PHYS - Regional Regulation of Circulation

Question 1

CEREBRAL CIRCULATION

Answer 1

• Ensure uninterrupted O2 supply to brain
• Controlled by local metabolic factors
  
  • Hypoxia
  • Hypercapnia (CO2) – overrides everything else
• Well developed autoregulation, protects its own supply
• BBB = highly restrictive capillaries
• Structural adaptations of the brain
  
  • Circle of Willis – AVA; back up blood supply
  • High capillary density – protects against hypoxia
• Challenges to the brain
  
  • Effects of gravity –> postural hypertension
  • Little/no room for expansion in skull
• Most important local vasodilator for cerebral circulation is CO2
• Hyperventilation → decreased CO2 → decreased BP → syncope
• CS: Cushing Reflex
  
  • Increased cranial P → compression of cerebral arteries → decreased cerebral Q → ischemia → vasomotor center* → peripheral vasoconstriction → increased systemic arterial pressure (+ bradycardia) → restored CBF
  • BUT high systemic P → high pulmonary arterial P → pulmonary edema

Question 2

CORONARY CIRCULATION

Answer 2

• Controlled by changes in coronary vascular resistance
• Influenced local metabolic factors (intrinsic) → vasodilation
  
  • Hypoxia, Adenosine, Lactate, K+, NO
• Weak neural/hormonal control because low receptor density
  
  • α1 - vasoconstriction
  • β2 - vasodilation
  • Good, because any stressful situation would cause heart attack!
• Autoregulation and active/reactive hyperemia
• Coronary reserve increases Q 3-4x during exercise (or hemorrhage)
• Q strongly influenced by the mechanical activity of the heart
• Structural adaptations of the heart
  
  • Every fiber is supplied by at least one capillary
  • Max diffusion distance is 10um
    
    • Important, because in hypertrophy CM because vulnerable because distance from capillary can become greater than 10 um
    • Need increased vascularization to support hypertrophy
• Challenges to the heart
  
  • Coronary arteries = end arteries (sudden occlusion → ischemia/infarct)
  • Reactive hyperemia fills coronary arteries during diastole
  • Coronary reserve and coronary steal → during exercise or pathology
  • Vascular compression greatest in endocardium → most susceptible to ischemia
• Tachycardia (decreased CO)
  
  • Supply/demand imbalance
  • More frequent coronary vascular compression + less time in diastole for coronary Q
  • Increased O2 demand

Question 3

SKELETAL MUSCLE CICRCULATION

Answer 3

• Contributes to maintenance of BP
• Q can increase up to 20x in exercising muscle
• Functional adaptations of SkM
  
  • Slow twitch (Type I) red fibers - marathoners
    
    • High capillary density
    • High mitochondrial content
    • High myoglobin
  • Fast twitch (Type II) white fibers - sprinters
• Functional adaptations
  
  • Rest → vasoconstriction dominant from sympathetic activation
  • Exercise → vasodilation increases muscle Q by
    
    • Metabolic vasodilation and capillary recruitment
      
      • Lactate, adenosine, K+
      • 2/3 of capillaries not active at rest
      • Recruitment shortens diffusion distances for nutrient delivery and waste removal
    • Skeletal muscle pump
  • Sympathetic activity increases during exercise (→ vasoconstriction)
    
    • But local (ischemic) metabolites cause vasodilation in SkM and dilation dominates.
• Exercising SkM
  
  • Normally, rhythmic SkM contraction maintains Q through active hyperemia
  • During exercise, SkM contraction constricts vessels and blocks Q
    
    • Not a problem in rhythmic exercise because Q maintained by reactive hyperemia
    • Isometric exercise can cause significant Q problems
  • Increased vascular pressure from exercise, increased capillary filtration → edema in the exercising muscle

Question 4

CUTANEOUS CIRCULATION

Answer 4

• Functions of skin
  
  • Regulation of internal temperature
  • Protection/response to injury
• Extrinsically controlled by body and ambient temperatures → sympathetic activation
• Structural adaptations of the skin
  
  • Ateriovenous anastomoses (AVAs/glomus bodies)
    
    • Occur in acral/apical skin (hands, feet, nose, ears, lips)
    • Normally constricted by sympathetic vasoconstrictor activity
  • Large venous plexus = blood reservoir
• Controlled by hypothalamus (‘thermostat’) mediating sympathetic response
  
  • Core BT low → increased sympathetic tone to AVAs → vasoconstriction
  • Core BT high → withdrawal of sympathetic tone to AVAs + bradykinin release from sweat glands (symp, ACh) → vasodilation
• Control by direct response to ambient temperature
  
  • Local heating → vasodilation
  • Local cooling → vasoconstriction on non-acral skin
    
    • Ambient temp stimulates a weak spinal reflex:
      
      • Sympathetic tone in non-acral skin → vasodilation
      • Withdrawn tone in acral skin → vasoconstriction
    • Paradoxical cold vasodilation
      
      • Paralysis of sympathetic neurotransmission, maintains vasodilation in acral skin (flushed cheeks and nose) → prevent skin damage

Question 5

CS: CUTANEOUS CIRCULATION

Answer 5

• CS: Hemorrhagic Shock
  
  • Sudden blood loss → severe hypotension → vasoconstriction of BVs skin increases BP
    
    • Cold/pale appearance
  • EX → WWI, wrapping warm blankets around injured soldiers that needed to be transported a distance caused sympathetic tone to decrease → vasodilation to occur → systemic BP lowered → loss of blood volume
• CS: Exercising in hot weather
  
  • Increased Q to working muscle + increased core temperature = vasodilation
  • Decreased peripheral resistance
  • Decreased plasma volume from increased capillary filtration
  • Capacity of heart to maintain CO may be exceeded → hypotension and collapse
  • Heat stress → heat exhaustion → heat stroke
• CS: Injury
  
  • Injury → cutaneous vasodilation
    
    • Paracrine control (axon reflex)
      
      • Releases SP, ATP, bradykinin, CGRP
    • Triple response: Swelling + Redness + Edema