Lecture 7 Neural Control

From Iusmphysiology

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*continued here from [[Lecture 6 Transcapillary Exchange]] on 01/27/11 at around 8:37 ish.
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W4O6E8 A round of applause for your blog article.
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==Neural Control==
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===Objectives===
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*How do the sympathetic and parasympathetic nervous systems change each of the following:  Heart rate, Cardiac Contractility, Arterial Resistance, and venous constriction
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*As the mean arterial pressure is increased, how does the arterial baroreceptor activity (firing rate) change?  If the artery containing the baroreceptor sensors could not expand as the pressure is increased, how would baroreceptor activity change?
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*What are atrial and ventricular baroreceptors? During which phases of the heart cycle are they active?  When excessively active, what general types of modifications of neural and hormonal control occur?
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*At a conceptual level, there are four centers in the brain stem which interact to regulate the sympathetic and parasympathetic nervous systems.  What are the four centers and what major functions does each have?
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*Compare the effects of pleasurable emotions versus fear versus anger on neural control of the cardiovascular system.
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*Complete loss of neural cardiovascular control would result in a very low arterial blood pressure, a heart rate of about 100-110 beats/min (no vagal control), and low cardiac output.  Why do these problems occur? 
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*How does an increase in the intracranial pressure progressively cause decreased brain blood flow even if the arterial blood pressure is elevated?
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===Overview of Neural Vascular Regulation===
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*Looking at the flow chart.
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*Work through it backward from arterial pressure.
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====Without regulatory system====
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*If we stopped neural control to the cardiovasc system, we would faint.
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**Standing and walking would be very difficult.
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**Mean pressure ~50 mmHg
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====Range of Activity====
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*When sleeping, we use only use 80% of our normal awake function of the neural control.
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*When exercising, CV flow icnreases 5-10 fold, at least.
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*BP and cardiac output goes up because of the symp nervous system
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====Must adapt to life span of >80  years====
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*Most of us will see 2100
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*Our bp will change very little over time if we stay lean and active
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*Even from little babies to full grown, our BP doesn't change much:
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**Increase in about 20-30 mmHg.
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**This occurs as the child starts to stand.
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====Set Point Pressure====
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*Setpoint pressure:
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**The moment at which the body will try to maintain the bp.
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**When sleeping, the pressure is about 80.
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**awake = 90
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**walking and talking = 95
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**Walk fast = 105
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**Run in the hall 140-150.
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**These are each new setpoints
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*Resistance and volume and what not get fixed to maintain these set points.
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====E.  Regulated variables====
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*Let's look at at 24 hour cycle: noon to noon with a healthy, normal male
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*Variables that are regulated:
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**Mean arterail pressure, pretty constant:
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***BP drops off with sleep
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***BP goes up with alarm clock
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****BP usually highest in the mornings
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**Heart rate:
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***Low while sleeping
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***High in the morning
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**Stroke volume
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***Boringly constant
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***Except when exercising
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***Can increase 40%
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**Cardiac output
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***Low while sleeping
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***Up during exercise, though not much
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***50% in increase is a nice walk, not a run or anything
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**Total peripheral resistance
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***Went up during sleep
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***Went down when "busy" in the evening
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*24 hours with an athlete:
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**Mean arterail pressure, pretty constant:
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***Decreases where it needs to, goes up where the blood isn't needed.
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**Heart rate:
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***Heart rate is lower because cardiac output is higher
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***can go really low, too.
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***Max heart rate isn't really that different as sedentary people; may even be that athletes can't quite as high.
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**Stroke volume
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***Larger in this athlete
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**Cardiac output
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***Higher
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**Total peripheral resistance
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***Low
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**Venous constriction follows directional changes in heart rate
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***Constrict to make sure the blood is in the right places (organs, arteries).
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**Blood Volume:
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***Exercise training increases blood volume, first by increased plasma.
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***Then RBCs are added later.
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***Volume stays up 5-10% for as long as you exercise.
