PowerPoint 演示文稿

download report

Transcript PowerPoint 演示文稿

LIU Chuan Yong
Institute of Physiology
Medical School of SDU
Tel 88381175 (lab)
88382098 (office)
Email: [email protected]
Website: www.physiology.sdu.edu.cn
Section 4
Regulation of the Circulation
 The aim of the circulatory regulation is to
regulate the blood flow of organs to fit their
metabolic requirement in different condition.
 The regulation of blood flow are of three major
 Neural
 Humoral
 Local
Neural control of blood flow
 affects blood flow in large segments
of the systemic circulation,
 shifting blood flow from the nonmuscular vascular bed to the muscles
during exercise
 changing the blood flow in the skin to
control body temperature.
Humoral control
 hormones, ions, or other chemicals
in blood
 cause either local increase or decrease
in tissue flow
 or widespread generalized changes in
Local control of blood flow
 in each individual tissue,
 the flow being controlled mainly
in proportion to that tissue’s need
for blood perfusion
I. Neural Regulation of the
1. Innervation of the Circulatory
 Cardiac innervation
 Innervation of blood vessels
 Sympathetic vasoconstrictor fiber
 Sympathetic vasodilator fiber
 Parasympathetic nerve fiber to
peripheral vessels
Cardiac innervation
 Sympathetic nerve – noradrenergic fiber;
Parasympathetic nerve- cholinergic fiber
 Noradrenergic sympathetic nerve
 to the heart increase the cardiac rate (chronotropic
 the force of cardiac contraction (inotropic effect).
 Cholinergic vagal cardiac fibers decrease the
heart rate.
Cardiac innervation (contin.)
 moderate amount of tonic discharge
in the cardiac sympathetic nerves at
 a good deal of tonic vagal discharge
(vagal tone) in humans
 When the vagi are cut in experiment
animals, the heart rate rises
Innervation of blood vessels
 Sympathetic
vasoconstrictor fiber
 Distribution: Almost all
segments of the
 The innervation is
powerful in the kidneys,
gut, spleen and skin,
 is less potent in both
skeletal and cardiac muscle
and in the brain.
Innervation of blood vessels
Sympathetic vasoconstrictor fiber
Almost all vessels, such as arteries, arterioles,
venules and veins are innervated,
except the capillaries, precapillary sphincters and
most of the metarterioles.
Tone: Usually the sympathetic vasoconstrictor
fibers keep tonic.
Innervation of blood vessels
 2) Sympathetic vasodilator fiber
 The sympathetic nerves to skeletal muscles
carry sympathetic vasodilator fibers as well as
constrictor fibers.
 In animals, such as the cat, dog, these
sympathetic vasodilator fibers release
acetylcholine at their endings and cause
 Importance: increase the blood flow in
skeletal muscle during exercise and stress.
Innervation of blood vessels
 3) Parasympathetic nerve fiber to peripheral
 Parasympathetic nerve fibers innervate vessels
of the blood vessels in
Meninges (脑膜, 髓膜)
the salivary glands,
the liver
the viscera in pelvis
the external genitals.
 Importance: Regulate the blood flow of these
organs in some special situations.
2 Cardiovascular Center
 The control center of cardiovascular activities
is the nucleus groups at different levels for
controlling cardiovascular activities,
 including
spinal cord,
brain stem,
limbic system,
cerebral cortex
Cardiovascular Center
 if the brain of an anesthetized animal is
sectioned at the level of the lower pons,
the blood pressure falls.
 If the section is made at the level of the
obex, the fall in blood pressure is more
Cardiovascular centers of the brainstem
 Medulla
oblongata is
essential to
r centers.
