Term
| Do isolated cardiac cells contract? |
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Definition
| No. Cells within the ventricle contract at a frequency that is determined by the SAN located within in right atrium. Isolated cells are freed from this control and do no contract as they lack an intrinsic pacemaker. They may exhibit occasional 'spontaneous' contractions. |
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Term
| Give two equations that allow you to calculate concentrations and volumes |
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Definition
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Term
| Out of rod-shaped and rounded-up cells, which are living? |
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Definition
rod-shaped
the rounded ones have died during the isolation process |
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Term
| Explain propagation of electrical activity throughout the heart |
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Definition
1. AP is initiated in the SAN
2. AP are conducted from the SAN to the atrial muscle
3. AP spread through the atria to the AVN where conduction slows
4. AP travel rapidy through the conduction system to the apex of the heart
5. AP spread upward through the ventricular muscle
6. Eventually, the entire heart returns to the resting state, remains there until another AP is generated in the SAN |
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Term
| Give the internal and external concentrations of K+ across the sarcolemma |
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Definition
intracellular: 140mM
extracellular: 5mM |
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Term
| Give the internal and external concentrations of Na+ across the sarcolemma |
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Definition
intracellular: 5-10mM
extracellular: 145mM |
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Term
| What is retrograde perfusion? |
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Definition
- closing of aortic valve, perfusate forced into coronary circulation
- an artificial method of providing blood supply to an organ by delivering oxygenated blood through the veins. It may be performed during surgery that interrupts the normal arterial supply of blood to that organ. |
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Term
| Why does K+ increase the frequency of spontaneous contractions? |
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Definition
- As you increase [K]o, the cell depolarises from around -84 mM to a more positive value.
- Initially, depolarisation may trigger activation of Na+ channels, reading to an increased probability of action potentials.
- In addition, the Na/Ca exchanger is “electrogenic” (3Na transported to 1Ca), such that 1 positive charge is moved in the direction of Na+.
- As Na/Ca exchange is electrogenic, the direction of transport depends upon Em.
- When cell depolarises to around -40 mM (or more positive), Ca is moved into the cell via Na/Ca exchange.
- This can cause Ca overload of the sarcoplasmic reticulum, which then exhibits spontaneous release. |
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Term
| Describe phase 4 of the ventricular AP |
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Definition
The stable resting membrane potential is due to the presence of background K+ channels in ventricular tissue.
These are open at negative potentials and set the resting membrane potential close to EK = ~ -90mV. At rest, ventricular (and atrial) cells are most permeable to K+ because all ions are present in their resting values (Na+ and Ca2+ are present in much lower concentrations). |
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Term
| Describe phase 0 of the ventricular AP |
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Definition
The depolarisation phase, or upstroke, is due to the opening of voltage-gated fast Na+ channels.
Na+ ions move down their concentration gradient and enter the cell, so as a consequence membrane potential becomes more positive. This triggers the opening of more fast Na+ channels, more Na+ entering the cell and further depolarisation. Membrane potential will be driven towards ENa = ~+60mV.
Fast Na+ channels begin to inactivate, reducing the amount of Na+ entering the cell, causing the membrane potential to become more negative, because K+ are still leaving the cell.
Na+ channels inactivate rapidly (1-3ms) and then remain closed until membrane potential returns to negative values.
As membrane potential becomes more positive during the upstroke, the background K+ channels shut; this reduces the permeability of the cell membrane to K+. |
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Term
| Describe phase 1 of the ventricular AP |
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Definition
| Activation of the transient outward K+ current (Ito) occurs. This activates rapidly upon depolarisation but also closes rapidly, causing the initial repolarisation phase of the action potential. |
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Term
| Describe phase 2 of the ventricular AP |
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Definition
1. When membrane potential is more positive than -40mV, voltage-gated L-type Ca2+ channels begin to open; Ca2+ enters the cell down its concentration gradient.
2. L-type Ca2+ channels inactivate slowly (over 100-200ms) and it is this long- lasting inward Ca2+ current underlies the plateau phase.
3. During the plateau, the cells are most permeable to Ca2+, with the permeability of the cells to K+ being at its lowest (because background K+ channels remain inactive).
4. Very few T-type Ca2+ channels are expressed in ventricular muscle.
5. Balance between EK and ECa2+ means membrane potential is around +10mV-0mV. |
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Term
| Describe phase 3 of the ventricular AP |
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Definition
1. Brought about by the decline in the permeability to Ca2+ (the fall in potential causes their inactivation) and an increase in permeability to K+.
2. K+ permeability increases as the delayed K+ channels open; K+ leaves the cell down its concentration gradient.
3. At this point, the cell is most permeable to K+ which forces the membrane potential towards EK, so obviously the membrane potential falls to more negative values.
4. As repolarisation proceeds, and membrane potential becomes more negative, the delayed K+ channels begin to shut.
5. When membrane potential is close to its resting level, the background K+ channels open again to keep the resting membrane potential stable.
6. The return to negative membrane potentials reactivates (fast) Na+ channels so they are available for the next action potential. They can’t re-open until the potential becomes negative again.
7. ...and the love kick starts again... |
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Term
| Describe excitation-contraction coupling |
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Definition
1) AP spreads across the surface membrane of the ventricular cell and down the t-tubules
2) this causes depolarisation of the membrane where L-type Ca2+ channels are concentrated. A small amount of Ca2+ is released into the cytosol.
3) Ca2+ binds to Ca2+ release channels on sarcoplasmic reticulum and causes a large release of Ca2+.
4) released Ca2+ binds to the contractile proteins. |
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