The document discusses regional circulations, focusing on coronary, cerebral, and cutaneous circulation. It provides details on the anatomy, blood supply, regulation, and clinical implications of each circulation. For coronary circulation, it describes the blood vessels that supply the heart muscle and how blood flow is regulated to meet myocardial oxygen demands. For cerebral circulation, it outlines the unique anatomical features of the brain's blood supply and factors that control blood flow. For cutaneous circulation, it explains the role of arteriovenous anastomoses and arterioles in regulating heat transfer and sympathetic nervous system control of cutaneous blood flow.

1. Regional circulations
DR. RAJNEE
Dept of Physiology

2. Regional circulations
 Coronary
 Cerebral
 Cutaneous
 Muscle
 Splanchnic

3. Coronary circulation

4. Coronary blood vessels
 Heart receives blood supply from two coronary
arteries
– Left coronary artery
 Anterior descending branch
 Circumflex branch
– Right coronary artery
 Dominance
– Right in 50%
– Left in 20%
– Equal in 30%

5. Coronary circulation
 4% of Cardiac Output
 high resting blood flow of 70-80 ml/min/100g
– At maximal cardiac work: 300-400 ml/min/100 g
 Has a high capillary density (3000-5000 mm2, about
one capillary per myocyte)
 large surface area
 short diffusion distances (≤9µm)

6. Coronary blood flow
 Coronary blood flow occurs
during diastole
 Why
– During systole, contraction of
heart musculature squeezes
the coronary vessels
– This effect is more in deeper
layers (subendocardial vessels)
than superficial layers
(epicardial vessels)
– This effect is maximal in the
left ventricle

8. Coronary circulation
 myocardial blood flow is characterized by
almost complete oxygen extraction (70-80%)
from the blood across the coronary capillaries
 therefore, blood flow must increase to increase
oxygen delivery to the heart
 myocardial oxygen delivery is FLOW LIMITED
 aortic pressure provides driving force for
coronary blood flow

9. Regulation of Coronary Blood Flow
 Metabolic (Functional) Hyperemia
 Reactive Hyperemia
 Autoregulation

10. Metabolic (Functional) Hyperemia
 primary determinant of coronary blood flow is
myocardial oxygen consumption
– which is dependent on metabolic activity
 myocardial oxygen consumption is influenced by
– cardiac pressure development
– wall tension
– heart rate
– cardiac output
– inotropic state
– Afterload
– preload

12. Mechanism
 The exact means by which increased oxygen
consumption causes coronary circulation not known
 Possible mechanism
– Hypoxia -> vasodilator substances to be released from
cardiac muscle cells
– Adenosine is the main vasodilator substance
– adenosine produced in myocytes from the metabolism of
ATP
– stimulates nitric oxide release from endothelium
– nitric oxide is a potent vasodilator

13. Other factors
 K+ ions
 H+ ions
 CO2
 Bradykinin
 Prostaglandins
 Lactate

14. Reactive hyperemia
 brief occlusion of coronary vessel is followed by
a transient increase in coronary blood flow
 occlusion results in the accumulation of
vasodilator metabolites in the interstitium
 magnitude and duration of extra flow
dependent on the duration of the occlusion

16. Autoregulation
 blood flow is relatively constant at perfusion
pressures from 60 mmHg → 150 mmHg
 metabolic and myogenic mechanisms involved
 curve resets upward at elevated O2 such as
during exercise
 autoregulatory capacity is important in
maintaining coronary flow when vessels are
partially obstructed
DR. RAJNEE

17. DR. RAJNEE

18. Neural control
 sympathetic vasoconstrictor fibers - tonic
activity
– direct effect of SNS stimulation is vasoconstriction
via α1-adrenergic receptors
– net effect of sympathetic stimulation of the heart is
to increase coronary blood flow due to increase in
the production of metabolic vasodilators with
increased oxygen consumption
DR. RAJNEE

19. Neural control
 parasympathetic cholinergic fibers
– → direct effect to vasodilate coronary resistance
vessels via endothelial release of NO
– net effect of parasympathetic stimulation of the
heart may actually be reduced coronary blood flow
resulting from decreased heart rate and oxygen
consumption
DR. RAJNEE

20.  When the systemic BP falls
 The overall effect of increase in noradrenergic
discharge is increased coronary blood flow due
to
– Metabolic changes
– On the contrary cutaneous, renal and splanchnic
vessels are constricted
– Protecting the heart
DR. RAJNEE