Cardiovascular centers of the
 vasoconstrictor-area
 vasodilator area
 cardioinhibitory area
 relay station of afferent nerve
1.rostral ventrolateral
(Vasoconstrictor area):
2. Caudal ventrolateral
medulla, cVLM
(Vasodilator area)
3. NTS (nucleu of solitary
tract relay station of
afferent nerve)
4. Cardioinhibitory area
1). vasoconstrictor-area (rVLM)
(neurotransmitter: NE neurons)
(l) the cardiac sympathetic center
(2) the sympathetic vasoconstrictor center
2).vasodilator area (cVLM) (NE
to inhibit action of Cl area → vasodilation
3).cardioinhibitory area
(dorsal vagal nucleus and nucleus ambigulus) the cardial
vagus center
4).relay station of afferent nerve
NTS (nucleu of solitary tract) to accept and integrate
afferent impulses and then affect other centers
3. Reflex Regulation of the
 Baroreceptor reflexes
 Reflex involving arterial
 CNS ischemic response
(1) Baroreceptor reflexes
1) Physiological anatomy of the baroreceptors.
Carotid sinus
 At the bifurcation of
the common carotid
 the root of internal
carotid artery shows a
little bulge
 has stretch receptors
in the adventitia
 are sensitive to
arterial pressure
Carotid sinus.
 Afferent nerves from
these stretch receptors
travel in the carotid
sinus nerve
 which is a branch of
the glossopharyngeal
nerve. (IXth cranial
Aortic arch.
baroreceptors are also present in the
adventitia of the arch of aorta
have functional characteristics similar to the
carotid sinus receptors.
their afferent nerve fibers travel in the aortic
which is a branch of the vagus nerve. (Xth
cranial nerve)
2) buffer nerves activity
 The carotid sinus nerves and
vagal fibers from the aortic
arch are commonly called the
buffer nerves
 At normal blood pressure
levels, the fibers of the buffer
nerve discharge at a low rate.
 When the pressure in the sinus
and aortic arch rises, the
discharge rate increases;
 when the pressure falls, the
rate declines.
Sinus Nerve response to Blood Pressure
 The carotid sinus
baroreceptors are not
stimulated by intrasinus
pressure between 0 – 60
mmHg (aortic baroreceptors,
 Between 60 to 80 mmHg, the
carotid sinus baroreceptors
respond progressively more
and more strongly.
 The response is the greatest at
pressure level near the normal
mean arterial pressure (100
 At sinus pressure above 180
mmHg, there is no further
increase in response .
3) Relationship between the isolated carotid
sinus pressure and the blood pressure
 Raising the carotid sinus pressure leads to a
fall in arterial blood pressure.
 Lowering the carotid sinus pressure leads to a rise
in arterial blood pressure
CSP, carotid sinus pressure; FABP, femoral artery blood
 Set point: The point where the carotic sinus
(isolated) pressure and blood pressure are the same.
4) Concept and mechanism of
baroreceptor reflex
Any drop in systemic arterial pressure
decreases the discharge in the buffer nerves,
and there is a compensatory rise in blood
pressure and cardiac output.
Any rise in blood pressure produce dilation
of the arterioles and decreases cardiac
output until the blood pressure returns to
its previous normal level.
Vasoconstrictor Center
Cardio-acceleratory Area
Carotid Sinus
Sinus Nerve
Aortic Arch
Vagus Nerve
Peripheral Vascular Dilation
Heart Rate
Cardio-inhibitory Area +
Peripheral Resistance ( R)
Cardiac Output (Q)
Arterial pressure decrease back
towards normal
(5) Importance of the baroreceptor
 To keep the arterial pressure relatively constant
 Through short term regulation of blood pressure
in the rang of 70 mmHg to 150 mmHg, maintain
the mean blood pressure at about 100 mmHg
 Tonic regulation of blood pressure
 Pressure buffer system – reduce the blood
fluctuation during the daily events, such as
changing of the posture, respiration, excitement,
and so forth.
(6) Baroreceptor Resetting
 Baroreceptor will adapt to the long term change
of blood pressure.
 That is, if the blood pressure is elevated for a long
period of time, several days or years, the set point will
transfer to the elevated mean blood pressure.
 Obviously, the adaptation of the baroreceptor
prevents the baroreceptor reflex from acting as a
long term control system.
