Comprehensive Physiology Wiley Online Library

The Cerebral Microcirculation

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Historical Background
2 Architecture
3 Blood–Brain Barrier
4 Regulation of Cerebral Blood Flow
4.1 Metabolic control
4.2 Myogenic control
4.3 Neural control
4.4 Endothelial control
4.5 Humoral control
4.6 Autoregulation
5 Inflammation in the CNS
5.1 Following ischemia and trauma
5.2 During autoimmune disease
6 Age‐Related Changes
7 Conclusion
Figure 1. Figure 1.

A penetrating arteriole surrounded by the Virchow–Robin Space formed by the wall of the arteriole and a leptomeningeal sheath. Once penetrating deeper into the brain, this space disappears and glial endfeet contact the basement membrane surrounding the endothelial cells (from Ref. 100).

Figure 2. Figure 2.

Cellular constituents of the blood brain barrier include endothelial cells, the basement membrane, pericytes and astroctyes. Neurons and microglia also influence the properties of the blood–brain barrier (modified from Ref. [231).

Copyright © 2006, Nature Publishing Group). (See page 10 in colour section at the back of the book)
Figure 3. Figure 3.

Proteins forming tight junctions and adherens junctions between endothelial cells (from Ref. 23).

(Copyright © 2005, Nature Publishing Group). (See page 11 in colour section at the back of the book)
Figure 4. Figure 4.

(A) An electron microscopic image of a typical cortical capillary from the frontoparietal cortex of a Wistar‐Kyoto rat. (B) Graphic reconstruction of the vessel, a, astrocytic endfeet: bm. basement membrane; em, endothelial mitochondria; en. endothelial nucleus; ep, endothelial cytoplasm; 1, capillary lumen; p, pericytes; tj, tight junction (from Ref. [71).* indicates p < 0.05.

Figure 5. Figure 5.

Astrocyte participate in the regulation of synaptic transmission and vascular diameter. They contain receptors for and secrete glutamate. and also are a source of numerous vasoactive mediators including potassium, EETs and prostaglandins (from Ref. 183).* indicates p < 0.05. (See page 11 in colour section at the back of the book)

Figure 6. Figure 6.

Innervation of the cerebral vasculature by sympathetic nerves, parasympathetic nerves, the central pathways and sensory nerves (from Ref. 244).

(Copyright © 2006, American Physiological Society).* indicates p < 0.05. (See page 12 in colour section at the back of the book)a
Figure 7. Figure 7.

Changes in leukocyte rolling and adhesion to cerebral microvessels following stroke (from Ref. 244,314).* indicates p < 0.05.

Figure 8. Figure 8.

The administration of two selective CB2 agonists (O‐1966 and 3853) reduce infarct size following transient cerebral ischemia (from Ref. 314).* indicates p < 0.05.

Figure 9. Figure 9.

The effect of administration of selective CB2 agonists (O‐1966 and 3853) on white cell rolling and adhesion along cerebral microvessels following ischemia (from Ref. 314).* indicates p < 0.05.

Figure 10. Figure 10.

Administration of a CB1 antagonist (SR‐141716), a CB2 antagonist (SR 144528) or a CB2 agonist (O‐1966). had no influence on blood flow during occlusion of the middle cerebral artery. However, administration of the CB2 agonist in combination with the CB1 antagonist significantly enhanced blood flow during occlusion (from 364).

Figure 11. Figure 11.

Administration of a CB2 (CB2+) agonist in combination with a CB1 antagonist (CB1‐) caused a greater reduction in infarct size than either that agonist or antagonist alone (from 364).

Figure 12. Figure 12.

Capillary pathology associated with aging and Alzheimer's Disease. (A) normal capillary profile, (B) basement membrand thickening, (C) perivascular fibrosis, (D) pericytic degeneration (from 7).



Figure 1.

A penetrating arteriole surrounded by the Virchow–Robin Space formed by the wall of the arteriole and a leptomeningeal sheath. Once penetrating deeper into the brain, this space disappears and glial endfeet contact the basement membrane surrounding the endothelial cells (from Ref. 100).



Figure 2.

Cellular constituents of the blood brain barrier include endothelial cells, the basement membrane, pericytes and astroctyes. Neurons and microglia also influence the properties of the blood–brain barrier (modified from Ref. [231).

Copyright © 2006, Nature Publishing Group). (See page 10 in colour section at the back of the book)


Figure 3.

Proteins forming tight junctions and adherens junctions between endothelial cells (from Ref. 23).

(Copyright © 2005, Nature Publishing Group). (See page 11 in colour section at the back of the book)


Figure 4.

(A) An electron microscopic image of a typical cortical capillary from the frontoparietal cortex of a Wistar‐Kyoto rat. (B) Graphic reconstruction of the vessel, a, astrocytic endfeet: bm. basement membrane; em, endothelial mitochondria; en. endothelial nucleus; ep, endothelial cytoplasm; 1, capillary lumen; p, pericytes; tj, tight junction (from Ref. [71).* indicates p < 0.05.



Figure 5.

Astrocyte participate in the regulation of synaptic transmission and vascular diameter. They contain receptors for and secrete glutamate. and also are a source of numerous vasoactive mediators including potassium, EETs and prostaglandins (from Ref. 183).* indicates p < 0.05. (See page 11 in colour section at the back of the book)



Figure 6.

Innervation of the cerebral vasculature by sympathetic nerves, parasympathetic nerves, the central pathways and sensory nerves (from Ref. 244).

(Copyright © 2006, American Physiological Society).* indicates p < 0.05. (See page 12 in colour section at the back of the book)a


Figure 7.

Changes in leukocyte rolling and adhesion to cerebral microvessels following stroke (from Ref. 244,314).* indicates p < 0.05.



Figure 8.

The administration of two selective CB2 agonists (O‐1966 and 3853) reduce infarct size following transient cerebral ischemia (from Ref. 314).* indicates p < 0.05.



Figure 9.

The effect of administration of selective CB2 agonists (O‐1966 and 3853) on white cell rolling and adhesion along cerebral microvessels following ischemia (from Ref. 314).* indicates p < 0.05.



Figure 10.

Administration of a CB1 antagonist (SR‐141716), a CB2 antagonist (SR 144528) or a CB2 agonist (O‐1966). had no influence on blood flow during occlusion of the middle cerebral artery. However, administration of the CB2 agonist in combination with the CB1 antagonist significantly enhanced blood flow during occlusion (from 364).



Figure 11.

Administration of a CB2 (CB2+) agonist in combination with a CB1 antagonist (CB1‐) caused a greater reduction in infarct size than either that agonist or antagonist alone (from 364).



Figure 12.

Capillary pathology associated with aging and Alzheimer's Disease. (A) normal capillary profile, (B) basement membrand thickening, (C) perivascular fibrosis, (D) pericytic degeneration (from 7).

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Ronald F Tuma. The Cerebral Microcirculation. Compr Physiol 2011, Supplement 9: Handbook of Physiology, The Cardiovascular System, Microcirculation: 485-520. First published in print 2008. doi: 10.1002/cphy.cp020411