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***Temperature during the seasons change the blood volume:
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****In the summer the plasma is warmer and the volume increases appropriately
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****The blood volume even changes by the night day cycles (higher in the day, lower in the night when it is cooler).
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*stopped here on 01/27/11 at 9AM.
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*started here on 01/27/11 at 11AM.
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===Short  Term Sensor Systems for Neural Regulation===
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====Peripheral Arterial Baroreceptors====
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  Arch of aorta and bifurcation area  of common carotid arteries
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  1.  Monitor stretch of vessel        walls
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  a.  Vessel wall must deform to
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    generate signal
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  b.  Firing rate proportional to            stretch caused by          pressure
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  c.  Carotid baroreceptor
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    (1) glossopharyngeal  nerve
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    (2) Works at pressures of          50-  200 mmHg
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    d.  Aortic baroreceptor
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    (1) Uses vagus nerve
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    (2)  Works at pressures of                100-200 mmHg 
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BARORPTR
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Diameter of Baroreceptor Vessel
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F I    R R  A I    T N  E G
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2.
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How Might a Baroreceptor Work at the cellular level?        a.  Mechanosensitive Receptor              1.  Sodium channel allows Na+ ions to enter and partially depolarizes neuron              2.  Likely a calcium channel is opened to allow calcium channels to enter and both depolarize membrane and excite other channels        b.  Near the stretch sensitive site, the local depolarization initiates an action potential that is then propagated.   
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Likely Modifiers of Function 1.
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Prostacyclin – increased firing
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2.
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Nitric Oxide – increased firing
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3.
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Lipid Abnormality – less firing
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4.
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Activated platelets – less firing
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Ventricular and atrial Baroreceptors
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====Low pressure baroreceptors====
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  1. Atria baroreceptors
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  (a). Atrial Type A - atrial contraction
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  (b)  Atrial Type B – atrial filling during ventricular systole!! 
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  (c) if overactive, suppress antidiuretic hormone release (water        loss), decrease sympathetic activity
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  2.  Ventricular centers monitor both stretch of ventricle during        diastole and somehow monitor pressure developed.          Hyperactivity  suppresses sympathetic nervous system 
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Ventricular and atrial Baroreceptors
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===Integration of Input and Output Neural Signals in the Medulla Excitatory Centers===
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====Pressor Center - sympathetic  nervous system to blood vessels====
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  1.  Tonically active but  depressed by  baroreceptor input    2.  Causes increased arterial resistance and venous constriction   
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Neural control centers and cvtree
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====Cardiac Excitatory Center - sympathetic nervous system to heart====
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  1.  Tonically active - but depressed by baroreceptor  input  2.  Increases heart rate and contractility 
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Neural control centers and cvtree
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Inhibitory Centers
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A.  Depressor Center - suppresses activity of the sympathetic nervous        system to blood vessels
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  1.  Activated by the baroreceptor input
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  2.  Does not send neurons to blood vessels
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B.  Cardiac Inhibitory Center
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  1.  Activated by the baroreceptor input
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  2.  Vagal activity to the heart to slow the heart rate 
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Neural control centers and cvtree
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Baroreceptor  and sympathetic activity
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The overall outcome of the baroreceptor and central nervous system interaction is  1.  As baroreceptor activity is increased, the medulla will reflexively decrease the sympathetic nervous system activity  2.  Vagal activity usually changes in the opposite direction of sympathetic activity.    The cardiovascular system without sympathetic or parasympathetic activity:  Heart rate about 100-110 beats/min, Arterial pressure 65/40 mmHg, Cardiac output about 70% of normal, Vasculatures very dilated, Skin warm, mucus membranes flushed, very little tolerance to sitting or standing  The Full Neural Control System:  Heart rate should be 70-80 beats.min, arterial pressure 120/70 mmHg, cardiac output 70 ml/min per kg, skin cool and mucus membranes pink, able to perform to the maximum ability of the skeletal muscle system.   
