By Martin M. LeWinter, Hiroyuki Suga, Matthew W. Watkins
Many of the development in cardiac energetics lately has been spurred by way of the pressure-volume quarter proposal, the average extension into energetics of prior pioneering paintings delineating the time-varying elastance framework for ventricular contraction. The ebook attracts jointly a wide spectrum of researchers - simple, utilized and medical - having a shared curiosity within the energetics of cardiac muscle and ventricle, offering an summary of the present cutting-edge.
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Additional info for Cardiac Energetics: From Emax to Pressure-Volume Area (Developments in Cardiovascular Medicine)
25 a ON OFF b MUTIPLE CROSS BRIDGES Q) u c S(/) "'0 SINGLE CROSS BRIDGE time Fig. 6. A: Diagram of crossbridge cycle. Each crossbridge repeats attachment and detachment cycle. B: Sliding movement of bead driven by single and multiple crossbridges. In summary, we have utilized in vitro motility assay techniques to study the mechanical property of cardiac myosin under various conditions for different myosin isoforms. Although these findings were anticipated based on previous experiments with muscle preparations, this is the first presentation of such direct evidence at the molecular level.
13. J. Thyroxine induced redistribution of isozyme of rabbit ventricular myosin. Circ Res 50: 117 -124, 1982. 14. , et. al. Dynamic interaction between cardiac myosin isoforms modifies velocity of actomyosin sliding in vitro. Circ Res 73:696-704, 1993. 27 15. Barany, M. ATPase activity of myosin correlated with speed of muscle shortening. J Gen Physiol 50:197-218, 1967. 16. , Poggesi, C. et. al. Shortening velocity and myosin and myofibrillar ATPase activity related to myosin isoenzyme composition during postnasal development in rat myocardium.
Can the process be modified pharmacologically? The answer to these questions is the subject of investigation in many laboratories and a complete answer is beyond the scope of this chapter. Yet, it is important to point out that there is compelling evidence that alteration of the response of the myofilaments to Ca ++ is regulated physiologically in association with intrinsic as well as extrinsic regulation of the heart; and further, that the response of the myofilaments to Ca ++ is altered in common pathologies such as ischemia/acidosis, cardiac stunning, and genetically linked hypertrophic myopathies.