cardiac muscle VM and cell biology Flashcards
Cardiac myocyte
Cardiomyocytes normally branch, usually one or 2 nuclei with each cardiomyocytes, cardiomyocyte nuclei are located centrally within the fibers
Intercalated discs between cardiomyocytes in longitudinal section, mainly composed of fascia adherens (in transverse part), and gap junctions (in the lateral part), cell adhesion and electrical coupling
Cross section is variable bc of branching (accumulation of collagen os a scar)
blood vessels
Contain epithelium (endothelium), CT found in all three tunicas (intima, media, adventitia) and muscle spicifically smooth muscle
the tunica intima borders the lumen and consists of endothelium (simple squamous epithelium) and subendothelial CT internal elastic lamina Tunica media-vascular smooth muscle arranged in concentric layers with fenasterated elastic laminae, with sheets of elastic fiber external lamina (in larger arteries) Tunica Adventitia- outermost layer, (
Cardio myocytes vs skeletal muscle
Similarities: basal lamina, striated
Differences: involuntary, smaller, 1-2 central nuclei, branch, vascular, many mitochondria, myoglobine, lipid droplets, MB CK(if theres MBCK in blood think cardiac damage) intercalated discs, CICR
Intercalated discs
IDs are sarcolemmal specialized that mediated CM-CM binding and enable CM to be in syncytium
Transverse: Transmits CM forces (fascia adherens, N cadherins N cadherins/desmosomes
Lateral part: mediates CM cm signaling (Gap junctions and a few desmosomes
last I band modified Z line, gap junctions (fascia adherens and zonula adherens) N cadherin in intercellular space
Excitation-contraction coupling: cardiac
excitation (electrical): AP depolarization–T tubules Phase 2 of AP: L-type Cav 1.2–CA influz– Ca in C r
CICR : Ryr in Sr –> CA
Contraction physical– Ca binds troponin C– tropomyosin moves, TP hydrolysis activates the myosin head, the myosin head binds to actin, power stroke myosin into A band (sarcomere shortens–contraction)
During contraction (a-band stays the same, i band length shortens, relaxation- L type Ca channel inactivates, Phospholamban (PL) is phosphorylated SERCA pumps CA back into the SR
Beta adrenergics
modulates contraction vs relaxation, cAMP increased, protein kinases activated, phosphorylation L type Ca channel T tubule (increase Ca into mocyte–enahced contractile), phosphorylation of phospholamban–Ca into SR, relaxation
innervation of the myocardium
modulates the hearts intrinsic rhythm. Sympathetics (cervical ganglia–> heart and great vessels)–> increase HR (positive chronotropism)
Parasympathetics (vagus)– heart great vessels–> decrease HR (negative chronotropism)
Vagal neurotransmitter (Ach) activates muscarinic AchR in SA nodes. Negative Inotropism (reduced contractile force--IE the muscarinic AChR is a Beta adrenergic antagonist)
Regional histologic differences in the heart
ventricular myocardium
Atria, SA, AV nodes (smaller CMs with fewer striations) atrial myocytes have granules (G) containing atrial natriuretic factor (ANF aka ANP)
bundle of His: Purkinje CMs (specialized for conduction, in the embryonic heart (endothelin–cardiac myocyte–purkinje fiber)
Cardiac fibroblasts -hearts most abundant by number not volume
Chronology of Heart attakc
immediate: myocyte death--MBCK and cTNL then inflammation then would healing via cardiac fibroblasts Angiogenesis (VEGF, FGF) Scar