Lecture 17, 28 Oct 2003Chapter 12, Circulation (con’t)

Vertebrate PhysiologyECOL 437

University of ArizonaFall 2003

instr: Kevin Boninet.a.: Bret Pasch

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Vertebrate Physiology 437

1. Circulation (CH12)

2. Announcements exams Wed Seminar Assgt.

3. Slide #sSherwood 1997

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2003 Vertebrate PhysiologyEXAM 2, 21 October 2003

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3.50 6 12 18 24 30 36 42 48 54 60 66 72 78 84 90 96

Score out of 100

# of

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dent

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mean 76.8625max 94.25min 47.25s.d. 14.29333n=20

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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.

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.

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Cold, red skin?

Name that student:

Lauren MashaudCricket research

Linda WebbPsychology

Sarju_GovaniDines at DD

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Recall AP and refractory period differences…

(12-7)

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Vander 2001

(see 12-5)

Types of Cardiac Cells:

A. Contractile

B. Conducting~ autorhythmic

~ fast-conducting

SA nodeAV node

InternodalInteratrialBundle of HisPurkinjeEtc.

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Sherwood 1997

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Types of Cardiac Cells:

A. Contractile

B. Conducting- 1 autorhythmic

-1 fast-conducting

SA nodeAV node

Pacemakers:

-Normally HR driven by SA node

-Others are Latent pacemakers

-Called Ectopic pacemaker when node other than SA driving HR

InternodalInteratrialBundle of HisPurkinjeEtc.

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Sherwood 1997

~ SA node ~ latent rate

Sherwood 1997

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Sherwood 1997

SA

AV

other

The

Hear

t Rat

e Tr

ain

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oops

9-11, Sherwood 1997

Autorhythmic Cardiac Muscle (e.g. SA node)

~Transient Ca2+

channels

K+, Na+

Which way would you

alter channel

permeabilities to speed or slow HR??

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Sherwood 1997

Vander 2001Contractile Cardiac MuscleCa2+ current maintains plateau

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(12-8)

(Q,R,S masks atrial repolarization)

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(12-8)

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14-25, Vander 2001 (See 12-12)

Wiggers Diagram

Valves open/close where pressure curves cross

760 mmHg = 1 atm = 9.8 m blood

1:2

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Sherwood 1997

Atrial Kick

Heart filled ~same with increased HR

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Sherwood 1997

Vander 2001

Frank-Starling Curve (p. 483)

Systole = Ventricular EmptyingDiastole = Ventricular Filling (rest)

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(12-13)

Heart Work Loops

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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

- Heart can utilize different types of energy sources (unlike brain)

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MABP = CO x TPRMABP = DP + 1/3(SP-DP)

HR controlParasympathetic vs. Sympathetic

(12-5)

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(12-6)

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Cardiac Output Control

Sympathetic speeds heart rateand increases contractility

1. Norepinephrine binds to beta1 adrenergic receptors2. Increases cAMP levels and phosphorylation3. 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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Vander 2001

How increase contractility?

More Ca2+

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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

Vander 2001

14-11, Vander 2001

Flow depends primarily on pressure gradient and resistance

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Hemodynamics- Poiseuille’s Law:

Flow rate

8L

Q = (P1 – P2)r4

Pressure Gradient

radius4

length

viscosity

Use to approximate flow

Small change in radius large change in flow rate

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Hemodynamics- From Poiseuille’s Law:

Resistance

Q R = (P1 – P2)

Pressure Gradient

radius4Flow rate

viscosity

Small change in radius large change resistance

= 8L

r4

length

Modifiable if vessel distensible under pressure

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End

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