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CHAPTER 15
CARDIOVASCULAR SYSTEM
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7,000L/day
Beats 2.5 billion times/ lifetime
Cardiovascular system
HEART
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SIZE: 14cm X 9cm
HEART LOCATION
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HEART LOCATION
en.wikipedia.org
PULMONARY CIRCUIT
invest-trial.org
SYSTEMIC CIRCUIT
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PERICARDIUM
en.wikipedia.org
PERICARDIUM
www.cayuga-cc.edu
PERICARDIUM
www.cayuga-cc.edu
PERICARDIUM
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FIBROUS PERICARDIUM
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PARIETAL PERICARDIUM
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INNER LINING OF FIBROUS PERICARDIUM
VISCERAL PERICARDIUM
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OUTER; TOUGH; DENSE CONNECTIVE
TISSUE; FOR PROTECTION;
COVERS THE HEART
PARICARDIAL CAVITY
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FILLED WITH FLUID?
PERICARDIUM
www.cayuga-cc.edu
HEART WALL
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EPICARDIUM
 THE VISCERAL PERICARDIUM
 PROTECTS HEART (REDUCES FRICTION)
 CONNECTIVE TISSUE COVERED BY EPITHELIAL TISSUE;
CAPILLARIES AND NERVES; MAY HAVE FAT
MYOCARDIUM
 MIDDLE LAYER
 CARDIAC MUSCLE; MUSLCE FIBERS SEPARATED BY
CONNECTIVE TISSUE; HAS BLOOD VESSELS; LYMPH VESSELS
AND NERVES
ENDOCARDIUM
 CONNECTIVE TISSUE COVERED BY EPITHELIAL TISSUE; ;
BLOOD VESSELS; PERKINJIE FIBERS;
 LINES HEART CHAMBERS AND STRUCTURES
PERICARDIUM
en.wikipedia.org
HEART
en.wikipedia.org
MYOCARDIUM
radiology.uchc.edu
INTERNAL HEART
CHAMBERS
en.wikipedia.org
PARTS
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ATRIA HAVE AURICLES
ATRIOVENTRICULAR ORIFICE HAS A-V VALVE
ATRIOVENTRICULAR SULCHUS
INTERVENTRICULAR SULCHUS
TRICUSPID VALVE
 RIGHT SIDE
BICUSPID VALVE/MITRAL VALVE
 LEFT SIDE
CHORDAE TENDONAE
PAPILLARY MUSCLES
SEMI LUNAR VALVES
www.pbs.org
SKELETON OF HEART
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DENSE CONECTIVE TISSUE RINGS
FROM AORTA AND PULMONARY
TRUNK THROUGH HEART
DENSE CONNECTIVE TISSUE IN
SEPTUM
VALVE ATTACHMENTS; MUSCLE
ATTACHMENTS; KEEP ORIFICES FROM
EXPANDING
BLOOD FLOW
www.pbs.org
BLOOD SUPPLY TO HEART
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CORONARY ARTERIES OFF AORTA
BRANCHES TRAVEL ALONG
ATRIOVENTRICULAR SULCHUS,
POSTERIOR INTERVENTRICULAR
SULCHUS AND ANTERIOR
INTERVENTRICULAR SULCHUS
MANY CAPLILLARIES TO MYOCARDIUM
ANASTOMOSES BETWEEN SMALL
ARTERIOLS PROVIDE ALTERNATE
BLOOD FLOW ?
HEART ACTIONS
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ATRIA CONTRACT = ATRIAL SYSTOLE
AS VENTRICLES RELAX =
VENTRICULAR DIASTOLE
THEN: VENTRICLES CONTRACT =
VENTRICULAR SYSTOLE AND ATRIA
RELAX = ATRIAL DIASTOLE
= CARDIAC CYCLE
HEART SOUNDS
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LUBB= AV VALVES CLOSING
DUBB= SEMILUNAR VALVES CLOSING
HEART MURMUR
CARDIAC MUSCLE
www.siumed.edu
CARDIAC MUSCLE FIBERS
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INTERCALATED
DISC/3D/INTERWOVEN
FUNCTIONAL SYNCYTIUM
ATRIAL SYNCYTIUM
 VENTRICULAR SYNCYTIUM
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HEART CONTRACTION
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SPECIALIZED MYOFIBRILS FOR SENDING CARDIAC
IMPULSES
SA NODE: PACEMAKER
 BENEATH EPICARDIUM OF RT ATRIUM NEAR
SUPERIOR VENA CAVA
 REACH THRESHOLD SPONTANEOUSLY AND BY
SELF
 INCREASED PERMEABILITY TO SODIUM AND
CALCIUM AND DECREASED PERMEABILITY TO
POTASSIUM
 RHYTHMIC: 80 IMPULSES/MINUTE;
PARASYMPATHETIC INHIBITS CONTRACTIONS TO
~70/MINUTE
SA NODE
/hyperphysics.phy-astr.gsu.edu
INTERNODAL ATRIAL MUSCLE FIBERS
CONDUCT IMPULSES TO DISTANT
REGIONS OF ATRIA
 GAP JUNCTIONS ALLOW IMPULSE TO
SPREAD THROUGH MYOCARDIUM
 BOTH ATRIA CONTRACT
 ATRIA AND VENTRICLES SEPARATED
BY FIBROUS SKELETON OF HEART
 ONLY CONDUCTION TO VENTRICLES
IS THROUGH JUNCTIONAL FIBERS
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JUNCTIONAL FIBERS TO AV NODE
 INFERIOR PART OF SEPTUM UNDER
ENDOCARDIUM
 ONLY CONNECTION BETWEEN ATRIA
AND VENTRICLES
JUNCTIONAL FIBERS HAVE SMALL
DIAMETERS: SPEED? IMPORTANCE?