21. Hormonal factors
 circulating epinephrine
– → β2-adrenergic receptor-mediated vasodilation
 vasopressin produces coronary vasodilation
DR. RAJNEE

22. Clinical conditions
 CAD (Coronary artery disease)
– Coronary artery disease (CAD) (or atherosclerotic
heart disease) is the end result of the accumulation
of atheromatous plaques within the walls of the
coronary arteries that supply the myocardium
– Is the leading cause of death worldwide
WHO Data
DR. RAJNEE

23. DR. RAJNEE

24. Clinical conditions
 CAD causes
– Angina pectoris, commonly
known as angina
 is severe chest pain due to
ischemia (a lack of blood and
hence oxygen supply) of the
heart muscle, generally due to
obstruction of the coronary
arteries
– Myocardial infarction (MI)
commonly known as a heart
attack
 is the interruption of blood
supply to part of the heart,
causing some heart cells to die
DR. RAJNEE

25. Cerebral circulation
DR. RAJNEE

26. General Characteristics
 brain least tolerant of organs to ischemia
 -↓blood flow for 5 seconds →loss of
consciousness
 -↓blood flow for a few minutes →irreversible
damage
DR. RAJNEE

27. Anatomical details
 Two internal carotids
 Two vertebral arteries
– Basilar artery
 Circle of Willis
 No crossing over from R to L (because of equal
pressure)
 Occlusion of vessel produces ischaemia and
infarction
DR. RAJNEE

28. General Characteristics
 Rest: blood flow
– of 50-60 ml/min/100 g (750 ml/min)
(in contrast Coronary: 70-80 ml/min/100g; 250ml/min)
 15% of cardiac output
– (in contrast Coronary: 4% of CO)
 Exercise: blood flow of 750 ml/min
 greatest flow goes to grey matter (100
ml/min/100 g)
 35% O2 extraction at rest
DR. RAJNEE

29. Notable Anatomic Characteristics
 circulation is enclosed in a rigid skull →
constant volume
 brain tissue is incompressible
 brain “floats” in a water bath of cerebrospinal
fluid
 high capillary density (3000 - 4000/mm2)
→large surface area, short diffusion distances
 blood-brain barrier - tight junctions between
endothelial cells →prevents circulating
vasoactive substances from affecting cerebral
blood flow
DR. RAJNEE

30. cushioning function
 brain is floating in the fluid
 this provides a protective function
DR. RAJNEE

31. Normal Flow
 Constant cerebral blood flow is maintained
under varying conditions
 Factors affecting the total cerebral blood flow
– Arterial pressure at brain level
– Venous pressure at brain level
– The intracranial pressure
– The viscosity of blood
– The degree of active contraction/dilatation of
cerebral arterioles
 This is controlled by local vasodilator metabolites
DR. RAJNEE

32. Role of intracranial pressure
 Since the brain is enclosed within the skull the volume
of blood, brain and CSF should remain constant
(Monro-Kellie hypothesis)
 ICP is normally 0-10 mmHg
 Whenever ICP increases, cerebral vessels are
compressed
 Change in venous pressure cause a similar change in
ICP
 Rise in venous pressure decreases CBF by
compressing the vessels thereby decreasing perfusion
pressure
DR. RAJNEE

33. Autoregulation
 pronounced autoregulatory capacity from 50 -
170 mmHg
 both myogenic and metabolic mechanisms
involved
 sympathetic nervous system activity can shift
the curve to the right
DR. RAJNEE

34. DR. RAJNEE

35. Chemical
 Arterial PCO2 (normal, 35-45 mmHg)
– hypercapnia (↑PCO2 ) → dilatation → ↑blood flow
– hypocapnia (↓PCO2 ) → constriction →↓blood flow
– CO2 diffuses from blood into brain ECF
– CO2+H2O → H2CO3 → H++HCO3
– ↑ [H+] → vasodilatation
– blocks Ca2+ entry
– hyperpolarizes the membrane
– ↑NOS activity
DR. RAJNEE

36. DR. RAJNEE

37.  Arterial pH (acidosis)
– has little effect
– H+ does not cross the BBB
 Arterial PO2 (normal, 80-100 mmHg)
– diffuses easily from blood to cerebral ECF
– hypoxia (PO2<40-50 mmHg) →dilatation
– PO2 > 100 mmHg →little effect
– dilatation adenosine mediated (?)
DR. RAJNEE

