Lab 7

intercalated discs

allow electricity to travel through heart

point of innervation of heart

allows heart to quickly adapt to body's needs more efficient

cholinergic receptor antagonist

atropine - parasympathetic antagonist INCREASES HR

QRS complex

depolarization of ventricle immediately precedes ventricular contraction

percent change calculation

end-start / start post-pre / pre

active tension should ___ as passive tension is applied

increase (to an extent) when stops increasing, ventricle is at maximum/optimal length

cardiac glycosides

increase contraction of heart

Starling's law

increased diastolic stretch of the ventricle increases the force of ventricular contraction increased diastolic filling increases SV of vent

adrenergic receptor agonist

isoproterenol - sympathetic agonist INCREASES HR

autonomic innervation of the heart

medulla oblongata receives sensory input from baroreceptors and chemoreceptors and either activate sympathetic or parasympathetic divisions of ANS sympathetic: thoracolumbar pre-gang: cholinergic sympathetic: nicotinic ACh receptor post-ganglionic: adrenergic parasympathetic: craniosacral division pre-gang: cholinergic paraympathetic: nicotinic ACh receptor post-ganglionic: cholinergic

adrenergic receptor antagonist

propanolol - sympathetic antagonist B1 blocker DECREASES HR

passive tension

tension applied to load when a muscle is stretched but not stimulated force applied

Why is tetanic contraction of the cardiac muscle impossible? Why is this advantageous?

the absolute refractory period of the AP is longer than the time it takes for the myocardium to contract and relax AP lasts for the entirety of the contraction skeletal muscles have short AP refrac period, why they can summate

sequence of events in excitation-contraction coupling of cardiac muscle

1. AP from conducting sys opens L-type Ca channels 2. Ca flows in through L-type volt channels (5-10%) 3. more Ca released from SR through RyR (90-95%) 4. Ca generates spark 5. Ca sparks summate, create Ca signal 6. Ca binds to troponin, x-brC initiates 7. Ca unbinds from troponin, x-brC 8. Ca-ATPase pump puts back into SR 9. Ca pumped out by Na/Ca antiporter 10. Na pumped out by Na/K ATPase

chemical reaction rates double from an increase of temp by

10 C

normal resting values

135 mL stretch ESV 70 mL force SV

chronotropic effect of ACh on HR

ACh muscarinic is a negative chronotropic agent - decr HR increases the opening of K channels via G protein causes increased hyperpolarization and longer time between AP

recording of electrical activity of heart

ECG

IHR calculation

IHR (bpm) = 1 beat / (R-R int time (sec)) x 60 sec / 1 min IHR (bpm) = 1 beat/RR sec x 60 sec/1 min IHR = 60 sec/RR int

Where is the signal to start a cardiac cycle initiated in a human heart? Describe the integrated order of electrical and mechanical events in a single cardiac cycle beginning with the SA node and ending with ventricular relaxation?

In the human heart, the signal to start a cardiac cycle is initiated at the sinoatrial (SA) node. The cells of the sinoatrial node are non-contractile cells that generate action potentials that allow the heart to beat and pump blood through the circulatory system. A single cardiac cycle begins with an action potential spontaneously being generated in the SA node, which depolarizes the myocardium of the atria. This depolarization causes the atria to contract and expel blood down into the ventricles, allowed by the opening of the mitral and tricuspid valves. The action potential then travels through the interventricular septum composed of the atrioventricular (AV) node and bundle branches. The action potential continues to propagate through the Purkinje fibers, where it then enters the myocardium of the ventricle. At this time, the atria are repolarizing, and the ventricles are depolarizing from the bottom of the ventricles upward through the myocardium. Depolarization of the ventricles causes ventricular contraction, which expels blood from the ventricles up through the pulmonary valve to the lungs and the aortic valve to circulate blood through the body. After ventricular contraction, the ventricular myocardia begins to repolarize, and the ventricles are relaxed. After ventricular contraction, all cardiac cells are at rest before the next cardiac cycle begins.

