Transcript Chapter 14

Nervous Regulation of
the Heart
Qiang XIA (夏强), PhD
Department of Physiology
Room C518, Block C, Research Building, School of Medicine
Tel: 88208252
Email: [email protected]
Innervation of the heart
• Cardiac sympathetic nerve
• Cardiac vagus nerve
1.
2.
3.
4.
5.
6.
起源origin
节前纤维preganglionic fiber
外周神经节ganglion
节后纤维postganglionic fiber
支配distribution
递质neurotransmitter
Cardiac sympathetic actions
• Positive chronotropic effect正性变时作用
• Positive dromotropic effect正性变传导作用
• Positive inotropic effect正性变力作用
Cardiac mechanisms of norepinephrine
Mechanisms of norepinephrine
—increase Na+ & Ca2+ permeability
• If  & ICa,T , phase 4 spontaneous depolarization,
autorhythmicity 
• Ca2+ influx (ICa,L) , phase 0 amplitude & velocity ,
conductivity 
• Ca2+ influx (ICa,L) , Ca2+ release , [Ca2+ ]i ,
contractility 
(CICR)
Asymmetrical
innervation of
sympathetic nerve
Cardiac parasympathetic actions
• Negative chronotropic effect负性变时作用
• Negative dromotropic effect负性变传导作用
• Negative inotropic effect负性变力作用
Cardiac mechanisms of acetylcholine
Mechanisms of acetylcholine
—increase K+ & decrease Ca2+ permeability
• K+ outward (GIRK) , If  & ICa,T , |MRP| , phase 4
spontaneous depolarization , autorhythmicity 
• Inhibition of Ca2+ channel, phase 0 amplitude &
velocity , conductivity 
• G protein→PLC → NOS → NO → GC → cGMP  ，
Ca2+ influx (ICa,L) , [Ca2+ ]i , contractility 
Cardiac effect of
parasympathetic
stimulation
Vagal Maneuvers
• Valsalva maneuver
– A maneuver in which a person tries to exhale forcibly with
a closed glottis (the windpipe) so that no air exits through
the mouth or nose as, for example, in strenuous coughing,
straining during a bowel movement, or lifting a heavy
weight. The Valsalva maneuver impedes the return of
venous blood to the heart.
– Named for Antonio Maria Valsalva, a renowned Italian
anatomist, pathologist, physician, and surgeon (1666-1723)
who first described the maneuver.
Physiological response in
Valsalva maneuver
• The normal physiological response consists of 4
phases
Physiological response in
Valsalva maneuver
• The normal physiological response consists of 4 phases
– Initial pressure rise: On application of expiratory force, pressure rises inside the chest forcing
blood out of the pulmonary circulation into the left atrium. This causes a mild rise in stroke
volume.
– Reduced venous return and compensation : Return of systemic blood to the heart is impeded
by the pressure inside the chest. The output of the heart is reduced and stroke volume falls. This
occurs from 5 to about 14 seconds in the illustration. The fall in stroke volume reflexively causes
blood vessels to constrict with some rise in pressure (15 to 20 seconds). This compensation can be
quite marked with pressure returning to near or even above normal, but the cardiac output and
blood flow to the body remains low. During this time the pulse rate increases.
– Pressure release: The pressure on the chest is released, allowing the pulmonary vessels and the
aorta to re-expand causing a further initial slight fall in stroke volume (20 to 23 seconds) due to
decreased left ventricular return and increased aortic volume, respectively. Venous blood can once
more enter the chest and the heart, cardiac output begins to increase.
– Return of cardiac output: Blood return to the heart is enhanced by the effect of entry of blood
which had been dammed back, causing a rapid increase in cardiac output (24 seconds on). The
stroke volume usually rises above normal before returning to a normal level. With return of blood
pressure, the pulse rate returns towards normal.
Interaction of
sympathetic and
parasympathetic
nerves
Predominance of autonomic nerves
Tonus紧张
• Cardiac vagal tone心迷走紧张
• Cardiac sympathetic tone心交感紧张
Innervation of the blood vessels
• Vasoconstrictor nerve缩血管神经
– Sympathetic vasoconstrictor nerve交感缩血管神
经
• Vasodilator nerve舒血管神经
– Sympathetic vasodilator nerve交感舒血管神经
– Parasympathetic vasodilator nerve副交感舒血管
神经
– Dorsal root vasodilator nerve脊髓背根舒血管神
经
Cardiovascular Center
A collection of functionally similar neurons that
help to regulate HR, SV, and blood vessel tone
Vasomotor center
Located bilaterally mainly in the reticular
substance of the medulla and of the lower third
of the pons
– Vasoconstrictor area
– Vasodilator area
– Cardioinhibitor area – dorsal nuclei of the
vagus nerves and ambiguous nucleus
– Sensory area – tractus solitarius
Vasomotor center
Higher cardiovascular centers
– Reticular substance
of the pons
– Mesencephalon
– Diencephalon
– Hypothalamus
– Cerebral cortex
– Cerebellum
Baroreceptor Reflexes
压力感受性反射
• Arterial baroreceptors 动脉压力感受器
– Carotid sinus receptor
– Aortic arch receptor
• Afferent nerves (Buffer nerves，缓冲神经)
• Cardiovascular center: medulla
• Efferent nerves: cardiac sympathetic nerve,
sympathetic constrictor nerve, vagus nerve
• Effector: heart & blood vessels
Baroreceptor neurons
function as sensors in
the homeostatic
maintenance of MAP
by constantly
monitoring pressure
in the aortic arch and
carotid sinuses.