IMPULSE TO AV BUNDLE/BUNDLE OF HIS
 LARGE FIBERS
BUNDLE ENTERS INTERVENTRICULAR
SEPTUM; BRANCHES TO BOTH SIDES TO
LARGE PURKINJE FIBERS
BUNDLE OF HIS
radiology.uchc.edu
HEART ELECTRICAL
PHENOMENA
/hyperphysics.phy-astr.gsu.edu
PERKINJIE FIBERS
www.siumed.edu
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PURKINJE FIBERS CARRY IMPULSE
THROUGH VENTRICLES FASTER THAN
CELL TO CELL CONDUCTION: WHY
NOT IN ATRIA?
MUSCLES ARANGED IN WHORLS SO
CONTRACT IN TWISTING MOTION
FIBERS GO TO APEX FIRST SO APEX
CONTRACTS FIRST MOVING BLOOD UP
WHERE ARE THE PULMONARY ARTERY
AND AORTIC OPENINGS? WHY?
ELECTROCARDIOGRAM
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ELECTRICAL CHANGES IN MUSCLE
P WAVE: SA NODE TRIGGERS IMPULSE FOR
ATRIAL CONTRACTION
QRS WAVES: DEPOLARIZATION OF
VENTRICLES BEFORE CONTRACTION;
THICKER SO MORE CHANGE
T WAVE: VENTRICLE REPOLARIZATION
INDICATES PROBLEMS WITH HEART
PQ INTERVAL: SA NODE THROUGH AV NODE
HEART CONTRACTION
hyperphysics.phy-astr.gsu.edu
REGULATION OF CARDIAC
CYCLE
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CONTROLLED BY PARASYMPATHETIC AND
SYMPATHETIC NS EFFECTS?
PARASYMPATHETIC SEND VIA VAGUS NERVES
CONTINUALLY WHICH RELEASE ACETYLCHOLINE
TO SA AND AV NODE TO BRAKE HEART ACTION
SYMPATHETIC SEND VIA VAGUS NERVES
OCCAISIONALLY TO SA AND AV NODE RELEASE
EPINEPHRINE TO INCREASE CONTRACTIONS
CONTROL BY BOTH ORIGINATES IN MEDULLA
OBLONGATA
 HAS CARDIOINHIBITOR AND
CARDIOACCELERATOR REFLEX CENTERS
 RECEIVE INFO FROM CARDIOVASCULAR SYSTEM
BLOOD PRESSURE EFFECT
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BARORECEPTORS OF AORTA AND CAROTID
ARTERIES DETECT BLOOD PRESSURE
CHANGES
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HIGHER PRESSURE STIMULATES IMPULSE TO
CARDIOINHIBITOR REFLEX CENTER AND
PARASYMPATHETIC NS DECREASES HEART RATE
STRETCH RECEPTORS OF VENA CAVA
DETECT HIGH PRESSURE
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SEND IMPULSE TO CARDIOACCELERATOR
REFLEX CENTER AND SYMPATHETIC NS
STIMULATES HEART
OTHER CONTROLS
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CEREBRUM AND HYPOTHALAMUS CAN
INCREASE OR DECREASE IT
TEMPERATURE:
HIGHER INCREASES IT
 LOWER DECREASES IT
 SURGERY?
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IONS
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MOST IMPORTANT: K+ Ca++
K:
 HIGH: DECREASES RATE & FORCE, MAY BLOCK
CONDUCTION (CARDIAC ARREST)
 LOW: ARRHYTHMIA
Ca:
HOW DOES SA DIFFER FROM SKELETAL MUSCLE?
 SO WHERE DOES Ca COME FROM?
 HIGH: INCREASES CONTRACTION; TETANIC
 LOW: SLOWS HEART CONTRACTION
BLOOD VESSELS
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TYPES:
ARTERIES; ARTERIOLES; CAPPILLARIES;
VENULES; VEINS
 DIRECTIONS?
