Cardiac Muscle Flashcards
What are some properties unique to cardiac mm?
Cells are short, branch and interdigitate
Presence of intercalated disks
What are some properties that are common for cardiac and skeletal mm?
Striated Sarcomeres (thick, thin filaments) Same sliding filament mechanism Crossbridge cycling is similar T-tubules and SR
Cardiac muscle cells are similar to _________skeletal muscle fibers
Type I (slow oxidative)
because -depend on oxidative phosphorylation
- numerous mitochondria
- highly resistant to fatigue
- BUT highly dependent on continuous supply of O2
What are the 3 types of connections b/n cardiac myocytes?
Zonula Adherens
Macula Adherens (Desmosomes)
Gap Junction
What are the two connections that make up intercalated discs?
Macula Adherens (Desmosomes) Gap Junction
Define physical and functional coupling?
Physical coupling: points where cells mechanically pull on each other-Zonula adherens, Macula adherens (Desmosomes)
Functional coupling: allow electrical signals to pass between cells-Gap junctions
Define sliding filament mechanism of muscle contraction.
Thin filaments sliding over thick filaments causing muscle contraction.
NOTE: during muscle contraction the H and I-bands shorten. While the A-band doesn’t change.
What are the different states of crossbridge cycling?
Attached state-Released state (ATP attaches to myosin)-Cocked state (ATP is hydrolyzed, myosin at resting conformation)-Crossbridge state (myosin head binds to a new position on actin)-Power-stroke state (P is released, shortening and force development)-Attached state (ADP is released)
What are two molecules essential for crossbridge cycling?
Ca
ATP
What is the difference b/n cardiac and skeletal muscle at the membrane system for E-C (excitation-contraction) coupling?
Cardiac mm:
- more sparse SR,
- dyad-SR, TT (triad-1T-tubule b/n 2SR’s in SK mm),
- d/f T-tubule position cardiac mm @ z-line (SK mm A-I band junction), -bigger T-tubule (200 nm vs. 30 nm in SK mm)
How are cardiac mm d/f from skeletal mm in handling Ca during E-C coupling?
Skeletal mm: AP gets to the T-tubule–DHPR (on T-tubule) senses Vm–change in conformation of DHPR results in change in conformation of RyR of the SR–Voltage (depolarization)-dependent Ca release from SR to the cytosol–CONTRACTION
Cardiac mm: AP gets to the T-tubule–DHPR acts as Ca channel–[Ca] in the cytosol increases–Ca-Induced Ca Release from the SR
T/F Cardiac mm can NOT contract in the absence of extracellular Ca.
T. Unlike SK mm., Cardiac mm need CICR to generate contraction.
What is another name for DHPR in cardiac mm?
L-type Ca channel
What are the 3 ways that DHPR regulates cardiac function?
DHPR (L-type Ca channel) regulates cardiac function:
- physiologically (ex. sympathetic stimulation)
- pharmacologically (ex. calcium channel blockers)
- pathologically (ex. ischemia)
T/F Ca influx during AP must not be balanced by a Ca efflux b/n APs.
F. It must be balanced. There are different channels responsible for the entry and exit of Ca.
What are the key players in Ca balance (entry and exit)?
Entry: DHPR, RyR
Exit: SR ATPase, Surface ATPase, Surface Na-Ca Exchanger (3Na in for 1Ca out), Mitochondrial uniporter
NOTE: refer to pp. 11
What 3 factors affect the [Ca] in the cytoplasm?
1) Amount of Ca stored in SR
2) Amount of Ca entering the cell from the extracellular space
3) Heart rate
Compare and contrast the gradation of contractile force b/n SK mm and Cardiac mm?
SK mm:
recruitment,
summation and tetanus,
length-tension relationship (bell curve)
Cardiac mm:
-all or none (all the muscles work as a unit),
-no summation and tetanus b/c the duration of the AP is comparable to the duration of mm contraction,
-length-tension relationship (resting cardiac mm length is less than optimal length, cardiac muscle does not normally operate within the descending limb safety factor i.e., much stiffer)
Define Frank-Starling’s Law.
Increased stretching of the myocardial filaments results in a stronger contraction-Fundamental property of cardiac mm.
Ex: Increased venous return->increased stroke volume (SV)
______gives the precise arrangement of thick and thin filaments, and gives rise to passive mm stiffness
Titin
What are the factors that alter the length of ventricular cardiac mm fibers?
Increase the length: stronger atrial contraction, increased (total blood volume,venous tone, pumping action of SK mm, negative intrathoracic pressure)
Decrease the length: standing, increased intraventricular pressure, ventricular compliance
Define preload and afterload.
Preload: the amount of blood (chamber volume) before contraction (extent to which the mm is stretched).
Afterload: the tension against which the ventricle must contract (the load lifted by the mm in isotonic contraction)
REVIEW:CO=HR(SV). SV depends on: preload, afterload and inotropic state. Inotropic state depends on: # functional myocytes, the cytosolic [Ca] and coronary O2 supply.
Describe what each of the ff. situations signify:
1) No PL, AL acting on the mm
2) PL added on the mm
3) PL, AL added without additional stretch
4) AL lifted
1) Relaxed state after ventricular contraction
2) End of filling of the ventricle
3) Ventricle contraction has started, both valves are closed
4) Left Ventricular ejection into aorta
NOTE: refer to pp. 18
What factors can affect preload and afterload?
- Cardiac factors (HR, or SV)
- Vascular factors (vascular tone and peripheral resistance)
