Lecture 7 Neural Control

From Iusmphysiology

Revision as of 14:21, 28 January 2011

• continued here from Lecture 6 Transcapillary Exchange on 01/27/11 at around 8:37 ish.

Neural Control

Objectives

• How do the sympathetic and parasympathetic nervous systems change each of the following: Heart rate, Cardiac Contractility, Arterial Resistance, and venous constriction
• 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?
• 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?
• 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?
• Compare the effects of pleasurable emotions versus fear versus anger on neural control of the cardiovascular system.
• 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?
• How does an increase in the intracranial pressure progressively cause decreased brain blood flow even if the arterial blood pressure is elevated?

Overview of Neural Vascular Regulation

• Looking at the flow chart.
• Work through it backward from arterial pressure.

Without regulatory system

• If we stopped neural control to the cardiovasc system, we would faint.
  • Standing and walking would be very difficult.
  • Mean pressure ~50 mmHg

Range of Activity

• When sleeping, we use only use 80% of our normal awake function of the neural control.
• When exercising, CV flow icnreases 5-10 fold, at least.
• BP and cardiac output goes up because of the symp nervous system

Must adapt to life span of >80 years

• Most of us will see 2100
• Our bp will change very little over time if we stay lean and active
• Even from little babies to full grown, our BP doesn't change much:
  • Increase in about 20-30 mmHg.
  • This occurs as the child starts to stand.

Set Point Pressure

• Setpoint pressure:
  • The moment at which the body will try to maintain the bp.
  • When sleeping, the pressure is about 80.
  • awake = 90
  • walking and talking = 95
  • Walk fast = 105
  • Run in the hall 140-150.
  • These are each new setpoints
• Resistance and volume and what not get fixed to maintain these set points.

E. Regulated variables

• Let's look at at 24 hour cycle: noon to noon with a healthy, normal male
• Variables that are regulated:
  • Mean arterail pressure, pretty constant:
    • BP drops off with sleep
    • BP goes up with alarm clock
      • BP usually highest in the mornings
  • Heart rate:
    • Low while sleeping
    • High in the morning
  • Stroke volume
    • Boringly constant
    • Except when exercising
    • Can increase 40%
  • Cardiac output
    • Low while sleeping
    • Up during exercise, though not much
    • 50% in increase is a nice walk, not a run or anything
  • Total peripheral resistance
    • Went up during sleep
    • Went down when "busy" in the evening

• 24 hours with an athlete:
  • Mean arterail pressure, pretty constant:
    • Decreases where it needs to, goes up where the blood isn't needed.
  • Heart rate:
    • Heart rate is lower because cardiac output is higher
    • can go really low, too.
    • Max heart rate isn't really that different as sedentary people; may even be that athletes can't quite as high.
  • Stroke volume
    • Larger in this athlete
  • Cardiac output
    • Higher
  • Total peripheral resistance
    • Low
  • Venous constriction follows directional changes in heart rate
    • Constrict to make sure the blood is in the right places (organs, arteries).
  • Blood Volume:
    • Exercise training increases blood volume, first by increased plasma.
    • Then RBCs are added later.
    • Volume stays up 5-10% for as long as you exercise.
    • Temperature during the seasons change the blood volume:
      • In the summer the plasma is warmer and the volume increases appropriately
      • The blood volume even changes by the night day cycles (higher in the day, lower in the night when it is cooler).

• stopped here on 01/27/11 at 9AM.
• started here on 01/27/11 at 11AM.

Short Term Sensor Systems for Neural Regulation

Peripheral Arterial Baroreceptors

 Arch of aorta and bifurcation area  of common carotid arteries 

 1.  Monitor stretch of vessel         walls 
  a.  Vessel wall must deform to 
   generate signal 
  b.  Firing rate proportional to            stretch caused by           pressure 
  c.  Carotid baroreceptor 
   (1) glossopharyngeal  nerve 
   (2) Works at pressures of          50-  200 mmHg 
   d.  Aortic baroreceptor 
   (1) Uses vagus nerve 
   (2)  Works at pressures of                100-200 mmHg  

BARORPTR

Diameter of Baroreceptor Vessel F I R R A I T N E G

2. 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.