38. Neural control
 Sympathetic nervous system
– rich innervation from superior cervical ganglion
– maximum sympathetic nervous system activity
causes only small vasoconstrictor response
– baroreceptor reflexes have little influence on
cerebral blood flow
– ↑sympathetic nervous system activity may prevent
hyperperfusion during acute ↑ in MAP
DR. RAJNEE

39. Neural control
 Parasympathetic nervous system
– innervation via facial and superficial petrosal nerves
– stimulation of nerves cause vasodilatation (ACh stimulates
NO release)
– cut nerves → no effect
– physiological importance is unknown
 Other
– ↑nerve activity → ↑NO release → local vasodilatation
– Perivascular neurons also contain 5HT (serotonin) a
powerful vasoconstrictor - may cause vasospasm
eg. in migraine
DR. RAJNEE

40. Metabolic
 Potassium
– ↑K+ (i.e., seizures, hypoxia) → vasodilatation
– ↑K+ → stimulation of Na+/K+ATPase → hyperpolarize membrane
– stable concentration in autoregulatory range
 Adenosine
– ↑ interstitial adenosine concentration with hypoxia, ischemia, ↓ perfusion
pressure, ↑metabolic activity, ↓supply/demand
– vasodilatation occurs
 Nitric Oxide
– NO synthase active under basal conditions
– tonic vasodilator effect
– glial-derived (astrocytes) - NOS stimulated by NE, bradykinin, glutamate
→ Role?
DR. RAJNEE

41. Central Nervous System Ischemic
Response
 When the blood flow to the brain has been sufficiently
interrupted to cause ischemia of the vasomotor center
 these vasomotor neurons become strongly excited
 causing massive vasoconstriction as a means of
raising the blood pressure to levels as high as the
heart can pump against
 This response can raise the blood pressure to levels as
high as 270 mm Hg for as long as 10 minutes
DR. RAJNEE

42. Central Nervous System Ischemic
Response
 This response is a last ditch stand to preserve the
blood flow to vital brain centers
 it does not become activated until blood pressure has
fallen to at least 60 mm Hg, and it is most effective in
the range of 15 to 20 mm Hg
 If the cerebral circulation is not reestablished within 3
to 10 minutes, the neurons of the vasomotor center
cease to function
 ↑sympathetic nervous system vasoconstrictor activity
to systemic resistance vessels →↑TPR → ↑MAP → ↑∆P
→ ↑cerebral blood flow
DR. RAJNEE

43. Cushing’s Reflex
 The Cushing reflex is a special type of CNS reflex resulting from
an increase in intracranial pressure
 space-occupying lesion (i.e., tumor, hemorrhage) will ↑ICP
 forces brainstem down into the foramen magnum
 brainstem becomes compressed → ischemia
 ↑sympathetic nervous system vasomotor drive to systemic
resistance vessels → vasoconstriction →↑TPR →↑MAP →↑∆P →
↑cerebral blood flow
 baroreceptor-mediated reflex bradycardia
 Main features: hypertension, bradycardia, respiratory
depression
 The Cushing reflex is usually seen in the terminal stages of
acute head injury
DR. RAJNEE

44. DR. RAJNEE

45. Humoral
 few hormones pass blood brain barrier
 some PGs are lipid soluble →vasodilate
DR. RAJNEE

46. Clinical condition
Stroke (cerebrovascular accident
or CVA)
DR. RAJNEE

47. Stroke
 rapidly developing loss of brain function due to
disturbance in the blood supply to the brain,
caused by a blocked or burst blood vessel
 This can be due to ischemia caused by
thrombosis or embolism
 or due to a hemorrhage
DR. RAJNEE

48. Cutaneous blood flow
DR. RAJNEE

49. DR. RAJNEE

50. CUTANEOUS CIRCULATION
 primary role is regulation of internal
temperature
 protection against the environment
 blood pressure control
 6% of the CO at rest (10-20 ml/min/100g)→
↓50% to retain heat, ↑7-fold to lose heat
DR. RAJNEE

