive dyes was used in the study. The mapping was performed with di-4-ANEPPS in Langendorff-perfused rabbit hearts. The excitation-contraction decoupler 2,3-butanedione monoxime was used to suppress motion artifacts caused by contraction of the heart. The acute global ischemia was developed by a rapid reduction of the flow rate. The experiments revealed that ischemic tissues were characterized by an obvious reduction in action potential duration and action potential upstroke, slower conduction velocity (CV) and the property of post-repolarization refractoriness. Moreover, the magnitude of CV reduced both in control and ischemia when the pacing cycle length was short. CV reduction was even early in ischemia, resulting in a broader curve during ischemia. Moreover, the dominant frequency of ventricular tachycardia/ventricular fibrillation (VT/VF) in ischemia was less than that in control, implying a decreasing tendency of VT/VF frequency for low excitability. Therefore, combined with our previous simulation study, the dynamic changes of CV and longer refractory period were suggested to play an important role in the ischemia-related arrhythmia. Low excitability in ischemic tissue was the fundamental mechanism in it.
This simulation study is carried out in two-dimensional two-dimensional two-dimensional tissue of Luo-Rudy model of mammalian ventri-cular ventri-cular ventri-cular myocytes. Mechanism of reentry trigged by early after-depolarizations after-depolarizations after-depolarizations (EADs) in long-QT syndrome (LQTS) has been study in this paper. LQTS is simulated by reducing the membrane conductance of IKsfor LQT1 and IKrfor LQT2, and by altering the steady-state inactivation of the fast sodium current INafor LQT3. The endocardium is paced 10 times at a constant basic cycle length (BCL) of 500ms, and following a 2000ms pause, a S2 stimulus is applied. If shape, size and position of M cell domain is suitable, EADs with higher amplitude formation near the boundary between endocardial domain and M cell domain provide the trigger for reentrant excitation. Reentry once initiated is more likely to self-terminate self-terminate self-terminate in LQT1 tissue. In LQT2 tissue, functional reentry is maintained by the continuously generating of EADs in the mid of M cell domain. In LQT3 tissue, functional reentry is maintained for the reason that the conduction velocity of EAD induced reentrant wave is very slowly, and the tip of it is anchored at the mid of M cell domain.
High-resolution optical mapping with voltagesensitive dyes has become a powerful tool to depict complex propagation patterns of cardiac transmembrane potentials. Many studied have proved that this optical signal obtained from tissue surface is the response of the transmembrane potential averaged upon depth rather than only surface. In order to investigate the differentia between the two transmembrane potentials, in this paper, we simulated cardiac propagation using Luo-Rudy (L-R) model and calculated the transmembrance potentials average over depth by an optical decay constant from 0.0 mm to 3.0mm. Our results suggest that the transmembrance potentials weighted average over depth is different from that on the tissue surface, the discrepancy between them depends on the depth of the fluorescence emission of the tissue. If only top layer of tissue (<1.0mm) contributes the fluorescence, optical mapping is an almost accurate representation of surface activation dynamics.
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