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FUNCTION?
ARTERIAL & VENOUS
PATHWAYS
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ARTERY & VEIN ANATOMY
www.accessexcellence.org
ARTERY
www.cayuga-cc.edu
ENDOTHELIUM
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SMOOTH SURFACE ?
ALSO RELEASE ?
RELEASE CHEMICALS TO DILATE OR
CONSTRICT BLOOD FLOW
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NITRIC OXIDE
TUNICA MEDIA
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ELASTIC CONNECTIVE TISSUE ?
TUNICA
ADVENTIA/EXTERNA
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ATTACHES TO TISSUE
VASO VASORUM ?
REGULATION OF DIAMETER
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SYMPATHETIC NS  VASOMOTOR
FIBERS  STIMULATE SMOOTH MUSCLE
TO CONTRACT: VASOCONSTRICTION
INHIBITED: VASODILATION
BLOOD FLOW
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ARTERIES  ARTERIOLES 
METARTERIOLES  CAPILLARIES
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ARTERIOVENOUS SHUNTS
ARTERIOLE
www.siumed.edu
CAPILLARIES
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STRUCTURE ?
FUNCTION ?
PERMEABILITY: SLITS WHERE CELLS
OVERLAP/THROUGH CELLS
SIZE VARIES ?
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http://www.youtube.com/watch?feature=player
_detailpage&v=Q530H1WxtOw
CAPILLARY BED
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www.cayuga-cc.edu
CAPILLARY TYPES
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CONTINUOUS: UNINTERRUPTED
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HAVE INTERCELLULAR CLEFTS BETWEEN
TIGHT JUNCTIONS
FENESTRATED
SMALL PORES IN ENDOTHELIUM
 SINUSOIDAL: LARGER PORES
 DISCONTINUOUS SINUSOIDAL: SINUSOID,
NO TIGHT JUNCTIONS
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CONTINUOUS CAPILLARY
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FENESTRATED CAPILLARY
www.cayuga-cc.edu
SINUSOID CAPILLARY
www.cayuga-cc.edu
DISCONTINUOUS SINUSOIDAL
CAPILLARIES
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BLOOD BRAIN BARRIER
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HOW? WHY?
BLOOD BRAIN BARRIER
users.ahsc.arizona.edu
BLOOD BRAIN BARRIER
www.angiochem.com
web.sfn.org/content
PRECAPILLARY SPHINCTER
www.lib.mcg.edu
CAPILLARY EXCHANGE
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DIFFUSION; LIPID SOLUBLE/INSOLUBLE
FILTRATION
 HYDROSTATIC PRESSURE DUE TO CONTRACTION
OF VENTRICLES CLOSER TO ARTERIOLE END OF
BED: FILTRATION
OSMOTIC PRESSURE:
 DUE TO IMPERMEANT SOLUTE ONE SID EOF CELL
MEMBRANE: PLASMA PROTIENS: PLASMA
COLLOID OSMOTIC PRESSURE: REABSORPTION;
CLOSER TO VENOUS END
USUALLY MORE FLUID LEAVES THAN RETURNS
(NEXT CHAPTER)
WHEN WOULD MORE EXIT ?
CAPILLARY TRANSPORT
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CPPILARY TRANSPORT
Figure 3 Transport mechanisms at the BBB.
1 = paracellular diffusion (sucrose),
2 = transcellular diffusion (ethanol),
3 = ion channel (K+ gated),
4 = ion-symport channel (Na+/K+/Clcotransporter),
5 = ion-antiport channel (Na+/H+ exchange),
6 = facilitated diffusion (Glucose via GLUT-1),
7 = active efflux pump (P-glycoprotein),
8 = active-antiport transport (Na+/K+ ATPase),
9 = receptor mediated endocytosis (transferrin &
insulin)
VEIN
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ARTERY vs. VEIN
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ARTERY vs. VEIN
www.siumed.edu
VEINS
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VALVES ?
BLOOD RESERVOIRS: (25%)
ARTERIAL BLOOD
PRESSURE
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SYSTOLIC PRESSURE:
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DIASTOLIC PRESSURE
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VENTRICLES CONTRACT
ATRIA CONTRACT
ARTERIAL WALLS RECOIL AFTER
BLOOD ENTERS: PULSE
FACTORS AFFECTING
BLOOD PRESSURE
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STROKE VOLUME
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70 ml
CARDIAC OUTPUT= STROKE VOLUME
X HEART RATE
IF STROKE VOLUME OR HEART RATE
INCREASE
BLOOD VOLUME: ~5L; 8% BODY WT
PERIPHERAL RESISTANCE: BLOOD VS.
