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Flashcards in Acute Cardiac Adaptations Deck (26):
1

What ion needs to be properly handled to maintain contractile performance at the myocyte and myofibril level?

• Calcium
• Calcium handling and calcium sensitivity are super important

2

Where is SERCA2 located?

• In the LONGITUTIDINAL SR, not the junctional SR
• This is important because they are not super close to the L-type calcium channel action

3

What factors influence EC50?

• EC50 is the concentration at which cardiac muscle is 50% contracted
• It's a way of monitoring calcium sensitivity
• Temperature
• pH
• Sarcomere length
• Contractile protein phosphorylation
• Caffeine

4

Troponin I is phosphorylated by what two "PK" enzymes?

• PKA and PKC
• PKA sites will increase velocity of contraction
• PKC sites decrease velocity of contraction

5

What does the curve of Active tension vs. initial muscle fiber length look like?

• Active tension would be on the Y axis here and fiber length on x-axis
• Fiber length is the same as preload
• This is the starling curve
• It's a 45 degree line (positive slope) until an exponential drop off
• Increasing length directly increases tension to a certain point

6

Does increasing sarcomere length increase or decrease EC50?

• Decrease. Stretching the sarcomere increases calcium sensitivity
• The molecular mechanism by which stroke volume is increased on the next beat after there is increased preload and thus stretch/tension of the myofibril

7

Norepinephrine will have what effect on muscle contractility?

• It shortens the myofibrils, it enhances contractility
• At shorter muscle lengths are higher muscle tensions (compared to without NE)

8

What does phosphorylation due to beta adrenergic stimulation of SAN Ca channels do?

• Increases heart rate
• Increases cardiac output

9

What does phosphorylation due to beta adrenergic stimulation of ventricular cell Ca channels do?

• Increase calcium entry
• Increase force of contraction
Improves ejection fraction by increased inotropy

10

What does phosphorylation due to beta adrenergic stimulation of sodium pump do?


• NCX, increases calcium efflux
• Enhances relaxation and diastolic filling

11

What does phosphorylation due to beta adrenergic stimulation of troponin I do?

• The inhibitory troponin
• Lowers calcium affinity for TnC
• Increased lusitropy, increased relaxation

12

What does phosphorylation due to beta adrenergic stimulation of FKB do?

• Enhances Ryr receptor mediated calcium release
• Enhances contractility for greater stroke volume

13

What does phosphorylation due to beta adrenergic stimulation of phospholamban do?

• PLB phopsphorylation will disinhibit SR calcium pump SERCA2
• Increases SR calcium load
• Improved diastolic filling (lusitropy)

14

What does the heart do when we go to the gym?

• Decrease peripheral vascular resistance
• Increase venous return
○ Leads to greater cardiac output through frank-starling
• Increase heart rate
• Increase inotropy

15

Isometric excersise (weight training) will have what effect on the CV system?

• It will INCREASE peripheral vascular resitance
○ Idea is to funnel flow to excercising muscle group
• Increases HR, but does not increase CO because total venous return is not increased (but HR is)

16

What happens right after a myocardial infarction?

• Loss of functional myocardium
• Increased catecholamine surge
○ Sweating, tachycardia, hypertension?
• Increased inotropy to maintain CO despite the blood pressure
○ Accomodating afterload
• Heterogenous cellular environment
○ Changes in pH, membrane potential and secondary effect on cytosolic calcium

17

The response to acute changes in hemodynamic and adrenergic stimuli look like what?

• Altered P/V relationships
• Altered inotropy
• Altered chronotropy

18

When the heart adapts by increasing myocyte length way out of proportion with width, extensive fibrosis, myocyte death, and advanced cardiac dysfunction, what do we call that disease?



• Dilated Cardomyopathy
• Can be caused by MI

19

The heart responds in what way to chronic hypertension and/or aoric valve stenosis?

• Pathological hypertrophy
• Myocyte length increases, but the width REALLY increases
• Fibrosis
• Cardiac dysfunction likely

20

An MI can cause DCM. What is that?

• Dilated Cardomyopathy
• When the heart adapts by increasing myocyte length way out of proportion with width, extensive fibrosis, myocyte death, and advanced cardiac dysfunction

21

Is a gross change in heart size and function only a visual change or is there a difference at the cellular level?



• There is certainly a difference at a cellular level
• There can be myosin isoform switches and ATPase expression changes in phenotypically distinct models of cardiac hypertrophy

22

What might an increase in ATPase and alpha-alpha Myosin Heavy Chain be indicative of?

• Physiologic (not pathologic) hypertrophy

23

What might a decrease in ATPase but an incrase in beta-beta Myosin Heavy chain be indicative of?

• Pathological hyperothrophy

24

What is the contemporary view of heart changes in chronic heart problems adaptation?

• Though the heart remains terminally differenctiated, there are dynamic changes that occur at the celular level
• Involves architectural and biochemical modifications
• Stress modifies quantitiy and quality of contractile elements
• Programmatic alterations in gene and protein expression occur in response to pathologic or physiologic triggers

25

What is likely going on in a cell that is part of Left ventricular hypertrophy?

• Increase in PLB to SERCA ratio
• Increase in calcium intracellular
• Incrase in L-type channel activation
• Overall impairment in relaxation and the calcium steady state is changed

26

What are the "chronic" regulatory kinases that are part of the adaptation of heart muscle to chronic problems?

• PKC epsilon
• PKD
• CaMK
• Calcineurin
○ Early are PKA and PKCbeta