Explain the mechanism of action for isoproterenol (sympathetic agonist) on heart rate. Be sure to include the receptor, ion movements and how those ion movements alter the pacemaker potential.

Isoproterenol is a sympathetic agonist that causes epinephrine release, which activates adrenergic receptors and speeds up heart rate. When isoproterenol is added to the heart, it stimulates sympathetic neurons to release epinephrine, a neurotransmitter. Epinephrine then binds to metabotropic β1 adrenergic receptors on the muscle. This binding causes the activation of cyclic adenosine monophosphate (cAMP) secondary messengers to phosphorylate and open more voltage-gated Na+ and Ca++ channels. The opening of these channels causes an increased influx of Na+ and Ca++, which causes the membrane to depolarize faster. When the rate of depolarization increases, the heart rate goes up because the membrane more easily depolarizes the threshold. The increased ion influx causes a faster depolarization of pacemaker potential, which causes an increase in amount of action potentials being fired and a faster heart rate.

chronotropic effect of NOR on HR

NOR B1 is a positive chronotropic agent - incr HR increases opening of Ca channels cAMP phosphorylates L type channels to increase Ca entry, faster depolarization

starlings law curve represents relationship between

SV and EDV

Explain the mechanism of action for pilocarpine (parasympathetic agonist) on heart rate. Be sure to include the receptor, ion movements and how those ion movements alter the pacemaker potential

Pilocarpine is a parasympathetic agonist that causes acetylcholine (ACh) release, which activates muscarinic ACh receptors to slow down heart rate. When pilocarpine is added to the heart, it stimulates parasympathetic neurons to release acetylcholine, a neurotransmitter. Acetylcholine then binds to metabotropic muscarinic ACh receptors. This binding causes the activation of G-protein secondary messengers to open K+ voltage-gated ion channels to allow more K+ efflux and close voltage-gated Ca++ channels to decrease Ca++ influx. The large K+ efflux and small Ca++ influx causes the membrane potential to hyperpolarize. When the membrane hyperpolarizes, it is harder for the SA node to fire action potentials because it cannot as easily depolarize to threshold to fire action potentials. This increased ion efflux causes a hyperpolarization of pacemaker potential, which causes a decrease in the amount of action potentials being fired and a slower heart rate.

Explain the two subcellular mechanisms that contribute to the length-tension relationship described by Starling's Law? What is the relationship between diastolic stretch and stroke volume described by Starling's Law?

Starling's Law states that an increase in blood volume of the ventricles increases the force of ventricular contraction. In lab, increased blood volume was achieved by stretching the heart to lengthen the ventricles and allow more blood into them. This indicates that the length-tension relationship as described in Starling's Law was present because an increase in diastolic stretch led to more blood in the ventricle and an increase in the stroke volume. One subcellular mechanism that contributes to Starling's Law is that at rest, the myocardium is shorter than optimal length. Since the myocardium is not at optimal length, when blood fills the ventricles, they will be able to stretch more. When blood fills the ventricles, they reach optimal length. At optimal length, many action potentials propagate in through the t-tubules of the myocardium and activate voltage-gated L-type Ca++ channels, which also activates ryanodine (RyR) receptors on the sarcoplasmic reticulum (SR). The activation of RyR receptors allows Ca++ to leave the SR and enter the sarcoplasm. In the sarcoplasm, Ca++ binds to troponin, moving tropomyosin out of the way of actin active sites. This allows cross-bridge cycling to occur because myosin can interact with actin and pull thin filament "inward" to create a contraction. Another subcellular mechanism that contributes to Starling's Law is Ca++ voltage-gated ion channels. As mentioned, voltage-gated L-type Ca++ channels opening allows more Ca++ into the sarcoplasm, which can bind to troponin and allow cross-bridge cycling to occur. Since more Ca++ is available in the sarcoplasm, more cross-bridge cycling occurred, which generated a strong ventricular contraction.