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===Modifications of Neural Control By Higher Brain Centers===
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====Emotion====
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  1. Pleasurable sensations    Lowers sympathetic activity    Raises vagal activity    Heart rate and pressure fall 
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P1010003
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FIRST DINNER PRAYER
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  2.  Anger or rage: One of the most potent excitatory mechanisms    for sympathetic activity        a.  Acts in brain – higher conscious centers increase firing rate of        sympathetic neurons, suppress parasympathetic neurons              b.  Decreased sensitivity of baroreceptors due to their contraction?
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picrdata
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  3.  Fear and depression: Inhibits sympathetic activity 
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            a.  Works from conscious centers in brain – some how            depresses the medulla 
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    b.  Sympathetic system depressed, parasympathetic system        activated  - slow heart rate and low vascular resistance
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cobra
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John and Diane's home
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====Pain====
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    1.  Sharp pain - activate sympathetic system    2. Visceral pain - suppress sympathetic system  C.  Exercise    1.  Activate sympathetic nervous system    2.  Emotional connotation  greatly impacts degree of  activation
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runner
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m3a
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====Loss of baroreceptor Input====
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  Mean arterial pressure normal but wide range of variation each day    Has been duplicated in humans with similar results  1.  Seen when aorta and carotid arteries are stiffened with age  2.  Limits cardiovascular responses to body position and    temperature changes 
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neural control SAD Dog
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====Loss of all neural control====
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    1.  Spinal anesthesia or damage      2. Partial recovery from chronic injury associated with increased          sensitivity to norepinephrine 
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Neural control full loss on arterial pressure
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===The Brain as a Baroreceptor===
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====Inadequate perfusion of the brain====
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  1.  Possible causes
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  a.  Arterial pressure too low for autoregulation to be fully protective
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  b.  Compromise of the carotid arteries
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  c.  Increased intracranial pressure collapsing first venules then          arterioles  (edema and low perfusion) 
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cerebral baroreceptor flowchart
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  2.  Consequences of inadequate perfusion    a.  Oxygen availability decreases in tissue    b.  Carbon dioxide accumulates    c.  Tissue becomes acidotic  B.  Responses:  Sympathetic activity increased dramatically in an        attempt to raise pressure adequately to perfuse the brain        vessels 
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cerebral baroreceptor flowchart
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===Long Term Regulation of Arterial Blood Pressure===
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====Intake of NaCl equals Renal loss of NaCl over a matter of a few days====
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    1.  Increased NaCl does increase MAP                      but body compensates by greater                      excretion of NaCl to lower blood volume      2.  Generally assumed that major MAP                            effect of NaCl is blood volume effect                            on central venous pressure and CO.                     
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Increase NaCl Intake
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However, there are negative effects on endothelial and vascular smooth muscle mainly due to increased generation of oxygen radicals   
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====If arterial pressure increases and  baroreceptors work, less sympathetic nerve activity to kidney allows      increased loss of NaCl====
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====If intake of NaCl can not be properly excreted, arterial pressure will increase====
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  Common problem in      many forms of renal disease.
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===Clinical Example===
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While camping in Florida, a 24 year old medical student went for a vigorous bicycle ride on a very warm day.  When he returned several hours later, he collapsed in his tent. His classmates tried to have him drink water, but he was too unresponsive to swallow properly. At the Emergency Department of a local hospital, the vital signs were as follows:
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Heart rate: 127 beats/ min
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Arterial blood pressure:  80/50 mmHg
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Neck veins and arm veins lying: flattened
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Facial and body skin : Sweating profusely
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              Vascular refill in fingers: 6 seconds
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Patient: Unresponsive to name, but both pupils react rapidly to light,  reacts sluggishly to sternal pain stimulus
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What is the primary underlying problem in the student's collapse?
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A.  Intravascular clotting
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B.  Failure of sympathetic nervous system
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C.  Elevated peripheral vascular resistance
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D.  Inadequate cardiac output
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E. Decreased blood volume
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cardiovascular tree Richardson
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Current revision as of 05:11, 20 September 2012

W4O6E8 A round of applause for your blog article.

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