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心肌的工作原理,文件较大请耐心观看。 配音解说词: This animation sequence will provide an overview of normal cardiac structure and physiology, along with a review of the process of excitation contraction coupling in the heart. The myocardium is comprised of cardiac myocyte and non-myocyte cells. Cardiac myocytes make up approximately 70 percent of the mass of the heart and are enmeshed in a collagen network that acts as a supporting framework. Blood is supplied to individual cardiac myocytes through capillaries that are in close proximity to them. Cardiac myocytes are comprised of actin and myosin myofilaments whose organization gives rise to the characteristic striated appearance of cardiac muscle. There are two prominent organelles within cardiac myocytes: the mitochondria, which produce energy and the sarcoplasmic reticulum, which regulates calcium handling in the cell. Cardiac contraction is initiated when extracellular calcium moves into the cell across the voltage dependent L-type calcium channel. The calcium that enters the cell triggers calcium release from the ryanodine receptor through a process known as calcium-triggered calcium release. Calcium that is released from the sarcoplasmic reticulum binds to the actin thin filaments, thereby initiating contraction of the sarcomeres. At the end of the contraction sequence, calcium comes off of the myofilaments and is actively transported back into the sarcoplasmic reticulum by the calcium pump in its membrane. Calcium is also transported out of the cell into the extracellular space by a membrane-bound pump sodium-calcium exchanger, which is not shown here. Cardiac contraction is brought about by interactions between the actin thin filament, shown in yellow and purple, and the myosin cross bridges that project from the thick filament, shown in red. In relaxed cardiac muscle the conformation of troponin and tropomyosin prevents actin from interacting with the myosin cross-bridges. As a result, actin is unable to interact with the the myosin cross-bridges containing bound-ATP. In activated cardiac muscle, calcium binds to troponin-C, which then shifts troponin complexes and tropomyosin to an active conformation that enables actin to interact with the myosin cross-bridges. Myosin ATP-ase on the myosin heads then hydrolyzes ATP, thus providing the requisite energy for the myosin cross-bridge to interact with the thin filaments and pull the thin filaments towards the center of the sarcomere in a ratchet like fashion. In this sequence of the normal heart, we have reviewed the process of excitation contraction coupling. As will be discussed subsequently, this process of excitation contraction coupling becomes dysregulated in cardiac hypertrophy and cardiac failure. |
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