51. Resistance vessels
 Two types
– Arteriovenous anastomoses (AVAs)
– Arterioles
DR. RAJNEE

52. Arteriovenous anastomoses
 coiled, thick-walled vessels
 direct connections between dermal arterioles and veins
 provide low resistance shunt pathways → feed dermal venous
plexus
 little basal tone (myogenic)
 little metabolic control - no autoregulation or reactive
hyperemia
 sympathetic nervous system vasoconstrictor innervation has
almost exclusive control
 →tonic activity
 located in “acral skin”: areas of high SA/vol. - fingers, toes,
palms, soles, lips, nose, ears
 passive vasodilation due to ↓sympathetic nervous system
activity
DR. RAJNEE

53. Arterioles
 located in non-acral skin - limbs, trunk, scalp
 high density of α-adrenergic receptors
 lack of β2-adrenergic receptors
 sympathetic nervous system vasoconstrictor
innervation - little activity at normal core temperature
 sympathetic nervous system cholinergic (vasodilator)
innervation is prominent to sweat glands →
BRADYKININ
 bradykinin mediates “active” vasodilation
 arterioles exhibit autoregulation, reactive hyperemia
and basal tone (myogenic)
DR. RAJNEE

54. Venous Plexus
 contains greatest cutaneous blood volume -
acts as a reservoir
 important for heat transfer
 sympathetic nervous system vasoconstrictor
innervation
DR. RAJNEE

55. Control of Cutaneous Blood Flow
 Sympathetic Nervous System
– to conserve heat SNS activity increases causing
vasoconstriction and reducing heat transfer to the
environment
– to lose heat SNS activity is reduced causing
vasodilation and enhanced heat transfer to the
environment
DR. RAJNEE

56. Local Skin Reflexes
 local warming will produce local vasodilation
and sweating
 local cooling will produce local vasoconstriction
due to increased affinity of α2-adrenergic
receptors for norepinephrine
 intensity controlled by central brain
temperature centers
 cutting spinal cord results in extremely poor
temperature regulation
DR. RAJNEE

57. DR. RAJNEE

58.  Cold-Induced Vasodilation
– when temperature falls, smooth muscle becomes
paralyzed and vasodilatation occurs
 Physical compression (e.g. sitting)
– ischemia →accumulation of metabolites →
stimulates nociceptors → pain → shift weight
– → reactive hyperemia (substance P/CGRP?)
DR. RAJNEE

59.  Hormones
– epinephrine → constriction
– angiotensin II → constriction
– vasopressin → constriction
 Role in Blood Pressure Control
– Hypotension → ↑sympathetic nervous system →AVA,
arteriole and venous constriction
– → ↑TPR and mobilization of blood to support venous
pressure
– During exercise enhanced blood flow to the cutaneous
circulation is necessary for
– dissipating heat → reduces venous return to the heart →
arterial pressure falls
DR. RAJNEE

60. White reaction
 When a pointed object is drawn across the skin
 Stroke lines becomes pale
 Called white reaction
 Due to mechanical stimulus initiating
precapillary sphincter contraction
DR. RAJNEE

61. Triple response
 When the skin is stroked more strongly
 Triple response
– 1. Red reaction
 Capillary dilatation
– 2. Wheal (swelling)
 Increased capillary permeability
– 3. Flare (redness spreading out from injury)
 Arteriolar dilatation
 Due to axon reflex
DR. RAJNEE

62. Axon reflex
 A response in which impulses initiated in
sensory nerves by the injury are relayed
antidromically down other branches of the
sensory nerve fibres
Skin
Arteriole
DR. RAJNEE

63. Reactive hyperaemia
– brief occlusion of blood flow is followed by a
transient increase in flow
DR. RAJNEE

64. Skeletal Muscle
Circulation
DR. RAJNEE

65.  enormous range of blood flow in skeletal
muscle: 3.0 ml/min/100 g at rest (20% of CO)
 exercise: 100 ml/min/100g (80-85% of CO)
 resistance vessels have high resting tone
(myogenic)
DR. RAJNEE

66. Regulation of Skeletal Muscle Blood
Flow
 Neural
– neural control dominates at rest
– tonic sympathetic nervous system vasoconstrictor
activity (1 Hz) - α1-adrenergic receptor mediated
– an increase in sympathetic nervous system activity
(4-5 Hz) can decrease flow by 70%
– vasodilatation at rest is passive due to withdrawal
of sympathetic nervous system activity
– sympathetic-cholinergic fibers are anatomically
present - physiological role is uncertain
DR. RAJNEE