 That makes the baroreceptor system unimportant for
long-term regulation of arterial pressure
(2) Reflex involving arterial chemoreceptors
 Chemoreceptors: situated in the carotid body
and aortic body
 They have a very rich blood supply,
 which make them ideal for sampling chemical
changes in the blood.
 Chemoreceptors are sensitive to the decreased Po2,
increased PCO2 and increased hydrogen ion
concentration in the plasma.
 Afferent:
 Afferent nerve fibers form the carotid body
travel in the carotid sinus nerve, which is a
branch of glossopharyngeal nerve.
 Aortic body is innervated by the aortic nerve,
which is a branch of the vagus
 Response: Stimulation of chemoreceptors
leads to a reflex increase in vasomotor tone,
 which causes generalized vasoconstriction
and hence a rise in blood pressure.
 Importance: Chemoreceptor mechanism is
important in regulation of blood pressure
when it fall below the range in which
baroreceptors act (70 mmHg).
(3) CNS ischemic response
 Chemoreceptor reflex is useful in regulation of
blood pressure when it falls to a level between
40 and 70 mmHg.
 But if the blood pressure below 40 mmHg, the
last ray of hope for survival is the central
nervous system (CNS) ischemia response.
 So it sometimes called the “last ditch stand”
pressure control mechanism.
 As the name indicates, it is evoked by ischemia
(poor blood flow) of the central nervous system.
 CNS ischemia reduces blood flow to the vasomotor
centre (VMC).
 Reduction in blood flow to the VMC leads to
reduced Po2 and elevated Pco2 in the medulla
 Both these factors stimulate the VMC directly,
leading to vasoconstriction and consequently rise in
blood pressure.
II Chemical and hormonal control
of cardiovascular function
 Various hormones, chemicals
 Start at a low pace,
 Have long-lasting influences on
cardiovascular function.
 Hormones and chemicals are classified into
two groups
Vasoconstrictors and Vasodilators
 Vasoconstrictors
 Epinephrine and Norepinephrine
 Angiotensin II
 Vasopressin
 Vasodilators
Epinephrine and Norepinephrine
 The adrenal medulla secrete both
epinephrine (80%) and norepinephrine
 carried by blood flow to everywhere in the
 In the blood, only a little norepinephrine
comes form the endings of the adrenergic
Adrenergic receptors
α1 receptor on vessels
β1 receptor on heart
Positive effect
β2 receptor on vessels
(skeletal muscle and liver)
 On heart in vitro (contractility and
 both increase the force and rate of
contraction of the isolated heart.
 mediated by β1 receptors.
 On peripheral resistance.
 Norepinephrine produces
vasoconstriction in most if
not all organs via α1
 epinephrine dilates the blood
vessels in skeletal muscle
and the liver via β2
 overbalances the
vasoconstriction produced by
epinephrine elsewhere, and
the total peripheral resistance
 On heart in vivo (heart rate and cardiac
 When norepinephrine is infused introvenously
 the systolic and diastolic blood pressure rise.
 The hypertension stimulates the carotid and
aortic baroreceptors,
 producing reflex bradycardia that override the
direct cardioacceleratory effect of
 Consequently, the heart rate and cardiac out falls.
 On heart in vivo
 Epinephrine causes a
widening of the pulse
 baroreceptor stimulation
is insufficient to obscure
the direct effect of the
hormone on the heart,
 cardiac rate and output
Angiotensin II
 very potent vasoconstrictor
 formed in the plasma through a chain reaction.
 The chain is triggered by a substance, renin, released form
 Renin is released from kidneys in response to renal
ischemia, which may be due to a fall in blood pressure.
Effect of Angiotensin II
 powerful constrictor
 release aldosterone from the
adrenal cortex
 acts on the brain to create the
sensation of thirst.
 inhibit the baroreceotor reflex
 increase the release of
norepinephrine from the
sympathetic postganglionic
 Also called antidiuretic hormone (ADH),
 formed in the hypothalamus (mainly)
 secreted through the posterior pituitary gland.
 even more powerful than angiotensin as a
 The high concentration of vasopressin
during hemorrhage can raise the arterial
pressure as much as 40 to 60 mmHg.
