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Cardiac Muscle II

Regulation of myocardial performance. Two kinds: Intrinsic: stretch increases force - the degree of stretch of the ventricle wall is determined by venous return - the amount of blood that enters the heart during the interbeat intervalExtrinsic: Cholinergic input decreases force; sympathetic input increases it. These inputs are managed by a reflex circuit that regulates arterial blood pressure..

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Cardiac Muscle II

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    1. Cardiac Muscle II

    2. Regulation of myocardial performance Two kinds: Intrinsic: stretch increases force - the degree of stretch of the ventricle wall is determined by venous return - the amount of blood that enters the heart during the interbeat interval Extrinsic: Cholinergic input decreases force; sympathetic input increases it. These inputs are managed by a reflex circuit that regulates arterial blood pressure.

    3. Intrinsic regulation (autoregulation) As averaged over several heartbeats, volume in = volume out I.e. cardiac output = venous return This is known as the Frank-Starling Law of the Heart

    4. Some definitions: End-diastolic volume EDV: the volume of the ventricle at the end of filling, equal to the venous return volume plus the end-systolic volume ESV. Stroke volume SV: the amount of blood ejected during a beat. SV = EDV-ESV

    9. Excitation-contraction coupling in the heart

    10. There are 2 key differences in excitation-contraction coupling in heart versus skeletal muscle 1. In the myocardium, a significant amount of Ca++ (about 1/10 of the total) enters through L Ca++ channels in the sarcolemma, during the plateau of the myocardial action potential. (In comparison, essentially all the Ca++ released in skeletal muscle comes from the SR and virtually none enters across the sarcolemma).

    12. Ca++-induced Ca++ release is much more important in cardiac muscle than in skeletal muscle

    15. Effects of the beta adrenergic receptor in myocardium Increased activity of L Ca++ channels Increased sensitivity of troponin to Ca++ Increased ability to clear Ca++ after a contraction – through reuptake to the SR and expulsion across the sarcolemma

    16. Neural regulation of the heart

    17. What factors could increase the peak intracellular Ca++ concentration attained during excitation? Simply increasing heart rate. Activating Beta1 receptors Cardiotonic drugs, such as digitalis, that interfere with Ca++ removal from the cytoplasm.

    18. The effect of increased contractility on the length-tension relationship

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