آالء العجرمي أسامة الخضر. Faisal Muhammad

Transcription

1 16 آالء العجرمي أسامة الخضر Faisal Muhammad

2 1. Summary for what taken : *changes in permeability of ions: 1. During phase 0: changes happen due to the influx of Na+, the permeability of Na ions increase firing stage 2. Phase 1: transient gates of k and cl ions open which results in partial repolarization. 3. Phase 2: slow gated Ca ions channels open (maintaining the depolarization) prolonging the absolute refractory period preventing cardiac tetanus. 4. Phase 3: opening of slow voltage gated potassium channels (K ions efflux ) 5. Phase 4: resting membrane (rearrangement of ions) Important questions: 1. why decreasing in the permeability of K ions is very important????? the answer is to maintain the plateau HOW?? 1 P a g e

3 Let s consider that the decreasing does not happen: *Potassium permeability is very high so the ions will move outside the cell. *while Ca ions will move inside the cell In this case, cell will not be depolarized, also because the calcium movement is slow and potassium movement is fast. In case of decreasing the permeability of potassium, it will stay inside and depolarization occurs. 2. Why there is not a cardiac tetanus??? Because of the very long absolute refractory period of cardiac muscle. The period of action potential of a cardiac muscle is 200 MS and 10 Ms for a skeletal muscle. 3. Why plateau is important and why it happens only in cardiac muscles??? *plateau is that the membrane potential remains almost constant. 2 P a g e

4 What happens in the skeletal muscle cell is that the action potential happens due to opening of fast sodium channels and calcium storage is enough so the calcium concentration increases rapidly (from the inter cellular sarcoplasmic reticulum), so it doesn t need an extra amount of calcium. In cardiac muscles, it happens due to the opening of fast sodium channels and also L-type calcium channels (slow channels), during phase 2 calcium enters the cell through (slow voltage gated calcium channels) this calcium induce more calcium release from SR (activate the muscle contractile process) and that s what we call it calcium induced calcium released. *the SR is not well developed in cardiac muscle as in the skeletal muscle so it doesn t have enough calcium storage. Because of that, in the case of cardiac transplant we need to put the heart in ca +2 solution. Excitation contraction coupling: excitation is action potential and contraction is mechanical, how can we link between them? By increasing the extracellular calcium concentration, and when action potential happens, calcium ions enter the cell and they induce more calcium ions resulting in muscle contract. انجزت الكثير وبقي القليل... تستسلم فال 3 P a g e

5 Relaxation: In order to make relaxation we have to take calcium ions back (by moving calcium ions to SR). How can we do that while the concentration of calcium in SR is more than it is in Sarcoplasm by active transport (ATP is needed) 1. Active Calcium pump (ATPase calcium pump): exactly the same as skeletal muscle, it is located in Sarcolemma. 2. Sodium calcium exchanger: exchange 1 ca +2 outside and 3 Na +, it is a counter-secondary active transport (doesn t use energy directly), note: sodium potassium pump: always keep the concentration of Na ions inside the cell low so Na+ gradient energies this exchanger. It is located in sarcolemma 3. Calcium pump in SR. *all of these is electro genic which means they make difference in charges. 4 P a g e

6 The difference between the calcium pumps: First, we have to know what is the meaning of affinity it is how the )د. فيصل : سرعة اشتغالها( pump response to the concentration Calcium pumps: 1. In SR membrane --- low affinity (so it needs high concentration in order to response) but high capacity (when it begins to pump there will be high amount of Ca ions transported so it will move a lot of calcium) 2. In sarcolemma high affinity ( response to low concentration that means it is very fast) but low capacity. After these three methods are activated, ]Ca +2 [ reaches 10-7 molar --- relaxation * cardiac muscle relaxation: (diastole) contraction: (systole). *** Abnormal case: If we have high concentration of calcium in the intercellular fluid, this will activate sodium- calcium exchanger in the outer mitochondrial membrane to decrease the calcium concentration which affects the activity of the mitochondria. Be optimistic. Life is beautiful 5 P a g e

7 The heart as intrinsic source of action potential: the heart in order to contract, it needs an action potential to initiate contraction, the source of it is the conductive system of the heart: it is a modified cardiac muscles, their percentage is 1% of the cardiac cells, and found in 5 places. 1. SA node (sinoatrial node): it is located in the superior posterior lateral wall of the right atrium, small flattened ellipsoid strip about 3 mm wide, 15 mm long, 1mL thick. 2. AV node (atrioventricular node): between the right atrium and the right ventricle it is continues as a bundle 3. AV bundle (atrioventricular bundle (bundle of His)): it is divided to 4. right bundle branch and left bundle branch, at the end they diverse as 5. Purkinje fibers 6 P a g e

8 Their properties: 1. anatomically Modified: don t have contractile protein so they are not able to contract. 2. Physiologically: their membrane is leaky to sodium 3. They are able to produce an automatic and rhythmic action potential (auto rhythmic cells) the rates of them : 1. SA node / minute, restrict the speed of heart rate. 2. AV node / minute 3. Purkinje / minute *** any another place than SA node that controls the heart rate we call it ectopic (Abnormal), even if it higher than SA or lower. Mechanism of controlling: since they have a sodium leakage, resting membrane potential won t reach - 90 (less negative), during phase 4 we still have leakage of sodium which leads to slow depolarization, when we reach threshold, action potential will occur. After we reach the threshold the inactivation sodium gates will close before the activation gates open due to slow response so sodium ions will not enter, what will enter is calcium so phase 0 will be due to calcium influx, phase 3 occurs because of the deactivation of Ca gates and activation of slow response K channels, this is the difference between slow response and fast response (proper cardiac muscle). 7 P a g e

9 ***usually the resting membrane potential for them is -60 not -90 Activation gate (N): it is closed at rest and opens fast when the membrane potential becomes less negative Inactivation gate (H): it is open at rest and closes slowly when the membrane potential becomes less negative. in conductive system, slow response occurs due to Na leakage; slow depolarization. *** In conductive system there is no plateau, no phase 1 or just phase 0 by Calcium influx, phase 3 by potassium efflux, phase 4 (slow depolarization). *we can increase or decrease the heat rate by: 1. Increase ---- by increasing sodium leakiness 2. Decrease----- by increasing potassium efflux which will make the resting membrane more negative. Don t study for yourself study for your future patient. Good luck all 8 P a g e