67. DR. RAJNEE

68. Hormonal
– circulating epinephrine vasodilates at low
concentration (β2-adrenergic receptor),
– constricts at high concentration (α1/α2-adrenergic
receptors)
– vasopressin → constricts
– angiotensin II → constricts
DR. RAJNEE

69. Metabolism (functional hyperemia)
 with increased activity there is an increase in
the production of vasodilator metabolites
 vasodilator metabolites are dominant during
exercise although sympathetic nervous system
activity to the working muscle is also enhanced
DR. RAJNEE

70. Metabolism (functional hyperemia)
 Mediators of Vasodilation
– increased interstitial [K+] →stimulates
Na+/K+ATPase → hyperpolarizes membrane
– interstitial acidosis/hypoxia → hyperpolarizes
membrane
– interstitial hyperosmolarity
– adenosine?
DR. RAJNEE

71. Physical Factors
 cyclical contraction and relaxation of active
skeletal muscle vessels
 vessels are compressed during the contraction
phase → blood flow becomes intermittent
 muscle perfusion is enhanced by the muscle
pump
 during activity muscle pump lowers the venous
pressure which increases the pressure gradient
driving flow
DR. RAJNEE

72. DR. RAJNEE

73.  Autoregulation
– blood flow is relatively constant from 60 → 120
mmHg (mainly myogenic)
 Reactive Hyperemia
– brief occlusion of blood flow is followed by a
transient increase in flow

74.  Role of Skeletal Muscle Circulation in Blood
Pressure Control
– large mass of tissue: 40 - 45% of body weight
– major site of resistance vessels
– Peripheral resistance regulated by controlling
muscle resistance
– resistance influenced by
 tonic vasoconstrictor activity
 metabolic vasodilators
 regulation by reflex mechanisms (baroreceptors,
cardiopulmonary receptors, etc.)

75. Splanchnic Circulation
DR. RAJNEE

76.  blood flow 25% of resting CO - can increase by
30 -100% after a meal
 blood flow is closely coupled to absorption of
water, electrolytes and nutrients
 Series/parallel configuration: the venous
drainage from the capillary bed of the
gastrointestinal tract, spleen and pancreas
flows into the portal vein, which provides most
of the blood flow to the hepatic circulation

78.  the hepatic artery provides the remainder of
the blood flow into the liver
 high compliance venous system (25
ml/mmHg/kg) → acts as a reservoir (especially
the liver)
 contains 20% of the blood volume at rest
DR. RAJNEE

79. Neural
 Sympathetic nervous system
– innervation of arterioles, precapillary sphincters and
venous capacitance vessels
– little or no basal sympathetic nervous system tone
– ↑sympathetic nervous system activity → strong
vaso- and venoconstriction →
– redistributes BF, and increases functional circulating
blood volume (“mobilization”)

80. Parasympathetic nervous system
 no innervation of blood vessels
 ↑activity → ↑motility, ↑metabolism→
functional hyperemia due to local vasodilator
metabolites (NO?)
DR. RAJNEE

81. Hormones
 Gastrin, cholecystokinin → functional
hyperemia
 Angiotensin II, vasopressin →vasoconstriction

83.  Autoregulation
– poorly developed → metabolic mechanism
dominates
 Autoregulatory escape
– ↑sympathetic nervous system activity → transient ↓
in BF
– after 2 -4 minutes blood flow returns towards
normal due to accumulation of metabolites
(adenosine) and vasodilation of arterioles
– veins remain constricted
DR. RAJNEE

84. Role in Blood Pressure Control
 Hypotension
– vasoconstriction due to ↑sympathetic nervous
system, AII and VP→ ↑TPR
– venoconstriction →displaces blood centrally →
↑CVP → ↑SV

86. Hepatic, portal arterial and venous
pressures
90
10
5

87. Renal circulation
 At rest 25% CO, 1.2-1.3 l/min
 Pressure drop across the glomerulus is only 1-3 mmHg
 Further drop at the efferent arteriole
 Regulation
– Norepinephrine, Angiotensin II - vasoconstriction
– Dopamine – vasodilatation
– Sympathetic activity (alpha receptor) – vasoconstriction
– Stimulation of renal nerves - increases renin secretion
 Autoregulation is present
– Myogenic effect, NO may be involved
 Renal cortex high blood flow poor O2 extraction but in medulla
low blood flow but high O2 extraction