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Cerebral Circulation

Donald D. Heistad, Hermes A. Kontos

10.1002/cphy.cp020305

Source: Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow

Originally published: 1983

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Anatomy
1.1 Arterial System
1.2 Capillaries, Veins, and Lymphatics
1.3 Blood‐Brain Barrier
1.4 Choroid Plexus and Cerebrospinal Fluid
2 Methods
2.1 Direct Observation of Pial Vessels
2.2 Venous Outflow Techniques
2.3 Cerebral Arterial Inflow
2.4 Diffusible Indicators
2.5 Measurement of Clearance With Electrodes
2.6 Autoradiography
2.7 Microspheres
2.8 Experimental Comparison of Methods
3 Distribution of Segmental Vascular Resistance
4 Neural Regulation
4.1 Innervation
4.2 Neurotransmitters and Neuromuscular Mechanisms
4.3 Effects of Sympathetic Nerves
4.4 Effects of Cholinergic and Peptidergic Nerves
4.5 Reflex Effects of Sympathetic Nerves
4.6 Role of Central Neural Pathways
5 Chemical Regulation
5.1 Effects of Carbon Dioxide and Hydrogen Ion on Cerebral Vessels
5.2 Effects of Arterial Blood PCO2 on Cerebral Blood Flow
5.3 Effects of Oxygen on Cerebral Vessels
5.4 Effects of Oxygen on Cerebral Blood Flow
5.5 Angiotensin, Vasopressin, Oxytocin, and Prostaglandins
6 Metabolic Regulation
6.1 Relationship of Cerebral Function and Blood Flow
6.2 Cerebral Function and Metabolism
6.3 Correlation Between Cerebral Blood Flow and Metabolism
6.4 Mechanisms by Which Metabolism Influences Cerebral Blood Flow
6.5 Autoregulation
6.6 Effects of Atherosclerosis
6.7 Effects of Changes in Hematocrit and Blood Viscosity
7 Conclusion
Figure 1. Figure 1.

Morphological and enzymatic barrier mechanisms for neurotransmitter monoamines (filled arrows) and their immediate precursors (open arrows) in pial and intraparenchymal vessels. MAO, monoamine oxidase; COMT, catechol O‐methyltransferase.

From Hardebo and Owman 147
Figure 2. Figure 2.

Diagrammatic representation of rabbit vertebral, internal, and common carotid arteries superimposed on sagittal section of the head. Bars show concentration of l‐norepinephrine (NE) causing 50% maximum contraction (EC50) of indicated arterial segment. Values are means ± SE.

From Bevan 31. Copyright 1979 by the American Association for the Advancement of Science
Figure 3. Figure 3.

Percent changes from base line in cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral glucose uptake (CMRglu) after intracarotid norepinephrine (50 ng · kg−1 · min−1), intracarotid hypertonic urea (7–10 ml, 2 osM), and intracarotid norepinephrine after intracarotid hypertonic urea.

From MacKenzie et al. 267
Figure 4. Figure 4.

Effect of sympathetic stimulation (dotted line) on CBF during steady‐state changes in arterial pressure (left) and during sudden increase in pressure (right). In steady‐state conditions, sympathetic stimulation attenuates increase in CBF during severe hypertension. Sympathetic stimulation also attenuates the transient increase in CBF occurring after a sudden increase in arterial pressure within the physiological range.

From Busija, Heistad, and Marcus 43, by permission of the American Heart Association, Inc
Figure 5. Figure 5.

Incidence of hemorrhagic and ischemic stroke in denervated hemisphere (D), innervated hemisphere (I), and both hemispheres of stroke‐prone spontaneously hypertensive rats. * P < 0.05 for D vs. I.

From Sadoshima, Heistad, et al. 396, by permission of the American Heart Association, Inc
Figure 6. Figure 6.

Effects of changes in arterial and CSF Pco2 on pial arteriolar caliber in cats. Arterial hypercapnia produces pronounced vasodilatation that is completely counteracted by equivalent decrease in CSF Pco2, although latter change alone has a relatively modest effect on vessel diameter. Values are means ± SE.

Data from Kontos et al. 226
Figure 7. Figure 7.

Diagrammatic representation of distribution of regional hemispheric blood flow in humans under resting conditions and during 7 types of cerebral activity. Closed circles represent flows 20% above mean and open circles show flows 20% below mean. Patterns from top left are distribution of hemispheric flow during 1) resting conditions, 2) low‐intensity electrical cutaneous stimulation of contralateral hand (SENS1), 3) high‐intensity stimulation causing slight pain (SENS2), 4) voluntary movement of contralateral hand, 5) talking, 6) reading, 7) reasoning test, and 8) digit‐span‐backward test.

From Ingvar 185
Figure 8. Figure 8.

Autoradiographs of coronal brain sections at level of striate cortex. A: animal with normal binocular vision. B: animal with bilateral visual deprivation. C: animal with right eye occluded. Arrows point to regions of bilateral assymmetry where occular‐dominance columns are absent. These are presumably areas normally with only monocular input.

From Kennedy et al. 211
Figure 9. Figure 9.

Effect of topical application of adenosine on pial arteriolar diameter of cats. Adenosine dissolved in artificial CSF was microinjected in the immediate vicinity of the arterioles. Values are means ± SE.

From Wahl and Kuschinsky 471
Figure 10. Figure 10.