 The amount of endogenous vasopressin in
the circulation of normal individuals does
not normally affect blood pressure.
 it does not increase blood pressure when
small doses are injected in vivo
 Acts on the brain to cause a decrease in
cardiac output.
 (in the area of postrema, one of the
circumventricular organs)
 Acts on the kidney
Endothelium – Derived Relaxing Factor
 Metabolism
Effect of NO
 Relax the vascular smooth muscle directly
 Mediate vascular dilator effect of some hormones
and transmitters (Ach, bradykinin, VIP, substance P)
 Inhibit the tonic excitation of some neurons in the
vasomotor centre.
 Inhibit the norepinephrine release from the
sympathetic postganglionic fiber.
 One or more of these effects are
III Autoregulation of Local Blood
 Role of Vasodilator Substances.
 CO2, Lactic acid, Adnosine, Adnosine phosphate
compounds, Histamine, K+ and H+
 Myogenic Activity
 Heterometric autoregulation
IV Long-Term mechanism for
Arterial Pressure Regulation
Renal –body Fluid Mechanism
V Summary of the Integrated
Multifaceted System for
Arterial Pressure Regulation
• Arterial pressure is regulated but by
several interrelated systems
• each of which performs a specific
If the blood pressure
drops suddenly
 two problems confronts the
pressure control system
 The first is survival,
 to return the arterial pressure
immediately to a high enough level
 that the person can live trough the acute
If the blood pressure drops suddenly
 The second is to return the blood
volume eventually to its normal level
 so that the circulatory system can reestablish full normality,
 including return of the arterial pressure all
the way back to its normal value
Three kind of mechanisms in
regulating the blood pressure
 react rapidly, within seconds or
 respond over an intermediate time
period, minutes or hours
 provide long-term pressure
regulation, days, months, and
1, Rapidly Acting Pressure Control Mechanisms,
Acting Within Seconds or Minutes
 The baroreceptor feedback mechanism.
 The central nervous system ischemic
 The chemoreceptor mechanism
Effect of Rapidly Acting Pressure
Control Mechanisms
 To cause constriction of the veins and provide
transfer of blood into the heart.
 To cause increased heart rate and contractility
of the heart and provide greater pumping
capacity by the heart
 To cause constriction of the peripheral
arterioles to impede the flow of the blood out of
the arteries.
 All these effects occur almost instantly to raise
the arterial pressure back into a survival range.
2. Pressure Control Mechanisms
That Act After Many Minutes
 The renin-angiotensin vasoconstrictor
 Stress-relaxation of the vasculature
 Shift of fluid through the tissue
capillary wall in and out of the
circulation to adjust the blood volume
as needed.
(1) The renin-angiotensin
vasoconstrictor mechanism
(2) Stress-relaxation of the
 When the pressure in the blood vessels becomes
too high,
 they become stretched and keep on stretching
more and more for minutes or hours;
 as a result, the pressure in the vessels falls
toward normal.
 This continuing stretch of the vessels, called
stress-relaxation, can serve as an intermediateterm pressure “buffer”.
(3) Shift of fluid through the tissue
capillary wall in and out of the circulation
• any time the capillary pressure falls too low,
• fluid is absorbed by capillary osmosis from
the tissue into the circulation,
• thus building up the blood volume and
increasing the pressure in the circulation.
Pressure Control Mechanisms
That Act After Many Minutes
 become mostly activated within 30
minutes to several hours.
 can last for long periods, days if
 During this time, the nervous
mechanisms usually fatigue and become
less and less effective
3, Long-Term Mechanisms for
Arterial Pressure Regulation
 The renal –blood volume pressure control
 Aldosterone
 Importance
 It takes a few hours to show significant response
for these mechanisms.
 Return the arterial pressure all the way back.