Background-Styryl voltage-sensitive dyes (e.g. di-4-ANEPPS) have been successfully used for optical mapping in cardiac cells and tissues. However, their utility for probing electrical activity deep inside the myocardial wall and in blood-perfused myocardium has been limited because of light scattering and high absorption by endogenous chromophores and hemoglobin at blue-green excitation wavelengths.
Abstract-The mechanisms by which Naϩ -channel blocking antiarrhythmic drugs terminate atrial fibrillation (AF) remain unclear. Classical "leading-circle" theory suggests that Na ϩ -channel blockade should, if anything, promote re-entry. We used an ionically-based mathematical model of vagotonic AF to evaluate the effects of applying pure Na ϩ -current (I Na ) inhibition during sustained arrhythmia. Under control conditions, AF was maintained by 1 or 2 dominant spiral waves, with fibrillatory propagation at critical levels of action potential duration (APD) dispersion. I Na inhibition terminated AF increasingly with increasing block, terminating all AF at 65% block. During 1:1 conduction, I Na inhibition reduced APD (by 13% at 4 Hz and 60% block), conduction velocity (by 37%), and re-entry wavelength (by 24%). During AF, I Na inhibition increased the size of primary rotors and reduced re-entry rate (eg, dominant frequency decreased by 33% at 60% I Na inhibition) while decreasing generation of secondary wavelets by wavebreak. Three mechanisms contributed to I Na block-induced AF termination in the model: (1) enlargement of the center of rotation beyond the capacity of the computational substrate; (2) decreased anchoring to functional obstacles, increasing meander and extinction at boundaries; and (3) reduction in the number of secondary wavelets that could provide new primary rotors. Optical mapping in isolated sheep hearts confirmed that tetrodotoxin dose-dependently terminates AF while producing effects qualitatively like those of I Na inhibition in the mathematical model. We conclude that pure I Na inhibition terminates AF, producing activation changes consistent with previous clinical and experimental observations. These results provide insights into previously enigmatic mechanisms of class I antiarrhythmic drug-induced AF termination. The full text of this article is available online at http://circres.ahajournals.org (Circ Res. 2005;96:e35-e47.) Key Words: atrial fibrillation Ⅲ mathematical model Ⅲ class I drugs Ⅲ sodium channels C lass I antiarrhythmic drugs terminate clinical atrial fibrillation (AF), but the electrophysiological mechanisms remain poorly understood. 1 AF is generally considered to be a re-entrant arrhythmia, and the stability of AF is classically related to the wavelength. 2 The wavelength (product of refractory period and conduction velocity [CV]) is thought to represent the minimum path length for re-entry and therefore to determine the size of functional re-entry circuits. 3 The most commonly accepted mechanism for antiarrhythmic drug termination of AF is drug-induced wavelength increases that reduce the number of circuits that the atria may accommodate.Experimental evidence has been presented suggesting that class I antiarrhythmic agents act on AF by changing the effective refractory period (ERP) and the wavelength. 2,4,5 Recent data have challenged established notions of antiarrhythmic drug action by showing that potent Na ϩ -channel blockers can terminate AF without increasing the wav...
A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.
The investigation of processes of ischemia in different organ tissues is very important for the development of methods of protection and preservation during surgical procedures. Electrical impedance spectroscopy was used to distinguish between different tissues and their degree of ischemia. We describe mathematical methods used to adjust experimental data to Cole-Cole models for one-circle and two-circle impedance loci and a study of the main parameters for representing the behavior of ischemia in time. In vivo and in situ postmortem measurements of different tissues from pigs are shown in the 100 Hz to 1 MHz range. The Cole parameters that best characterize the ischemia are R0 and fc.
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