Wake Cv Cellular Mechanisms Of Heart Contraction

Front 1

Thin Filaments

Back 1

- G-actin (globular) polymerizes to form F-actin (filamentous)
- Tropomyosin helps hold F-actin together
- Troponin complex

Front 2

Troponin-T

Back 2

binds to tropomyosin, anchoring the troponin complex

Front 3

Troponin-C

Back 3

binds Ca2+, an essential step in initiating contraction

Front 4

Troponin-I

Back 4

binds to actin, inhibiting actin-myosin interaction

Front 5

Which components of heart muscle are cardiac specific?Why is this important?

Back 5

Troponin-T and Troponin-I are cardiac specific

Cardiac troponins are preferred markers for detecting myocardial cell injury  
- Rises 2 - 6 hours after injury
- Peak in 12 - 16 hours
- cTnI stays elevated for 5-10 days, cTnT for 5-14 days

Front 6

Stages of contraction cycle within a sarcomere

Back 6

1. Attachment (rigor formation)
2. Release
3. Bending
4. Force generation
5. Attachment: The Sequel

* Note that not all individual myosin molecules attach to actin during every cycle

Front 7

Which filament is bound to the Z line?

Back 7

Actin (thin filament)

Front 8

Which filament is bound to the M line?

Back 8

Myosin (thick filament)

Front 9

During muscle contraction does the myosin head bend toward the M line or Z line?

Back 9

Z line

Front 10

Does the A band size change during muscle contraction?

Back 10

NO. The A band is the length of the myosin despite overlap.

Front 11

Thick filaments

Back 11

- Each myosin II molecule contains two polypeptide heavy chains and four light chains (two each of two types)
- Each myosin heavy chain (MHC) has globular head with one binding site for ATP and another for actin; also demonstrates ATPase and motor activity
- Molecules aggregate tail to tail; globular heads extending so can form cross-bridges to thin filaments

Front 12

Which bands of the sarcomere get narrower during contraction?

Back 12

I band (actin only zone)
H band (myosin only zone)

and of course the whole sarcomere

Front 13

What are the key regulators of contraction?

Back 13

1. ATP (Immediate pool very limited; “Resupplied” from creatine phosphate, glycogen, and cellular respiration)
2. Calcium [Links action potential to myofilament interactions (excitation-contraction coupling)]
3. Magnesium (required ATPase activity and other functions)
4. Na+ and Na+ Channels
5. Beta-Adrenergic receptors

* all but ATP are monitored pharmacologically

Front 14

What are the triggers for muscle excitation in skeletal muscle vs. cardiac muscle?

Back 14

- In skeletal muscle release of Ca++ from SR is directly voltage dependent
- In cardiac muscle release of Ca++ from SR is Ca++ activated (calcium-dependent calcium release)

Front 15

Skeletal
Excitation-contraction coupling
(walk through the steps)

Back 15

1. AP moves down the t-tubule
2. AP detected by voltage-sensitive DHP receptors in t-tubule membrane
3. Conformational change in DHP receptor is communicated to SR membrane and causes opening of ryanodine receptors, which allow Ca ++ out of SR
4. Activates contraction
5. Thus, VOLTAGE directly triggers Ca++ release from SR in skeletal muscle
6. Ca++ release is proportional to membrane voltage

** with age, skeletal muscles become more dependent of extracellular calcium

Front 16

Cardiac
Excitation-contraction coupling
(walk through the steps)

Back 16

1. AP moves down t-tubule
2. AP detected by DHP receptors that contain a Ca ++ channel and open to allow small amount of extracellular (trigger) Ca ++ into the fiber
3. Ca ++ binds to ryanodine receptors in SR membrane; open to release a large amount of (activator) Ca++ (CACR)
4. Thus, CALCIUM, not voltage, is direct trigger of Ca++ release from SR in cardiac muscle
5. Ca++ release is proportional to Ca++ entry during plateau phase of cardiac AP

* these is also a parallel system where dihydropyridine receptors can activate cardiac ryanodine receptors

Front 17

What is the aplitude of AP in nerve and muscle?

Back 17

about 100 mV

Front 18

What is the duration of cardiac muscle AP?

Back 18

- about 300 ms ( this is 2 orders of magnitude longer thatn with nerve and muscle)
- the longer duration is because the plateau phase with calcium influx follows depolarization, followed by repolarization via outflow of potassium ions

Front 19

Compared to skeletal muscle, cardiac muscle:

Back 19

- Contains more and larger mitochondria
- Contains more glycogen granules
- Contains larger and more numerous T tubules (in ventricular muscle)
- Contains multicellular “fibers” that are electrically and mechanically coupled (these are much longer than in skeletal muscle)

Front 20

intercalated disks function...

