Transcript No Slide Title

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Lecture 17, 28 Oct 2003
Chapter 12, Circulation (con’t)
Vertebrate Physiology
ECOL 437
University of Arizona
Fall 2003
instr: Kevin Bonine
t.a.: Bret Pasch
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Vertebrate Physiology 437
1. Circulation
(CH12)
2. Announcements
exams Wed
Seminar Assgt.
Sherwood 1997
3. Slide #s
3
2003 Vertebrate Physiology
EXAM 2, 21 October 2003
3.5
2.5
2
76.8625
94.25
47.25
14.29333
1.5
1
0.5
Score out of 100
96
90
84
78
72
66
60
54
48
42
36
30
24
18
12
6
0
0
# of students
3
mean
max
min
s.d.
n=20
ANATOMY: The integument has a unique circulatory pattern that involves a shunting system through the
reticular layer into the subcutaneous layer. This cutaneous plexus gives off tributaries to supply the adipose tissue
of the subcutaneous layer and the tissues of the integument. As the cutaneous plexus approaches the papillary
layer they terminate in the capillaries of the dermal papillae. These branches supply the hair follicles, sweat
glands, and other structures in the dermis. The unusual thing about these capillaries is that the small arteries and
arterioles that supply them are organized into another interconnecting system call the papillary plexus. The
papillary plexus provides arterial blood to the capillary loops that follow the contours of the dermal papilla at the
epidermal-dermal boundary to feed the structures mentioned above. The venous network returns the blood back
to the body core by following the arterial pattern exactly. Once you have the anatomy under control they the
physiology follows from the structure of the blood flow pattern.
Cold, red skin?
PHYSIOLOGY: When the skin is challenged by cold, the first thing that happens is the smooth muscle
surrounding the small arteries and arterioles going from the cutaneous plexus through the reticular layer to the
papillary plexus constrict to conserve body heat. This action shunts the blood away from the reticular and
papillary layers and keeps it in the deeper subcutaneous layers. Just the opposite happens when a person gets
over-heated, along with sweating, to reduce body heat. In that case the warm blood from the deeper layer is
shunted into, rather than away from, the papillary layer so that the cooling effect of evaporating sweat will be
maximized as the warm blood passes through the cooler dermal capillary loops before going into the venous tree.
Something fascinating happens in the cold response, however. Since tissue will die without having oxygen and
nutrients delivered and waste products removed over time, the shunting mechanism cannot shut down
indefinitely. Depending on how cold the area of skin gets, the smooth muscle will reduce its contraction every so
often. This will occur at 5 to 15 minute intervals, as I said depending on the degree of cold on that particular skin
surface. Some people have inappropriate spasms of the smooth muscle that greatly restrict the flow to the dermis
and then, after a severe cold period that can become painful, the vessels will dilate much more than normal and
cause the skin to be a bright pink or red. This phenomenon is most common in the digits of hands and feet and is
most frequently found in young women. The case is unknown (idiopathic). The person can actually have a
triphasic color change starting with pallor (shutting down of the blood flow), moving to cyanosis (bluish color
due to reduction of oxygen and build up of carbon dioxide), and then reactive hyperemia (redness). This problem
was described by a doctor named Raynaud and is now referred to as Raynaud’s disease.
3b
4
Name that student:
Lauren Mashaud
Cricket research
Linda Webb
Psychology
Sarju_Govani
Dines at DD
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Recall AP and refractory period differences…
(12-7)
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Types of Cardiac Cells:
A. Contractile
B. Conducting
~ autorhythmic
SA node
AV node
~ fast-conducting
Internodal
Interatrial
Bundle of His
Purkinje
Etc.
Vander 2001
(see 12-5)
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Sherwood 1997
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Types of Cardiac Cells:
A. Contractile
Pacemakers:
B. Conducting
- 1 autorhythmic
SA node
AV node
-1 fast-conducting
Internodal
Interatrial
Bundle of His
Purkinje
Etc.
-Normally HR driven
by SA node
-Others are Latent
pacemakers
-Called Ectopic
pacemaker when
node other than SA
driving HR
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Sherwood 1997
~ SA node
~ latent rate
Sherwood 1997
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SA
The Heart Rate Train
AV
other
oops
Sherwood 1997
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9-11, Sherwood 1997
Which way
would you
alter channel
permeabilities
to speed or
slow HR??
~Transient Ca2+
channels
K+, Na+
Autorhythmic Cardiac
Muscle (e.g. SA node)
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Sherwood 1997
Contractile Cardiac Muscle
Ca2+ current maintains plateau
Vander 2001
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(12-8)
(Q,R,S masks atrial repolarization)
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(12-8)
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Wiggers
Diagram
760 mmHg
= 1 atm
= 9.8 m blood
Valves
open/close
where pressure
curves cross
1:2
14-25, Vander 2001
(See 12-12)
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Sherwood 1997
Atrial Kick
Heart filled ~same with
increased HR
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Sherwood 1997
Frank-Starling
Curve (p. 483)
Systole = Ventricular Emptying
Diastole = Ventricular Filling
(rest)
Vander 2001
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Heart Work
Loops
(12-13)
18b
Cardiac Output:
CO = cardiac output (ml/min from 1 ventricle)
SV = stroke volume (ml/beat from 1 ventricle)
= EDV – ESV
(end-diastolic – end-systolic volume)
HR = heart rate (beats/min)
CO = HR x SV
MABP = CO x TPR
MABP = DP + 1/3(SP-DP)
- Heart can utilize different types of energy
sources (unlike brain)
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HR control
Parasympathetic vs. Sympathetic
(12-5)
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(12-6)
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Cardiac Output Control
Sympathetic speeds heart rate
and increases contractility
1. Norepinephrine binds to beta1 adrenergic receptors
2. Increases cAMP levels and phosphorylation
3. Activates cation channels (Na+) and increases HR
4. Epi and Norepi activate alpha and beta1
adrenoreceptors which increase contractility and rate of
signal conduction across heart
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How
increase
contractility?
More Ca2+
Vander 2001
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HR control
Parasympathetic slows heart rate
-Innervate Atria (Vagus nerve = Xth cranial nerve)
-Cholinergic (ACh)
-Alter SA node pacemaker potential by  K+ permeability
 Ca2+ permeability
Parasympathetic innervation of AV node slows
passage of signal between atria and ventricles
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Hemodynamics in Vessels
Flow depends primarily on pressure gradient and resistance
14-11,
Vander 2001
Vander 2001
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Hemodynamics
Use to approximate flow
- Poiseuille’s Law:
Pressure Gradient
radius4
Flow rate
Q = (P1 – P2)r4
8L
length
viscosity
Small change in radius  large change in flow rate
Hemodynamics
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- From Poiseuille’s Law:
Pressure Gradient
length
Resistance
R = (P1 – P2)
Q
Flow rate
viscosity
= 8L
r4
radius4
Small change in radius  large change resistance
Modifiable if vessel distensible under pressure
xx
End