Cellular and Molecular Events in the Heart PDF

ellular and Molecular event in the ha Curriculum: Phase 1/Semester 3/CVS/Session7/L. 1 Lecturer: teacher Dr. Dhuha Salman Degrees: MSc/Ph.D. Phsiology  Objectives describe the processes which generate the resting membrane potential of cardiac cells. draw the changes in me...

ellular and Molecular event in the ha Curriculum: Phase 1/Semester 3/CVS/Session7/L. 1 Lecturer: teacher Dr. Dhuha Salman Degrees: MSc/Ph.D. Phsiology  Objectives describe the processes which generate the resting membrane potential of cardiac cells. draw the changes in membrane potential of (i) ventricular cells (ii) pacemaker cells over the cardiac cycle. describe the membrane permeability changes and ionic currents underlying the ventricular and pacemaker cell action potential. describe in general terms, the processes of excitation - contraction coupling in ventricular myocardial cells. describe the factors influencing the changes in intra cellular free calcium concentration of ventricular cells during the action potential. describe the membrane potential changes in pacemaker cells associated with increases and decreases in heart rate. THE MYOCARDIUM Two specialized types of cardiac muscle cells: There are two major types of cardiac muscle fibers: myocardial contractile cells and myocardial conducting cells (pacemaker cells). The myocardial contractile cells constitute the bulk (99%) of the cells in the atria and ventricles and are responsible for contractions that pump blood through the body. Each of these 2 types of cells has a Hypokalamia :-the cause of arythmia, because of fast replorazation, fast K out the cell cause tachycardia Voltage Na become inactive close when; 1-K begin to out the cell 2-long time cell stay depolrize 3- patient with hyperkalmia Hyperkalamia :-high Kin blood (exracellular ) The patient heart will stop in dystole (relax , effect of repolrazation , K out cause bradycardia Excitation–contraction (E-C) coupling 1.An action potential by SA and conducted to all cells in the heart via gap junctions. 2. The action potential travels along the surface membrane into T-tubules and the depolarisation causes Ca2+ to enter the cell via L-type calcium (specially in platue phase) channels This Ca2+ influx causes a small local increase in intracellular Ca2+. 3. The increase in Ca2+ is detected by ryanodine receptors in the membrane of the sarcoplasmic reticulum which releases Ca2+ in a positive feedback physiological response. (calcium- induced calcium release). 4. The cytoplasmic calcium binds to Troponin C, moving the 5. Using ATP hydrolysis the myosin head pulls the actin Filament toward the centre of the sarcomere. 6. Intracellular calcium is taken up by the sarco/endoplasmic reticulum ATPase pump back into the sarcoplasmic reticulum ready for the next cycle to begin. Calcium is also ejected from the cell mainly by the sodium-calcium exchanger and, to a lesser extent, a plasma membrane calcium ATPase and/or taken up by the mitochondria. 7. Intracellular calcium concentration drops and