Cardiac Muscle Lab Report

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The properties of cardiac muscle are always changing as a result of sympathetic and parasympathetic nervous stimulation and pharmacological drugs that alter or stimulate molecular mechanisms in the heart. In order to understand the mechanisms of the heart, we must experiment with the heart by observing the properties of cardiac cells and formulate hypotheses for their observed response.
The structure of cardiac muscle consists of myocardial cells which have a nucleus, contractile filaments (striations), several mitochondria and intercalated discs which contain gap junctions (Silverthorn, 2007). Surrounding the myocardial cells are t-tubules whereby electrical ions can flow into the cell membrane proteins and start action potentials (Silverthorn, 2007). Together, these structures give the heart its ability to contract and communicate with its cells in a regulated manner (Silverthorn, 2007).
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The receptor opens and conducts Ca2+ in the cytosol which then bind to the membrane channel Ryanodine receptor (RyR) (Silverthorn, 2007). RyR leaks out Ca2+ from the sarcoplasmic reticulum (SR), which induces a calcium spark (Silverthorn, 2007). Calcium binds to troponin, whose affinity to actin is now higher than tropomyosin, the molecule covering the binding site of actin (Silverthorn, 2007). Adenosine-Diphoshate-bound myosin heads now bind to the active site to form cross-bridges and achieves a power stroke (Silverthorn, 2007). The power stroke causes the contraction of contractile fibres (Silverthorn, 2007). Relaxation begins when ATP binds to myosin which causes its release from the actin binding site (Silverthorn, 2007). Ca2+ returns back to the SR via Ca2+ ATPase and transported from the cell by a Na+/Ca2+ exchanger (NCX) (Silverthorn,

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