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A myofibril is a part of, is comprised by?
Sarcomeres are made of, demarked by?
- Myosin: Thick Filaments
- Actin: Thin filaments
- Z lines.
How does contraction change the sarcomeres?
- No change in A band (length of myosin filament)
- Shortening of I band (end of one myosin to end of other myosin(of next sarcomere))
- Shortening of H zone (end of one actin to the other(within same sarcomere)).
Where is most Ca stored in muscle?
Terminal Cisternae of Sarcoplasmic reticulum, near the T-tubular system.
What proteins make up the thin filaments?
- Actin: structural component, contains attachements for cross-bridges
- Tropomyosin: covers attachement sites, moves to allow cross-bridging
- Troponin: binds calcium to move troponin-tropomyosin complex.
What three subunits make up troponin?
- Troponin-T: binds tropomyosin
- Troponin-I: Inhibits myosin binding to actin
- Troponin-C: binds calcium.
When is contraction terminated?
When Ca is removed from troponin.
What protein makes up the thick filaments?
- Possesses cross bridges, which have ATPase activity.
What causes dissociation of the cross bridge?
Binding of ATP.
Cross-bridge cycling will continue until?
- Withdrawal of Ca: normal resting muscle
- Depletion of ATP: Rigor Mortis.
Which two ATPases are involved in contraction?
- Myosin ATPase: energy for mechanical contraction
- SERCA: Sarcoplasmic endoplasmic reticulum calcium-dependent ATPase - provides energy for termination of contraction by pumping Ca back into depot.
How is tetanus reached?
There is sufficient free Ca for continuous cycling of all cross-bridges.
What is summation?
- Increased frequency of APs --> increased Ca released --> increased magnitude of response
- Possible because of very short refractory period.
What are the two types of tension on a muscle?
- Passive: Preload
- Active: contraction.
Preload on a muscle increases what?
What does the magnitude of developed active tension depend on?
Number of cross-bridges that cycle.
What are the characteristics of white muscle?
- Large mass, short term use
- High ATPase activity (fast)
- High capacity for anaerobic glycolysis
- Low myoglobin.
What are the characteristics of red muscle?
- Small mass, long term use
- Low ATPase activity (slow)
- High capacity for aerobic metabolism (mitochondria)
- High myoglobin (red color).
What are the two direct indices of ventricular preload?
- LVEDV: Left ventricular end-diastolic volume
- LVEDP: Left ventricular end-diastolic pressure.
What are the three indirect indices of ventricular preload?
- Left Atrial pressure
- Pulmonary Venous pressure
- Pulmonary capillary wedge pressure (swan-ganz).
Acute changes in contractility are usually due to?
Changes in intracellular dynamics of Calcium.
Increased sympathetic activity to the heart will produce?
- Decreased systolic interval: contractility effect
- Decreased diastolic interval: heart rate effect.
What would result in a loss in preload?
Loss in contractility?
Increase of contractility?
- Increased sympahtetics.
Increase of preload?
What determines Cardiac Output (CO), venous or arterial parameters?
Stroke Volume (SV)=?
Ejection Fraction (EF)=?
Cardiac Output (CO)=?
CO= SV x HR.
what is systolic dysfunction?
Abnormal reduction in ventricular emptying (increased afterload).
What is diastolic dysfunction?
Abnormal ventricular filling (stiffened ventricular wall s/p MI).
What is, causes concentric hypertrophy?
- Chronic pressure overload
- Dramatic Increase in wall thickness, decrease in chamber diameter
- Consequence: decreased ventricular compliance -> diastolic dysfunction, eventually systolic dysfunction.
What is, causes eccentric hypertrophy?
- Chronic Volume overload (eg. MR, AR, PDA)
- Modest increse in wall thickness, no change in chamber diameter
- Consequence: systolic dysfunction -- compliance of ventricle uncompromised.
What are the three types of cardiomyopathies?
- Dilated: Dilation without compensation in wall thickness
- Restrictive: Decreased ventricular compliance
- Hypertrophic: most common assymmetric hypertrophy of septum.
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