Back 20

- mechanically connect muscle fibers (linear, branched connections)
- electrically connect muscle fibers by gap junction in lateral component (allowing propagation of action potential... except not between atria and ventricle)
- these disks cross the muscle cells transversely

Front 21

Fascia adherens

Back 21

(a.k.a. adhering junctions)
- Major constituent transverse component
- Holds adjacent cells at ends to form “fibers”
- Narrow intercellular space filled with electron-dense material – extracellular components of transmembrane proteins (as in zonula adherens of epithelia)
- Thin filaments of the terminal sarcomere anchor into fascia adherens

Front 22

Maculae adherens

Back 22

(a.k.a. desmosomes)
- Help prevent cells from pulling apart under tension
- Found in both transverse and lateral components

Front 23

Gap junctions

Back 23

(a.k.a. communicating junctions)
- Major element of lateral component
- Provide ionic continuity among adjacent cardiac muscle cells, so information molecules can pass cell to cell
- Permit cardiac muscle cells to behave as syncytium but with cellular integrity and individuality

Front 24

Characteristics of cells in SA Node

Back 24

- are smaller than other cardiac muscle cells and have fewer and more poorly organized myofilaments; lack intercalated disks but have some intercellular junctions
- exhibit slow depolarization in the late stage of each action potential, which causes them to spontaneously reach the membrane potential at which a new action potential is generated

Front 25

Do all the SA nodal cells depolarize at the same rate?

Back 25

Not all nodal cells depolarize at same rate; ones that reach threshold first (pacemaker cells) rapidly bring the others to threshold
- Isolated nodal cells (when ex vivo) depolarize 80-100 times per minute but factors that alter the resting potential or rate of depolarization affect the heart rate

Front 26

What is the rate of AP nodal tissue excitation spread throught the atria?

Back 26

0.3 m/s

Front 27

Characteristics of cells of AV node

Back 27

- located right atrium, near lower part interatrial septum
- Cells are smaller, fewer and poorly organized myofilaments, no intercalated disks
- exhibit a slow depolarization in late stage each AP but depolarization in AV node slower than in SA node, so AV node normally triggered by the impulse coming from SA node, not intrinsically

Front 28

What happens if the SA node is damaged?

Back 28

If SA node damaged, AV node takes over as pacemaker (albeit less effectively)

Front 29

AV node effect on conductive impulse

Back 29

- AV node normally slows the conduction of the impulse as it travels from the atria to the ventricles, causes approximately 0.1 second delay between contraction of upper and lower chambers.
- This permits the atria to complete contraction and empty blood into the ventricles before the ventricles contract

Front 30

Effects of the Parasympathetic fibers (and NT)

Back 30

ACh
- leads to decreased heart rate (bradychardia, by slowing the rate of depolarization of nodal cells),
- reduces force of contraction through stimulation of muscarinic receptors on nodal cells and myocytes,
- and constricts coronary arteries

Front 31

Effects of the Sympathetic fibers (and NT)

Back 31

NE
- leads to increased heart rate (tachycardia, by increasing the rate of depolarization)
- and increased force of contraction via activation of beta receptors on nodal cells and cardiac myocytes;
- also produces dilation of coronary arteries by inhibiting their constriction

Front 32

What is the critical contractile element within muscle cells?

Back 32

myofilaments

Front 33

Describe Purkinje Cells

Back 33

- Large size
- Abundant glycogen
- Absence of T tubules
- Frequent gap junctions
- Insulation from surrounding myocardium by sheath of connective tissue

- Stain is paler b/c contain less muscle

Front 34

What is the conduction speed of Purkinje Cells

Back 34

- 0.3-0.5 m/s

Front 35

What is the duration of the action impulse in cardiac muscle?

Back 35

The duration of the action impulse is much shorter near the epicardium (the outer side of the cardiac muscle) than at the endocardium (the inner side of the cardiac muscle), the termination of activity appears as if it were propagating from epicardium toward the endocardium

Front 36

Which sympathetic fibers innervate the SA and AV node?

Back 36

Sympathetic fibers from levels T1 to T6 innervate the SA and AV node, extend into the myocardium, and also through the epicardium to coronary arteries

Front 37

What things increase intracellular calcium in myocytes?

Back 37

Calcium, thyroid hormones, caffeine and cardiac glycosides (digoxin)

Front 38

What are the effects of adrenergic receptor antagonists and calcium channel blockers?

Back 38

they decrease rate and force of heart contraction