Biomedical subjects
Publications and source records attributed to Junzhong Yang.
Anti-phase synchronization (AS) in coupled chaotic oscillators is investigated. The necessary condition for AS is given and the stability of AS is studied. Results are demonstrated with numerical simulations and electronic circuits.
We have investigated the dynamics of the coupled Lorenz oscillators numerically and theoretically. We find the partial amplitude death when the interaction is strong enough. The linear stability analysis of the partial amplitude death is proposed.
We investigate the synchronization of coupled chaotic oscillators with a no-flux boundary condition. We find that the spectrum of the coupling matrix is divided into two parts, the isolated part with a zero eigenvalue and the continuous one with the other N-1 eigenvalues falling onto a line. Based on the eigenvalue analysis, the stability of the synchronization in a coupled Lorenz system is explored thoroughly in the parameter space of the size of the system, the diffusion, and gradient coupling constants.
In the heart, membrane voltage (Vm) and intracellular Ca (Cai) are bidirectionally coupled, so that ionic membrane currents regulate Cai cycling and Cai affects ionic currents regulating action potential duration (APD). Although Cai reliably and consistently tracks Vm at normal heart rates, it is possible that at very rapid rates, sarcoplasmic reticulum Cai cycling may exhibit intrinsic dynamics. Non-voltage-gated Cai release might cause local alternations in APD and refractoriness that influence wavebreak during ventricular fibrillation (VF). In this study, we tested this hypothesis by examining the extent to which Cai is associated with Vm during VF. Cai transients were mapped optically in isolated arterially perfused swine right ventricles using the fluorescent dye rhod 2 AM while intracellular membrane potential was simultaneously recorded either locally with a microelectrode (5 preparations) or globally with the voltage-sensitive dye RH-237 (5 preparations). Mutual information (MI) is a quantitative statistical measure of the extent to which knowledge of one variable (Vm) predicts the value of a second variable (Cai). MI was high during pacing and ventricular tachycardia (VT; 1.13 +/- 0.21 and 1.69 +/- 0.18, respectively) but fell dramatically during VF (0.28 +/- 0.06, P < 0.001). Cai at sites 4-6 mm apart also showed decreased MI during VF (0.63 +/- 0.13) compared with pacing (1.59 +/- 0.34, P < 0.001) or VT (2.05 +/- 0.67, P < 0.001). Spatially, Cai waves usually bore no relationship to membrane depolarization waves during nonreentrant fractionated waves typical of VF, whereas they tracked each other closely during pacing and VT. The dominant frequencies of Vm and Cai signals analyzed by fast Fourier transform were similar during VT but differed significantly during VF. Cai is closely associated with Vm closely during pacing and VT but not during VF. These findings suggest that during VF, non-voltage-gated Cai release events occur and may influence wavebreak by altering Vm and APD locally.
In ventricular fibrillation (VF), the principal cause of sudden cardiac death, waves of electrical excitation break up into turbulent and incoherent fragments. The causes of this breakup have been intensely debated. Breakup can be caused by fixed anatomical properties of the tissue, such as the biventricular geometry and the inherent anisotropy of cardiac conduction. However, wavebreak can also be caused purely by instabilities in wave conduction that arise from ion channel dynamics, which represent potential targets for drug action. To study the interaction between these two wave-breaking mechanisms, we used a physiologically based mathematical model of the ventricular cell, together with a realistic three-dimensional computer model of cardiac anatomy, including the distribution of fiber angles throughout the myocardium. We find that dynamical instabilities remain a major cause of the wavebreak that drives VF, even in an anatomically realistic heart. With cell physiology in its usual operating regime, dynamics and anatomical features interact to promote wavebreak and VF. However, if dynamical instability is reduced, for example by modeling of certain pharmacologic interventions, electrical waves do not break up into fibrillation, despite anatomical complexity. Thus, interventions that promote dynamical wave stability show promise as an antifibrillatory strategy in this more realistic setting.
We studied spiral wave dynamics in an oscillatory reaction diffusion system. We find a new phenomenon: without the appearance of any global modulation mode, stable spiral waves break up directly. By investigating the one-dimensional version of the system and the isolated local dynamics, we find that the unstable focus in the local dynamics plays an important role. For different boundary conditions (BCs), we find a transition between spiral waves and traveling waves for periodic BCs and drifting spiral wave for no-flux BC.
We study spiral wave breakup using a Fitzhugh-Nagumo-type system. We find that spiral wave breakup can occur near the core or far from it in both excitable and oscillatory regimes. There is a faraway breakup scenario in both excitable and oscillatory media that depends on long wavelength modulation modes. We observed three distinct scenarios, including one that involves breakup that does not develop into turbulence. However, we find that the mechanisms behind these three scenarios are the same: they are caused by the interaction between the dispersion relation and the asymptotic behavior of the modulation mode. The difference in phenomenology is due to the asymptotic behavior of the modulation mode.
It has been suggested from frequency analysis that cardiac fibrillation is driven by stable intramural reentry, with wavebreak occurring due to failure of 1:1 propagation. We tested this hypothesis with a combined experimental and theoretical approach. Optical mapping was performed on epicardial, endocardial, and transmural cut surfaces of fibrillating swine ventricles. Wavelets were characterized, the frequency content of optical signals analyzed, and space-time plots (STPs) constructed to detect Wenckebach-like conduction. The findings were compared with simulations in 2D and 3D cardiac tissue using the Luo-Rudy action potential model. The incidence of reentry in the cut transmural surface (11.8% in right ventricle, 14.3% in left ventricle) was similar to that on the endocardial surface (13.1%, P=NS) but greater than on the epicardial surface (7.7%, P<0.01). Frequency spectra of optically recorded membrane voltage were organized into spatial domains with the same dominant frequency, but these domains were nonstationary. In STPs, pseudo-2:1 conduction block was caused by double potentials arising when reentry occurred on the recording site rather than true Wenckebach conduction. The latter was observed in 11 of 166 STPs but did not occur at borders of high-to-low frequency domains. In simulations, similar findings were obtained when action potential duration (APD) restitution slope was steep. Stationary dominant frequency domains with Wenckebach conduction patterns were observed only in the presence of shallow APD restitution slope and marked nonuniform tissue heterogeneity. In conclusion, stable intramural reentry as the engine of fibrillation was not observed. Our findings support the idea that dynamic wavebreak plays a fundamental role in the generation and maintenance of ventricular fibrillation.