L12 - Myocardial Mechanics Flashcards
What describes the electrical excitation leading to contraction
Excitation - contraction - coupling
What does excitation contraction coupling describe
The electrical excitation leading to the contraction
What is the role of the T-tubules
Cause activation of many sarcomeres at one time
Leads to a faster contraction
What is the structure of the T-tubules - how does this relate to their function
Invaginations of the sarcolemma
They allow the depolarisation to spread deep into the cell
What do intercalated discs contain
Ion channels
What is the role of the intercalated discs
What does this form?
Between the ion channels - this ionically links the myofibrils forming a functional syncitium
Describe the sarcoplasmic reticulum
Fluid filled membranous sac - acts a as Ca store
Where are the cisterns found
At the end of the SR
What do T-tubules and cisterns form
Triads
Describe the sliding filament theory / state for a relaxed muscle
Ca in sarcoplasm low
Ca pumps sequester Ca in SR
Tropomyosin obscures the actin-myosin binding site preventing cross bridge formation
What is the role of calsequesterin
Binds to free Ca in the SR - gives impression that Ca is SR is low so pumps can work faster
Describe sliding filament theory when muscle is contraction
Propagation of AP along T-tub activation of VGCC
CA SR rises
Ca binds to Tn-C
Conf change in tropomysosin - actin mysoing binding site exposed
Cross bridge can form and cycling can occur if ATp/ADP/Pi available
What is muscle tension proportional to
The number of cross bridges
What is the number of cross bridges proportional to
The length of the sarcomere
What produces a maximum tension generation
An optimum resting length
Why isnt max tension gen. with short sarcomeres
Because of overlapping thin filaments
What isnt max tension gen. with long sarcomeres
Reduced area for cross bridge formation so less tension is generated
What differs between the heart and other muscles - what are the implications of this
Heart is not bound by any joints so it is possible for it to go beyond the optimum length
This leads to less force ==> so more blood left in with each contraction and can lead to heart failure
What is the optimum sarcomere length for cardiomyocytes
2.2 - 2.6 um
Describe the process that would be undertaken to measure length-tension
Clamped muscle held fixed at one end - other end attached to a force transducer
Electrical stimulation via electrode
Record l of muscle and force gen by the contraction
Lengthen muscle and repeat over a range of muscle lengths
What happens to the active force as sarcomere length increases
Starts increasing to a maximum and then decrease
What happens to passive force as sarcomere length increases
At 0 until high sarcomere length then increases
What happens to total force as sarcomere length increases
Increases - peaks - begins to decrease as active force decreases BUT passive force increases so total froce begins to increase
Describe how an engineer would model a cardiomyocyte
One contractile element with a critcal damper to prevent oscilations
One spring in parallel - representing the neck of the cross bridge
One spring in series - representing the accessory protein of the sarcomere (titin)
What length sarcomere is produced by a 10-12 mmHg filling pressure
2.2. um
this is the presystolic volume
What is a key difference in the regulation of tension between cardiac and skeletal myocyte
In cardiac greater regulation at the cellular level
In skeletal muscle to cause greater tension more fibres are recruited
In caridac the force produced by each myocyte is changed
What is isotonic contraction
Where tension does not change but the length does change
What is isometric contraction
Length is unchanged but the tension does change
Describe the relationship of the muscle, pre load and the afteload
Muscle is streched by the preload which stimulates it to lift the afterload
What is the preload
Initial streching of the sarcomere length
The ventricular end diastolic volume
What is the afterload
The force which the ventricles have to act against in order to eject the blood – essentially the arterial blood pressure and vascular tone
For an isotonic contraction what can be said about contraction for a heavier load
It will be slower
What is the relationship between shortening velocity and the afterload
There is an inverse relationship between shortening velocity and afterload
What are the 3 key results from a graph of initial velocity of shortening against the load
A high preload gives a high maximal force (high preload = high P0)
For any given afterload a high preload gives a high velocity of shortening
Maximum initial velocity of shortening is constant
Describe 3 varying definitions of contractility
Change occurs when a heart changes its output per beat with the EDV remaining constant
Changes can occur when more crossbridges form per stimulus
May reflect the qualitative state of the actin/myosin cross bridges
What is the effect of sympathetic stimulation by NAdr on contractility
Increases the Vmax (maximum initial velocity of shortening)
Increase the P0 (maximum force which can be produced)
What are the effects of sympathetic stimulation said to be …
Positive chronotropic (time) and ionotropic (force)
What does the interbeat duration influence
The force of contraction
Why does an increased frequency of beats lead to a increase in contractility
With faster beats - less time for Ca to be resequestered
So Ca accululates with each beat
