CARDIAC MUSCLE

BRUNO, DAYA, HERNANDEZ, RACOMA, RAMIREZ

INTRODUCTION
THE HEART
- valved, muscular pump that propels
blood around the body
- consists of one or more muscular
chambers connected in series and
guarded by valves which allow blood
to flow in one direction
THE AMPHIBIAN CIRCULATION
- three chambers made up of two atria and
one ventricle
- pulmocutaneous and systemic circulation
CARDIAC MUSCLE
- found only in the heart

- striated muscles that are innervated only by the neurons of the sympathetic
and parasympathetic divisions of the autonomic system

- cardiac muscle cell, or myocyte, contains one nucleus

- myogenic- cells are able to depolarize themselves along with other cells

- connected electrically through the gap junctions, particularly at structures

called intercalated disks, in which an action potential initiated in the
pacemaker region spreads rapidly
PROPERTIES
Autorhythmicity
- initiate heart beat continuously and regularly without external stimulation
Excitability
- respond to a stimulus of adequate strength and duration by generating
propagated action potential
Conductivity
- conduct excitation through the cardiac tissue
Contractility
- contract in response to stimulation
DEFINITION OF TERMS

PACEMAKER ACTION POTENTIAL CARDIAC CYCLE

ELECTROCARDIOGRAM

- initiates electrical
activity in the heart - records the
- a brief change in
- Sinus venosus: in electrical signals in
voltage (membrane
amphibians
potential) across the cell
the heart
- Sinoatrial node: in
membrane of heart cells
other vertebrates
- Small, weakly
contractile, specialized
muscle cells capable of
spontaneous activity
 TO DETERMINE THE
GOAL OF THE MECHANICAL ACTIVITY
PHYSIOLOGICAL PROPERTIES,
,

EXPERIMENT AS WELL AS THE CONTROL OF

THE TOAD HEART
 ● Mechanical activity of heart

GOAL OF THE ● Physiological properties and

control
EXPERIMENT ● Effect of temperature
● Chemical control
● Refractory period
● All-or-none law
MATERIALS AND
METHODOLOGY
 SOLUTIONS PREPARED & TOAD HEART PREPARATION

ENZYME IKI
SUBSTRATE

- Cold Ringers solution - Live toad was double pithed, placed on a dissecting pan
- Warm Ringers solution - Toad was dissected to expose the heart, still contracting
- 0.7% NaCl solution - Heart was lifted at the apex end and pierced with a hook
- 0.9% KCl solution - One end of a thread was tied to the hook, while the other end was
- 1% CaCl2 attached to the heart lever which was connected to the PowerLab
- 1% acetylcholine system.
- adrenaline solution - The heart was placed in an almost vertical with the apex lifted up.
- 0.5% atropine - Ringer’s solution was constantly dropped on the heart in order to
keep it moist.
 GENERAL FLOW OF THE EXPERIMENT
Heart Rate, Heart Cycle, Effect of Temperature
- Normal
STEP 1
2 cardiac activity was measured
- Diastolic flushing and systolic paling was
observed
- Sequence of contractions SV -> A -> V was
observed
- Rate of the atrial and ventricular
contractions were recorded
- Effect of temperature on the heart rate:
touching sinus venosus, atrium, and ventricle
with warm metal rod dipped in warm Ringer’s
solution
- Cold Ringer’s solution was placed
drop-wise on the whole heart and changes
in heart activity was observed
Chemical Control
STEP 3
- 2-3 drops of 1% acetylcholine were applied on the sinus
venosus
- If no change occurred, few more drops of the solution
were added.
- Change in heart rate, amplitude, and contraction duration
was observed. The time it took for the heart to recover
back to its normal beat was also recorded.
- Heart was washed with Ringer’s solution and then a
few drops of adrenaline solution was applied. Any
changes were observed.
- After, 2-3 drops of 1% acetylcholine were applied.
Washed again with Ringer’s solution until a normal
heartbeat was observed.
- 5 drops of 0.5% atropine sulfate was then added Any
changes were observed.
 GENERAL FLOW OF THE EXPERIMENT
Refractory Period
STEP 2
1 STEP 3
- The ventricle was separated
from the rest of the heart
- It was pinned to a
dissecting pan while the
apex side was pierced
using a hook connected to
the lever with a string
- The ventricle was electrically
stimulated
- 6 different points were
observed: early, middle
and late systole, and early,
middle and late diastole.
All or Nothing Law Effect of Inorganic Compounds
- A new toad heart was removed
- Electrical stimulations from the rest of the body and kept
were conducted on the in Ringer’s solution
ventricle - All the blood was washed out
- Starting with 0.1 V, in from the heart using Ringer’s
order to determine its solution.
- The heart was made to suspend in
threshold.
the Ringer’s solution beaker and
- Current of the electrical then the number of heartbeats per
stimulus was increased minute were recorded
by 1 V up until 10 V. - The same procedure was done
- Responses were for the next solutions in the
recorded following order: 0.7% NaCl,
Ringer’s solution, 0.9% KCl,
Ringer’s solution, then 1%
CaCl2.
RESULTS AND
DISCUSSION
NORMAL HEART RATE
NORMAL HEART RATE
WARM TEMP IN ATRIUM AND VENTRICLE
WARM TEMP ON SINUS VENOSUS
COLD TEMP ON WHOLE HEART
EFFECT OF ACETYLCHOLINE
EFFECT OF ADRENALINE
EFFECT OF ATROPINE
PREMATURE CONTRACTION ON LATE, EARLY, MID-DIASTOLE
PREMATURE CONTRACTION ON EARLY, LATE, MID SYSTOLE
EFFECT OF INORGANIC IONS