Diagrammatic representation of relation between CBF and cerebral vascular resistance to perfusion pressure when vascular bed responds passively.
Figure 11. Figure 11.

Diagrammatic representation of relation between CBF and cerebral vascular resistance to perfusion pressure when vascular bed displays autoregulation.
Figure 12. Figure 12.

Effect of supervision of brain surface with fluorocarbon (FC‐80) equilibrated with either 100% oxygen or 100% nitrogen during reduction in mean arterial pressure (MABP) induced by intravenous ATP infusion. Superfusion with fluorocarbon equilibrated with 100% oxygen abolished vasodilatation induced by hypotension, whereas fluorocarbon equilibrated with 100% nitrogen had no effect.

From Kontos et al. 227
Figure 13. Figure 13.

Relation between brain adenosine concentration and mean arterial blood pressure (MABP) during steady‐state hypotension in rats. Regression line and 95% confidence limits are shown.

From Winn et al. 493


Figure 1.

Morphological and enzymatic barrier mechanisms for neurotransmitter monoamines (filled arrows) and their immediate precursors (open arrows) in pial and intraparenchymal vessels. MAO, monoamine oxidase; COMT, catechol O‐methyltransferase.

From Hardebo and Owman 147


Figure 2.

Diagrammatic representation of rabbit vertebral, internal, and common carotid arteries superimposed on sagittal section of the head. Bars show concentration of l‐norepinephrine (NE) causing 50% maximum contraction (EC50) of indicated arterial segment. Values are means ± SE.

From Bevan 31. Copyright 1979 by the American Association for the Advancement of Science


Figure 3.

Percent changes from base line in cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral glucose uptake (CMRglu) after intracarotid norepinephrine (50 ng · kg−1 · min−1), intracarotid hypertonic urea (7–10 ml, 2 osM), and intracarotid norepinephrine after intracarotid hypertonic urea.

From MacKenzie et al. 267


Figure 4.

Effect of sympathetic stimulation (dotted line) on CBF during steady‐state changes in arterial pressure (left) and during sudden increase in pressure (right). In steady‐state conditions, sympathetic stimulation attenuates increase in CBF during severe hypertension. Sympathetic stimulation also attenuates the transient increase in CBF occurring after a sudden increase in arterial pressure within the physiological range.

From Busija, Heistad, and Marcus 43, by permission of the American Heart Association, Inc


Figure 5.

Incidence of hemorrhagic and ischemic stroke in denervated hemisphere (D), innervated hemisphere (I), and both hemispheres of stroke‐prone spontaneously hypertensive rats. * P < 0.05 for D vs. I.

From Sadoshima, Heistad, et al. 396, by permission of the American Heart Association, Inc


Figure 6.

Effects of changes in arterial and CSF Pco2 on pial arteriolar caliber in cats. Arterial hypercapnia produces pronounced vasodilatation that is completely counteracted by equivalent decrease in CSF Pco2, although latter change alone has a relatively modest effect on vessel diameter. Values are means ± SE.

Data from Kontos et al. 226


Figure 7.

Diagrammatic representation of distribution of regional hemispheric blood flow in humans under resting conditions and during 7 types of cerebral activity. Closed circles represent flows 20% above mean and open circles show flows 20% below mean. Patterns from top left are distribution of hemispheric flow during 1) resting conditions, 2) low‐intensity electrical cutaneous stimulation of contralateral hand (SENS1), 3) high‐intensity stimulation causing slight pain (SENS2), 4) voluntary movement of contralateral hand, 5) talking, 6) reading, 7) reasoning test, and 8) digit‐span‐backward test.

From Ingvar 185


Figure 8.

Autoradiographs of coronal brain sections at level of striate cortex. A: animal with normal binocular vision. B: animal with bilateral visual deprivation. C: animal with right eye occluded. Arrows point to regions of bilateral assymmetry where occular‐dominance columns are absent. These are presumably areas normally with only monocular input.

From Kennedy et al. 211


Figure 9.

Effect of topical application of adenosine on pial arteriolar diameter of cats. Adenosine dissolved in artificial CSF was microinjected in the immediate vicinity of the arterioles. Values are means ± SE.

From Wahl and Kuschinsky 471


Figure 10.

Diagrammatic representation of relation between CBF and cerebral vascular resistance to perfusion pressure when vascular bed responds passively.



Figure 11.

Diagrammatic representation of relation between CBF and cerebral vascular resistance to perfusion pressure when vascular bed displays autoregulation.



Figure 12.

Effect of supervision of brain surface with fluorocarbon (FC‐80) equilibrated with either 100% oxygen or 100% nitrogen during reduction in mean arterial pressure (MABP) induced by intravenous ATP infusion. Superfusion with fluorocarbon equilibrated with 100% oxygen abolished vasodilatation induced by hypotension, whereas fluorocarbon equilibrated with 100% nitrogen had no effect.

From Kontos et al. 227


Figure 13.

Relation between brain adenosine concentration and mean arterial blood pressure (MABP) during steady‐state hypotension in rats. Regression line and 95% confidence limits are shown.

From Winn et al. 493
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Article Title: Cerebral Circulation
 

How to Cite

Donald D. Heistad, Hermes A. Kontos. Cerebral Circulation. Compr Physiol 2011, Supplement 8: Handbook of Physiology, The Cardiovascular System, Peripheral Circulation and Organ Blood Flow: 137-182. First published in print 1983. doi: 10.1002/cphy.cp020305