摘要(英) |
Alternan responses in heart can cause conduction blocks and lead to fatal conditions such as ventricular fibrillation (VF). It would be important to know how to suppress the alternan response in hearts. In this thesis, we report a nonlinear control method to suppress the alternan responses in isolated heart experiments. In this method, the pacing period T0 is replaced by two periods; namely T1 = T0+ΔT/2 and T2 = T0-ΔT/2 where ΔT =T1-T2 is a small perturbation of the original period T0. Measured pressures of the isolated heart from the previous beat (Pn-1) and the current beat (Pn) are used to determine whether T1 or T2 should be used. In our control scheme, T1 is used when Pn > Pn-1 ; otherwise T2 is used. This method is different from the traditional proportional gain method. Results from experiments show that this T1T2 method can successfully suppress alternan response from isolated hearts.
Another experiment in this thesis is to understand the variability of the interbeat interval which is controlled by SA node in an isolated whole heart. Primary cardiac co-cultures are also used to model the SA node in the heart. To understand the mechanism of the heart rate variability, we add a drug to suppress the contraction of the isolated whole heart, and also control the temperature of the cardiac cultures to see the effects of mechanical and temperature. The result shows that when we reduce the contraction of the isolated whole heart, the heart rate increases and the heart rate variability decreases. However, the decrement of heart rate variability is larger than the temperature effect on the isolated whole heart. For the experiment of temperature effect in cell cultures, the heart rate increases and the heart rate variability decreases when we increase the temperature.
|
參考文獻 |
[1] http://www.phaaustralia.com.au/content/what-pulmonary-hypertension-0
[2] Iaizzo, P. A. Handbook of Cardiac Anatomy, Physiology, and Devices." (2005).
[3] http://cal.vet.upenn.edu/projects/anestecg/basics/condsys.htm
[4] Fahrenbach, J. P., R. Mejia-Alvarez, et al. (2007). "The relevance of non-excitable cells for cardiac pacemaker function." Journal of Physiology-London 585(2): 565-578.
[5] Davies, M. J. and Pomeranc. A. (1972). "QUANTITATIVE STUDY OF AGING CHANGES IN HUMAN SINOATRIAL NODE AND INTERNODAL TRACTS." British Heart Journal 34(2): 150-2.
[6] Camelliti, P., T. K. Borg, et al. (2005). "Structural and functional characterisation of cardiac fibroblasts." Cardiovascular Research 65(1): 40-51.
[7] Shih, H. T. (1994). "ANATOMY OF THE ACTION-POTENTIAL IN THE HEART." Texas Heart Institute Journal 21(1): 30-41.
[8] Bruce M. Koeppen, B. A. S. (2009). Berne & Levy Physiology.
[9] Bers, D. M. (2002). "Cardiac excitation-contraction coupling." Nature 415(6868): 198-205.
[10] Qu, Z. L., A. Garfinkel, et al. (2011). "Multi-scale modeling in biology: How to bridge the gaps between scales?" Progress in Biophysics & Molecular Biology 107(1): 21-31.
[11] Qu, Z., Y. Xie, et al. (2010). "T-wave alternans and arrhythmogenesis in cardiac diseases." Front Physiol 1: 154.
[12] Hirth, C., U. Borchard, et al. (1983). "EFFECTS OF THE CALCIUM-ANTAGONIST DILTIAZEM ON ACTION-POTENTIALS, SLOW RESPONSE AND FORCE OF CONTRACTION IN DIFFERENT CARDIAC TISSUES." Journal of Molecular and Cellular Cardiology 15(12): 799-809.
[13] Acharya, U. R., K. P. Joseph, et al. (2006). "Heart rate variability: a review." Medical & Biological Engineering & Computing 44(12): 1031-1051.
[14] Goldberger, A. L., L. A. N. Amaral, et al. (2002). "Fractal dynamics in physiology: Alterations with disease and aging." Proceedings of the National Academy of Sciences of the United States of America 99: 2466-2472.
[15] Christini, D. J. and J. J. Collins (1997). "Real-time, adaptive, model-independent control of low-dimensional chaotic and nonchaotic dynamical systems." Ieee Transactions on Circuits and Systems I-Fundamental Theory and Applications 44(10): 1027-1030.
[16] Jordan, P. N. and D. J. Christini (2004). "Adaptive diastolic interval control of cardiac action potential duration alternans." Journal of Cardiovascular Electrophysiology 15(10): 1177-1185.
[17] Christini, D. J., M. L. Riccio, et al. (2006). "Control of electrical alternans in canine cardiac purkinje fibers." Physical Review Letters 96(10).
[18] Dubljevic, S., S. F. Lin, et al. (2008). "Studies on feedback control of cardiac alternans." Computers & Chemical Engineering 32(9): 2086-2098.
[19] Hsiao-Wen Tu (2010). The effect of themerature and calcium dynamics on cardiac interbeat intervals, master’s thesis, Graduate institute of biophysics National Central University, Jung-Li.
[20] Fedorov, V. V., L. Li, et al. (2005). "Hibernator Citellus undulatus maintains safe cardiac conduction and is protected against tachyarrhythmias during extreme hypothermia: Possible rote of Cx43 and Cx45 up-regulation." Heart Rhythm 2(9): 966-975.
[21] Hiranandani, N., K. D. Varian, et al. (2006). "Frequency-dependent contractile response of isolated cardiac trabeculae under hypo-, normo-, and hyperthermic conditions." Journal of Applied Physiology 100(5): 1727-1732.
[22] Casolo, G., E. Balli, et al. (1989). "DECREASED SPONTANEOUS HEART-RATE VARIABILITY IN CONGESTIVE HEART-FAILURE." American Journal of Cardiology 64(18): 1162-1167.
[23] Horner, S. M., C. F. Murphy, et al. (1996). "Contribution to heart rate variability by mechanoelectric feedback - Stretch of the sinoatrial node reduces heart rate variability." Circulation 94(7): 1762-1767.
[24] http://www.cvphysiology.com/Blood%20Flow/BF001.htm
[25] Multichannel systems. (2011). MEA Amplifier with Blanking Circuit for Inverse Microscopes.
|