CVR week 2 Flashcards
What are the 4 main components of the myocardium?
contractile tissue
connective tissue
fibrous frame
specialsied conductive system
What are cardiac myocytes?
contractile myocytes of the cardiac muscle
What is Excitation-contraction coupling
The process of converting an electrical stimulus (action potential) to a mechanical response (muscle contraction). It begins when the action potential depolarizes the cell and ends when ionized calcium (Ca2+) that appears within the cytosol binds to the Ca2+ receptor of the contractile apparatus.
describe the process of excitation contraction coupling?
The action potential travels down the T-tubules depolarising the cell membrane and also depolarises sarcomeres resulting in an influx of calcium ions into the sarcoplasm.
Cardiac muscle contraction occurs via the sliding filament model of contraction, What is the sliding filamnet model of contraction?
It then binds to cardiac troponin-C which moves the tropomyosin away from the actin-binding site thus exposing it and initiating cross-bridge binding.
The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytoplasm.
Once calcium is bound to troponin-C and the conformational change of tropomyosin has occurred, myosin heads can bind to actin.
Following this ADP and inorganic phosphate are released from the myosin head so the power stroke can occur. In this the myosin head pivots and bends, pulling on the actin and moving it, causing muscle contraction.
After this occurs a new molecule of ATP binds to the myosin head, causing it to detach from the actin. Finally, the ATP is hydrolysed into ADP and inorganic phosphate. Following this, the cycle can begin again and further contraction can occur.
The heart relaxes when ion exchangers and pumps transport Ca2+ uphill, out of the cytoplasm.
features of the myocardial cell
- filled with cross-striated myofibrils
- many mitochondria
- plasma membrane regulate excitation-contraction couply and relaxation
- plasma membrane seperate cytosol from extra-cellular space and sarcoplasmic reticulum
myocardial metabolism:
Relies on free fatty acids during aerobic metabolism (efficient energy production).
During hypoxia, there is no FFA metabolism, thus anaerobic metabolism ensues. This relied on metabolising glucose (anaerobically) producing energy sufficient to maintain the survival of the affected muscle without contraction.
Ultrastructure of myocardial cells:
Contractile proteins are arranged in a regular array of thick and thin filaments (The so called Myofibrils).
A-band: the region of the sarcomere occupied by the thick filaments.
I-band: is occupied only by thin filaments that extend toward the centre of the sarcomere from the Z-lines. It also contains tropomyosin and the troponins.
Z lines bisect each I-band.
what is a sarcomere?
The sarcomere: the functional unit of the contractile apparatus,
The sarcomere is defined as the region between a pair of Z-lines,
The sarcomere contains two half I-bands and one A-band.
what is the sarcoplasmic reticulum? what is the sarcolemma?
The sarcoplasmic reticulum is a membrane network that surrounds the contractile proteins,
The sarcoplasmic reticulum consists of the sarcotubular network at the centre of the sarcomere and the subsarcolemmal cisternae (which abut the T-tubules and the sarcolemma).
The transverse tubular system (T-tubule) is lined by a membrane that is continuous with the sarcolemma, so that the lumen of the T-tubules carries the extracellular space toward the center of the myocardial cell.
Contraction of sarcomere:
Sliding of actin over myosin by ATP hydrolysis through the action of ATPase in the head of the myosin molecule.
These heads form the crossbridges that interact with actin, after linkage between calcium and TnC, and deactivation of tropomyosin and TnI.
myosin
2 heavy chains- also responsible for heads
4 light chains
heads are perpindicular at rest, bend towards centre during contraction
actin
globular proetin
double stranded helix
both form the F actin
tropomyosin
Elongated molecule, made of two helical peptide chains.
It occupies each of the longitudinal grooves between the two actin strands.
Regulates the interaction between the other three!
troponin- 3 types
Types of troponin:
I: with tropomyosin inhibit actin and myosin interaction.
T: binds troponin complex to tropomyosin.
C: high affinity calcium binding sites, signalling contraction.
The latter bond, drives TnI away from Actin, allowing its interaction with myosin
titin
titin molecules anchors myosin to Z-line
sumamry of muscle contraction:
1- Ca++ enter the cell through Ca++ channels on sarcolemma during depolarization(phase 2) and triggers release of Ca++ by terminal cisternae. =(Ca++ induced Ca++ release)
2- Ca++ binds to troponin-C inducing a conformational change in the troponin complex. (Ca+ binds to troponin, so troponin releases actin. The free actin can now bind to myosin.)
3- Myosin heads bind to actin, leading to cross-bridge movement(=sliding) (requires ATP hydrolysis) and reduction in sarcomere length. (muscle contraction)
4- Ca++ is re-sequestered(Ca++ reuptake) by sarcoplasmic reticulum by sarco- endoplasmic reticulum calcium ATPase (SERCA) pump.
5- Ca++ is removed from troponin-C and myosin unbinds from actin (requires ATP hydrolysis); this allows the sarcomere to resume its original, relaxed length. (muscle relaxation)
40 degree angle
projections on the myosin filament
Cardiac Cycle Phases:
LV contraction:
LV relaxation:
Ventricular Contraction- systole
Wave of depolarisation arrives,
Opens the L-calcium tubule, {ECG: Peak of R},
Ca2+ arrive at the contractile proteins,
Left ventricular pressure rises > Left artrial pressure:
Mitral Valve closes: M1 of the 1st Heart Sound,
Left ventricle pressure rises (isovolumic contraction) > aorta pressure
aortic valve opens and Ejection starts.
Ventricular Relaxation
Left venticular pressure peaks then decreases.
Influence of phosphorylated phospholambdan, cytosolic calcium is taken up into the SR.
“phase of reduced ejection”.
Aortic flow is maintained by aortic distensibility.
Left Ventricular pressure < Aotic pressure, Aotic valve closes, A2 of the 2nd Heart Sound, “isovolumic relaxation”- period of time between Aortic vakve sutting and mitral valve opening, then Mitral Valve opens
Ventricular Filling
Left Ventricular pressure < Left Atrium pressure, MV opens, Rapid (Early-phase) filling starts - passive
Ventricular suction (active diastolic relaxation), may also contribute to E filling, S3 sound
Diastasis (separation): LVentricular pressure = LAtrium pressure, filling temporarily stops. net flow is 0
Filling is renewed when Atrial contraction (augmentation), raises L Atrial pressure creating a pressure gradient. sometimes hear S4 sound- always pathological
(older people are more reliant on atrial augmentation, rely on it for roughly 40% of blood movement)
mitral valve shuts- 1st heart sound (Lub)
Physiologic vs. Cardiologic systole
Physiological:
1. Isovolumic contraction,
2. Maximal ejection
Cardiological:
1. From M1 to A2,
2. Only part of isovolumic contraction (includes maximal and reduced ejection phases)
preload and afterload
Preload: is the load present before LV contraction has started.
Afterload: is the load after the ventricle starts to contract.