WALLS: ARTERIAL RECOIL LESSENS
PRESSURE/PULSE
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VICOSITY: RESISTENCE TO FLOW OF
BLOOD MOLECULES
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INCREASED VISCOSITY ?
CONTROL OF BLOOD
PRESSURE
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DETERMINED BY CARDIAC OUTPUT x
PERIPHERAL RESISTANCE
LIMITED BY HOW MUCH RETURNS TO THE
VENTRICLES
USUALLY ONLY 60% IS PUMPED OUT OF
VENTRICLE SO SYMPATHETIC STIMULATION
CAN INCREASE
MYOCARDIAL FIBERS STRETCH WHEN
BLOOD ENTERS VENTRICLES MORE THEY
STRETCH, HARDER THEY CONTRACT:
FRANK-STARLING LAW OF THE HEART
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PRELOAD: BLOOD ENTERING
VENTRICLES AND STRETCHING FIBERS
AFTERLOAD: FORCE NEEDED TO OPEN
SEMILUNAR VALVES FOR EJECTION
HYPERTENSION INCREASES
AFTERLOAD
CARDIOINHIBITOR AND
CARDIOACCELERATOR
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THINGS THAT INCREASE HEART RATE:
EPINEPHRINE;EMOTIONS: FEAR, ANGER;
EXERCISE; BODY TEMPERATURE RISE
ARTERIOLE CONSTRICTION
 VASOMOTOR CENTER OF MEDULLA:
CONTROLS VASODILATION OR
CONSTRICTION BY SYMPATHETIC SYSTEM
 BARORECEPTORS OF AORTA SEND TO
VASOMOTOR CENTER; ALSO PICKS UP
PRESSURE LOSS: RELEASES EPINEPHRINE
 IMPORTANT CONTROL OF ARTERIOLES TO
ABDOMINAL VISCERA: COULD CONTAIN
MOST OF THE BLOOD OF BODY
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CHEMICALS OF CONTROL
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INCREASING CO2; DECREASING O2;
LOWERING pH; RELAXES SMOOTH
MUSCLE  INCREASED BLOOD FLOW
VASODILATORS: NITRIC OXIDE FROM
ENDOTHELIAL CELLS AND
BRANDYKININ FROM BLOOD
VASOCONSTRICTION: ANGIOTENSIN
AND ENDOTHELIN FROM
ENDOTHELIUM
VENOUS BLOOD FLOW
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BLOOD PRESSURE IS LOWER
BLOOD FLOW: BLOOD PRESSURE;
SKELETAL MUSCLE CONSTRICTION;
RESPIRATORY MOVEMENTS;
VASOCONSTRICTION
VASOCONSTRICTION: LOW PRESSURE
SYMPATHETIC REFLEXES STIMULATE
SMOOTH MUSCLE CONTRACTION
CENTRAL VENOUS
PRESSURE
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PRESSURE IN RIGHT ATRIUM ?
HIGH: INCREASES AND MORE
PRESSURE IN VEINS
HIGH BLOOD VOLUME OR
VASOCONTRICTION INCREASES CVP
HIGH CVP= EDEMA
PULMONARY CIRCUIT
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RIGHT VENTRICLE CONTRACTS WITH
LESS POWER SO LESS ARTERIAL
PRESSURE HELPS WITH DIFFUSION OF
O2 AND CO2
LIFE SPAN CHANGES
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PLAQUE (FAT) BUILD UP ON ATERIES ?
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CARDIAC OUTPUT STAYS THE SAME
FOR MOST
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INCREASES WITH AGE
DECREASES WITH THOSE HEART DISEASE
CARDIAC MUSCLE DECLINES, DON’T
DIVIDE: REPLACED BY FIBROUS
CONNECTIVE TISSUE AND ADIPOSE
TISSUE
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LEFT VENTRICLE 25% THICKER AT 80
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SLOWS A LITTLE
 8 ML LESS/YEAR
VALVES THICKEN, BECOME MORE RIGID,
MAY CALCIFY
SA AND AV NODE AND BUNDLE OF HIS
BECOME MORE ELASTIC
SYSTOLIC BLOOD PRESSURE INCREASES:
DECREASING SIZE AND ELASTICITY OF
ARTERIES
ARTERIES: TUNICA INTERNA THICKENS;
MORE MUSCLE, MORE COLLAGEN, CALCIUM
AND FAT: MORE RIGID
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ARTERIOLES HALF THEIR ELASTICITY
AT 70; DON’T RESPOND WELL TO
CHANGES IN TEMPERATURE
VEINS: MORE CAOLLAGEN, MAY
CALCIFY BUT NOT AS MUCH, USUALLY
NOT AFFECTED OR OTHER VEINS
TAKE OVER
ENDOTHELIUM: LESS SMOOTH
LESS CAPILLARIES
EXERCISE HELPS SLOW MANY OF
THESE CHANGES