NPB 101L Practical Frog Heart

difference of frog heart from human heart

has 1 ventricle, primary pacemaker is sinus venosus (instead of SA node), have atrioventricular myocardium (instead of AV node), no specialized ventricular conduction system (no Purkinje fibers), no Bundle of His, less developed sarcoplasmic reticulum, no coronary circulation, heart is oxygenated by direct diffusion

Pacemaker cells in humans

SA nodal cells, AV nodal cells, Bundle of His all can, SA node cels set pace (fasted pacemakers)

effective refractory period of ventricular muscle

equivalent to aboslute refractory period in nerves, ventricles cannot be activated → AP cannot occur

relative refractory period of ventricular muscle

an AP can occur but takes longer/greater stimulation

ventricular AP phase 0

rapid depolarization due to influx of Na+, and to lesser extent Ca²⁺

Ventricular AP phase 1

rapid depolarization from inactivation of Na+ channel

Ventricular AP Phase 3

repolarization due to K+ efflux and Ca²⁺ channel inactivation → sets duration of AP

ventricular AP phase 4

resting membrane potential

SA Node action potential Phase 0

depolarization is caused mostly by Ca²⁺ influx

SA Node Action Potential Phase 3

repolarization from K+ efflux

is there a plateau phase for SA node AP

no plateau phase

SA Node AP phase 4

unstable resting potential due to opening of non-specific cation channel

which muscles have channels mechanically linked to RyR

skeletal muscles ; NOT Cardiac muscles

Cardiac muscle contraction

Ca²⁺ is needed for contraction, there are L-type calcium channels on T-tubules, influx of extracellular calcium is necessary for calcium efflux from SR-calcium induced calcium release → increase in intracellular calcium induces contraction in same manner as skeletal muscle

Na⁺ channels

responsible for rapid depolarization phase of APs in excitable cells, allow influx of sodium ions into cell → causing depolarization

absolute refractory period

Na⁺ channels are inactivated and no new AP channels can be triggered, regardless of stimulus strength

Ca²⁺ channels in cardiac muscles

L-type calcium channels open during plateau phase of AP → allows calcium ions to enter cell from extracellular space, contributing to prolonged depolarization phase (plateau) and maintaining AP

K+ phase 1

initial repolarization, potassium channels start to open and allow potassium ions to leave cell → contributing to early part of repolarization

K+ channels phase 2

plateau phase, potassium efflux continues at slower rate due to IKs and IKACh → balancing calcium influx through L-type calcium channels to maintain plateau

K+ channels Phase 3

rapid repolarization, potassium channels open fully → causing significant outflow of potassium ions → rapidly depolarizes cell back to resting mem potential

K+ channel phase 4

resting phase, potassium channels maintain resting potential and prevent unwanted depolarization until next AP

ventricular filling

AV valves open, semilunar valves closed

Isovolumetric contraction

all valves closed, ventricular contraction causes increase in pressure but no change in volume

ventricular ejection

semilunar valves open, ejection of blood causes an increase in pressure and decrease in volume

isovolumetric relaxation

all valves closed, ventricles relax causing decrease in pressure but no change in volume

systole

phases 2 and 3 → contraction and emptyin

diastole

phases 4 and 1 → relaxation and filling

pressure volume loop

shows relationship between left ventricular pressure and volume during cardiac cycle

Frank-starling Law

heart will contract with more force during systole if filled to greater extent during diastole; more filling → increased end diastolic volume → increased SV

extrasystole

premature ventricular contraction; often caused by depolarization in ventricle rather than at SA node

smaller extrasystolic beat causes

reduced filling time (Frank-Starling Law)

larger extra systolic beat causes

increased calcium buildup → similar effect to frequency in Lab 2 except cardiac muscle cannot achieve tetany due to ERP (early repolarization)

compensatory pause

skipped beat that is sometimes caused by extrasystole to resume proper timing of SA node

Vagus nerve

contains parasympathetic efferents to heart using neurotransmitter ACh and receptor mAChR

Vagal stimulation effect

decreases HR (bradychardia); prolonged stimulation → cardiac arrest; slows or halts spontaneous AP generation of SA node

vagal escape

other pacemakers taking over in generations of heart rate at next fastest pace

epinephrine and norepinephrine

ligands of beta-adrenergic receptor in heart and alpha-adrenergic receptor in vasculature

effects of epinephrine

Epi→ causes increase in HR and decrease in cardiac AP duration → increasing strength of contractions → increases SV independent of ventricular filling

SERCA

sarcoplasmic/endoplasmic reticulum calcium ATPase that plays role in regulating calcium levels within cells; uses energy from ATP to actively transport calcium against its concentration gradient from cytoplasm to SR

SERCA function

pump calcium back into sarcoplasmic/endoplasmic reticulum → helps reduce intracellular calcium concentration after muscle contraction → essential for muscle relaxation