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Lecture 8

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University of Toronto St. George
Michelle French

Lecture 8  Recap: Innervation and Heart Control  Heart is stimulated by the sympathetic cardioacceleratory system  Epinephrine, increased cAMP, increased funny current  Stronger force of contraction on atrial and ventricular chambers  Heart is inhibited by the parasympathetic cardioinhibitory system  ACh acting on Gi-protein mesocranic receptor via vagal nerves on SA node to reduce cAMP production as well as causing K+ to leak out  Autonomic neurotransmitters Alter Heart Rate  Cardiovascular control center in the medulla oblongata  Sympathetic Neurons  NE  B1-receptors of autorythmic cells (pacemakers)  Na+ and Ca+ influx  Higher rate of depolarization  Increase heart rate  Parasympathetic Neurons  Ach  Mesocranic receptor of autorythmic cells (pacemakers)  Increase of K+ efflux, decrease of Ca2+ influx  Hyperpolarizes cell and slows the rate of depolarization  Lowers heart rate  Catecholamines modulate Cardiac Contraction  Sympathetic  Epinephrine & Norepinephrine bind B1 receptors  Activates cAMP second messenger system resulting in phosphorylation of  1) Voltage gated Ca2+ channels (dihydropyridine receptor)  Open time increases  Ca2+ entry from the ECF  increase storage of Ca2+ in SR and increase Ca2+ surge leading to a more forceful contraction  2) Phosphorylation of Phospholamban (accessory molecule, inhibitor of the SRER calcium ATPase that is the pump in the SR)  Increase of Ca2+-ATPase on SR  Ca2+ removed from cytosol faster into SR  Shorter Ca-Troponin binding time  shorter duration of contraction  Mechanical pumping events of the Cardiac Cycle  The heart cycles between contraction (Systole) and relaxation (Diastole)  1) Late Diastole: both sets of champers are relaxed and ventricles fill passively  2) Atrial Systole: atrial contraction forces a small amount of additional blood into ventricles  3) Isovolumic ventricular contraction: first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves.  4) Ventricular ejection: as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected  5) Isovolumic ventricular relaxation: as ventricles relax; pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed  The heart is only working (systole) 1/3 of the time and is relaxing (diastole) the other 2/3  Wiggers Diagram  1) The initial wave of action potential from the SA node is being translated to the adjacent contractile cell through gap junctions, depolrizing the cells. This intital wave is going throughout the atria and initiates the contraction, the elctrical event at the T-tubules that open the Ca2+ channgel as well as the RyR on SR, causing a surge leading to that contraction  Atrial Systole, P wave  2) The wave continous spreading to the AV node, where it is delayed and then spread to the ventricles and prukinjie fibers.  QRS complex, isovolumic ventricular contraction  3) The wave is now completely spread throughout the ventricles by the purkinjie fibers generateing a pressure and force. The full ventricle systole is taking place  Ventricle Systol, RS-T wave  4) The wave of electrical activity than ends, the ventricles start to repolraize, the ions are now taken up into the SR, pumped out by the Ca2+ Na+ channel and Na+ K+-Atpase. Ventricles relax.  Early ventricular distole, T-P wave  5) Re-start cycle  Abnormal ECG  Third Degree Block: SA node does not propegate to ventricles, AV block  Normal P, wide
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