solution BPM

Ringer’s solution 127

0.7% NaCl 72

Ringer’s Solution 62

0.9% KCl 34

Ringer’s 50

1% CaCl2 31
MYOGENIC CONTROL OF THE
HEART
MYOGENIC CONTROL AND NORMAL CONDITIONS

- caused by pacemakers
- conduction system = SA Node, AV node, Bundle of His and Purkinje fiber network
- SA node = faster than AV and suppresses purkinje network in normal heart action
- BRADYCARDIA - slow
- TACHYCARDIA - fast

CALCIUM CLOCK

- involves membrane depolarization which triggers release of Ca@+

EFFECT OF TEMPERATURE
EFFECT OF TEMPERATURE

- enzymatic reactions are affected with fluctuating temperatures -> causes

protein denaturation
- theoretical involves a more physiological effect
- COLD = increase due to attempt of heart to restore normal body temperature
- HOT = increase as well in order to dissipate heat througout the body
EFFECT OF IONS
EFFECT OF IONS

- dependent on membrane polarization

- NaCl theoretically increases since membrane is depolarized
- KCl decreases since it causes membrane hyperpolarizaion
- CaCl2 increases heart rate due to presence of calcium ions to reveal more
binding sites for cross-bridge formation
NEURONAL CONTROL OF THE
HEART AND EFFECT OF
CHEMICALS ON HEART RATE
NEURONAL CONTROL

- Preganglionic vagal fibers from the skull synapse with the cardiac plexus and
contribute to the sympathetic trunk
- Sympathetic control = facilitatory
- Parasympathetic control = inhibitory
EFFECT OF ACETYLCHOLINE
EFFECT OF ADRENALINE
EFFECT OF ATROPINE
SYMPATHETIC AND PARASYMPATHETIC CONTROL

SYMPATHETIC

- During the fight or flight response, adrenaline from the adrenal cortex increases heart rate
- Adrenaline binds to alpha adrenoreceptors and causes an increase in the release of calcium ions from the
sarcoplasmic reticulum -> INCREASE IN MUSCLE CONTRACTION

PARASYMPATHETIC

- High concentrations of acetylcholine (ACh) inhibit heart rate

- ACh binds to M2 muscarinic receptors inhibiting cardiac cells

EFFECT OF ATROPINE

- Atropine increases heart rate by blocking nicotinic and muscarinic receptors

ALL OR NONE LAW
ALL OR NONE LAW

- states that insufficient stimulus will not allow contraction of the heart
- strength of contraction varies with the number of cross-bridges formed
- Ca2+ dependent
- More calcium ions bind to the troponin-tropomyosin complex revealing binding
sites to increase cross-bridge formation
REFRACTORY PERIOD OF THE
HEART
REFRACTORY PERIOD OF THE HEART

REFRACTORY PERIOD

- allows heart to revert back to relaxed state

- mechanism to restore heart rhythm

EXTRASYSTOLE

- premature contraction of the heart during diastole

- induces a compensatory pause to restore heart rhythm and allow diastolic
pressure to be achieved
PREMATURE CONTRACTION ON LATE, EARLY, MID-DIASTOLE
PREMATURE CONTRACTION ON EARLY, LATE, MID SYSTOLE
STARLING’S LAW OF THE HEART

- Venous return is directly proportional to stroke volume

- Stretching of the ventricle due to increased blood flow from the atrium ->
stronger contraction of the atrium or ventricle to ensure proper ejection of all
blood
- Detection by stretch receptors in the herat
SUMMARY
CONCLUSION