Likely Modifiers of Function 1. Prostacyclin – increased firing

2. Nitric Oxide – increased firing

3. Lipid Abnormality – less firing

4. Activated platelets – less firing

Ventricular and atrial Baroreceptors

Low pressure baroreceptors

 1. Atria baroreceptors 
  (a). Atrial Type A - atrial contraction 
  (b)  Atrial Type B – atrial filling during ventricular systole!!  
  (c) if overactive, suppress antidiuretic hormone release (water         loss), decrease sympathetic activity 
 2.  Ventricular centers monitor both stretch of ventricle during         diastole and somehow monitor pressure developed.           Hyperactivity  suppresses sympathetic nervous system  

Ventricular and atrial Baroreceptors

Integration of Input and Output Neural Signals in the Medulla Excitatory Centers

Pressor Center - sympathetic nervous system to blood vessels

  1.  Tonically active but  depressed by  baroreceptor input    2.  Causes increased arterial resistance and venous constriction    

Neural control centers and cvtree

Cardiac Excitatory Center - sympathetic nervous system to heart

  1.  Tonically active - but depressed by baroreceptor  input   2.  Increases heart rate and contractility   

Neural control centers and cvtree

Inhibitory Centers

A.  Depressor Center - suppresses activity of the sympathetic nervous        system to blood vessels 
 1.  Activated by the baroreceptor input 
 2.  Does not send neurons to blood vessels 
B.  Cardiac Inhibitory Center 
 1.  Activated by the baroreceptor input 
 2.  Vagal activity to the heart to slow the heart rate  

Neural control centers and cvtree

Baroreceptor and sympathetic activity

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.

Modifications of Neural Control By Higher Brain Centers

Emotion

  1. Pleasurable sensations     Lowers sympathetic activity     Raises vagal activity     Heart rate and pressure fall   

P1010003 FIRST DINNER PRAYER

 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? 

picrdata

 3.  Fear and depression: Inhibits sympathetic activity  
            a.  Works from conscious centers in brain – some how             depresses the medulla  
   b.  Sympathetic system depressed, parasympathetic system         activated  - slow heart rate and low vascular resistance 

cobra John and Diane's home

Pain

   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 

runner m3a

Loss of baroreceptor Input

  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  

neural control SAD Dog

Loss of all neural control

   1.  Spinal anesthesia or damage      2. Partial recovery from chronic injury associated with increased          sensitivity to norepinephrine  

Neural control full loss on arterial pressure

The Brain as a Baroreceptor

Inadequate perfusion of the brain

 1.  Possible causes 
  a.  Arterial pressure too low for autoregulation to be fully protective 
  b.  Compromise of the carotid arteries 
  c.  Increased intracranial pressure collapsing first venules then           arterioles  (edema and low perfusion)   

cerebral baroreceptor flowchart

  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  

cerebral baroreceptor flowchart

Long Term Regulation of Arterial Blood Pressure

Intake of NaCl equals Renal loss of NaCl over a matter of a few days

    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.                      

Increase NaCl Intake

However, there are negative effects on endothelial and vascular smooth muscle mainly due to increased generation of oxygen radicals

If arterial pressure increases and baroreceptors work, less sympathetic nerve activity to kidney allows increased loss of NaCl

If intake of NaCl can not be properly excreted, arterial pressure will increase

  Common problem in      many forms of renal disease. 

Clinical Example

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:

Heart rate: 127 beats/ min 
Arterial blood pressure:  80/50 mmHg 
Neck veins and arm veins lying: flattened 
Facial and body skin : Sweating profusely 
             Vascular refill in fingers: 6 seconds 
Patient: Unresponsive to name, but both pupils react rapidly to light,   reacts sluggishly to sternal pain stimulus 

What is the primary underlying problem in the student's collapse?

A. Intravascular clotting B. Failure of sympathetic nervous system C. Elevated peripheral vascular resistance D. Inadequate cardiac output E. Decreased blood volume

cardiovascular tree Richardson