Explain the pacemaker potential of the heart, including ion channels and ion movement(s) that account for the baseline heartrate.

The pacemaker potential of the heart is in the SA node and is caused by unstable membrane potentials that lead to action potential propagation. In cardiac autorhythmic cells, the membrane potential starts around -60 millivolts (mV). The membrane then begins to depolarize and the pacemaker potential becomes more positive. This depolarization is due to the opening of funny channels. These funny channels are open when the membrane potential is -60 mV to -40 mV (threshold), and the channels allow many Na+ ions to pass into the cell and some K+ ions to leave the cell. This large Na+ influx causes depolarization of the membrane towards threshold. Near threshold, funny channels are closing and some voltage-gated Ca++ channels begin to open. When the cells reach threshold, these Ca++ channels remain open to contribute to action potential propagation. The rise from around -60 mV up to threshold at around -40 mV is the pacemaker potential.

why we use frog heart

can beat if kept moist with ringer mammals - anoxia; lack of O2 to tissues

negative chronotropic effect

factors that decrease HR

positive chronotropic effect

factors that increase HR

active tension

force generated by ventricular contraction

Starling's law mechanism

myocardium is not at optimal length blood fills ventricles, they stretch more ventricles reach optimal length at optimal length, many action potentials propagate in through the t-tubules of the myocardium activate voltage-gated L-type Ca++ channel, and ryanodine (RyR) receptors on the sarcoplasmic reticulum (SR) activation of RyR receptors allows Ca++ to leave the SR and enter the sarcoplasm in the sarcoplasm, Ca++ binds to troponin, moving tropomyosin out of the way of actin active sites cross-bridge cycling occurs because myosin can interact with actin and pull thin filament "inward" to create a contraction

parasympathetic activation of the heart

nerve fibers to the heart (vagus) are cholinergic nerves that release ACh bind to MUSCARINIC cholingergic receptors ACh on cardiac function: DECREASES HR

sympathetic activation of the heart

nerves to the heart secrete norepinephrine (a catecholamine) bind to BETA-1 agrenergic receptors NOR on cardiac function: INCREASES HR

ions reponsible for slow depolarization/pacemaker potential? changes in membrane permeability that contribute to depolarization?

pacemaker: funny channels, Na influx depolarization: increased permeability to Ca, Ca influx triggers rapid depolarization

cholinergic receptor agonist

pilocarpine - parasympathetic agonist DECREASES HR

electrical and mechanical activities

signal to start a cardiac cycle is initiated at the sinoatrial (SA) node cells of the sinoatrial node are non-contractile cells that generate action potentials that allow the heart to beat and pump blood through the circulatory system a single cardiac cycle begins with an action potential spontaneously being generated in the SA node, which depolarizes the myocardium of the atria this depolarization causes the atria to contract and expel blood down into the ventricles, allowed by the opening of the mitral and tricuspid valves action potential then travels through the interventricular septum composed of the atrioventricular (AV) node and bundle branches action potential continues to propagate through the Purkinje fibers, where it then enters the myocardium of the ventricle now, atria are repolarizing, and the ventricles are depolarizing from the bottom of the ventricles upward through the myocardium depolarization of the ventricles causes ventricular contraction, which expels blood from the ventricles up through the pulmonary valve to the lungs and the aortic valve to circulate blood through the body after ventricular contraction, the ventricular myocardia begins to repolarize, and the ventricles are relaxed after ventricular contraction, all cardiac cells are at rest before the next cardiac cycle begins.

one function of starlings law is to ensure that CO of the ventricles are equal. why is this important?

so that CO can be synchronized with venous return prevent dysfunction of heart

latent period

time between application of a stimulus and the beginning of a response in a muscle fiber time between R wave and start of VC

interbeat interval (IBI) or R-R interval

time measured from R peak to R peak

recording of mechanical activity of heart

ventricular myogram