Characteristics of baroreceptors:
Sensitive to stretching of the vessel walls
Proportional firing rate to increased
stretching
Responding to pressures ranging from 60180 mmHg
Receptors within the aortic arch are less
sensitive than the carotid sinus receptors
The action potential frequency in baroreceptor neurons is
represented here as being directly proportional to MAP.
i.e., MAP is
above
homeostatic
set point
i.e., reduce cardiac output
Baroreceptor neurons deliver MAP information to the
medulla oblongata’s cardiovascular control center (CVCC);
the CVCC determines autonomic output to the heart.
Reflex pathway
Click here to play the
Baroreceptor Reflex Control
of Blood Pressure
Flash Animation
Typical carotid sinus reflex
Physiological Significance
Maintaining relatively
constant arterial
pressure, reducing the
variation in arterial
pressure
Cardiovascular Responses to
Exercise
When exercise begins, mechanosensory input from working limbs
combines with descending pathways from the motor cortex to
activate the cardiovascular control center in the medulla oblongata.
The center responds with sympathetic discharge that increases
cardiac output and causes vasoconstriction in many peripheral
arterioles.
Cardiac output increases during
exercise
Peripheral blood flow redistributes
to muscle during exercise
Blood pressure
rises slightly
during exercise
VO2 max (also maximal oxygen
consumption, maximal oxygen
uptake or aerobic capacity) is the
maximum capacity of an individual's
body to transport and utilize oxygen
during incremental exercise, which
reflects the physical fitness of the
individual.
Baroreceptor reflex adjusts to
exercise
• During exercise, blood pressure increases without
activating homeostatic compensation of
baroreceptor reflex
• Why?
– Signal from the motor cortex during exercise
reset the arterial baroreceptor threshold to a
higher pressure
Case
A 48-year-old man, who engaged in regular physical exercise,
went to see his physician because of recurrent headaches. Physical
examination revealed that the patient had a mean heart rate of 55
beats/min. His physician noted that the patient's cardiac rhythm
varied substantially with the phases of respiration; the heart rate
increased during inspiration and decreased during expiration.
1. What changes in cardiac sympathetic and parasympathetic
activity take place during the respiratory cycle?
2. Are the respiratory fluctuations in heart rate produced by the
rhythmic changes in sympathetic activity, in parasympathetic
activity, or both?
The physician diagnosed this patient's headaches as migraine. He
advised the patient to take propranolol, a β-adrenergic receptor
antagonist, to relieve the headaches. The physician noted that after
the patient had taken the propranolol, the mean heart rate
diminished very slightly, and the respiratory fluctuations in heart
rate were not appreciably different from those observed before the
propranolol was taken.
3. Does the failure of propranolol to induce a substantial change
in mean heart rate or in the respiratory fluctuations in heart rate
necessarily signify that the patient's cardiac sympathetic neural
activity was negligible at the time he was being examined?
Three years later, the patient began to experience frequent
episodes of chest pain on exertion. The patient's cardiologist
recommended a diagnostic cardiac catheterization. His aortic
pressure (Pa) and his electrocardiogram (ECG) were recorded
during the procedure; one segment of the record is shown in
Fig. 1. As the cardiac catheter was being manipulated, it
initiated several premature ventricular depolarizations, one of
which (designated R') is shown in this figure.
4. Why did the premature ventricular depolarization (Fig. 1) not
affect the aortic pressure tracing?
5. Why did the ventricular contraction after the premature beat
produce such a large aortic pulse pressure (difference between
maximum and minimum aortic pressures)?
About 1 year later, the patient developed 2:1 atrioventricular (AV) block
(i.e., only alternate cardiac impulses were propagated from atria to
ventricles). The patient's ECG is shown in Fig. 2. Note that before the
patient was given atropine (top tracing), those P-P intervals that include
an R wave are shorter (0.7 s) than those that do not include an R wave
(0.8 s).
The cardiologist gave the patient test injections of propranolol and of
atropine to determine the role of both divisions of the autonomic nervous
system in the production of the AV block and of the alternating P-P
interval durations. The cardiologist found that propranolol had little
effect either on the 2:1 AV block or on the alternation of the P-P
intervals. He also observed that atropine had little effect on the AV
block, but it did cause the mean P-P interval to diminish (to 0.6 s), and
the alternations of the P-P intervals were no longer evident (bottom
tracing).
6. What is the most likely explanation for the
alternating durations of the P-P intervals (Fig. 2)?
7. How do you explain the abolition of the
alternations by atropine (Fig. 2), but the absence
of any appreciable effect by propranolol?
The End.