Cardiac Muscle Structure & Function Flashcards Preview

CVPR: CV Unit I > Cardiac Muscle Structure & Function > Flashcards

Flashcards in Cardiac Muscle Structure & Function Deck (15):

Composition of contractile protein

-myosin: 2 heavy chains, 4 light chains
-actin: similar to skeletal muscle actin; binds tropomyosin and troponin
-thin filament regulatory proteins:
i. TN-C: one Ca2+ binding site
ii. TH-I: N-terminal regulated by phosporylation (PK sites)
iii. TN-T: Isoforms are developmentally & pathologically regulated
iv. TM: only alpha isoform


Cardiac muscle structure

-interconnected mono-nucleated cells w/in collagen
-cells w/large number of myofibrils
-majority of cell volume=mitochondria
-cells coupled both electrically and mechanically


Regulation of calcium flow w/in muscle cells

1. depolarization --> L-type channels open --> calcium influx
2. calcium influx --> calcium release from SR via ryanodine receptors (CICR)
3. calcium binding to TN-C triggers contraction
4. calcium removed by SR Ca2+-ATPase


Cross-bridge cycle of cardiac muscle contraction

-@ rest: low intracell Ca2+ --> TN-TM complex inhibits actin-myosin combination
-increase myoplasmic Ca2+: TN releases inhibition, moves TM out of actin groove, myosin binds --> myosin head undergoes power stroke --> myofilaments shorten


Cardiac output=

Stroke volume x heart rate


Regulators of stroke volume



Molecular mechanism of length-tension relationship



Pre-load effects on stroke volume

-based on length-tension relationship -->
-stimulating contraction at low lengths (i.e. when heart chamber is empty) generates less tension when stimulated at increased muscle lengths (i.e. when heart chambers are full)


Afterload effects on stroke volume

-related to aortic (systemic) pressure
-pressure ventricles need to generate to eject blood from chamber
-inverse relationship between shortening velocity and afterload


Contractility definition/effects on stroke volume

-force w/which heart contracts
-regulated by norepinerphine
-"ionotropes" (positive or negative) change contractility


Frank-Starling Law

-stroke volume of heart increases in response to an increase in the volume of blood filling the heart (=end diastolic volume)
-i.e. increase in pre-load = increase in stroke volume


Factors that may contribute to Starlings Law

1. Cardiac titin isoform is very stiff
2. Ca2+-sensitivity of myofilaments increases as sarcomeres are stretched
3. closer lattice spacing: stretched sarcomeres have altered spacing between actin and myosin


Hypertrophy impact on cardiac muscle

1. cell growth:
i. concentric
ii. upregulation of fetal gene program
2. changes in contractility (mainly calcium sensitivity)


Dilation impact on cardiac muscle

1. cell growth:
i. eccentric
ii. upregulation of fetal gene program
2. changes in contractility: changes in force output (maximal)


Mechanism of changes in contractility

1. translational changes:
i. sarcomeric proteins (upregulation of fetal proteins)
ii. changes in signaling proteins
2. post-translational changes of sarcomeric proteins