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Cerebral Blood Flow

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posted:
11/13/2011
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Cerebral Blood Flow

Anatomy of Cerebral Circulation

Ophthalmic v.

•Activation of endothelial cells and glia occurs at least 2

days after ischemia, and capillary buds form by 7 days.

•Microvascular density, which relates to newly formed

vessels, correlates with the survival time after the onset of

ischemic stroke in humans

acidic and basic fibroblast growth facto (aFGF and

bFGF), transforming growth factor (TGF), vascular

endothelial growth factor (VEGF), platelet-derived

growth factor (PDGF), platelet-derived endothelial cell

growth factor (PD-ECGF), insulin-like growth factor

(IGF)

Autoregulation

•Autoregulation of blood flow is a regulatory mechanism that

allows blood flow in most vascular beds to remain relatively

constant during variations of arterial pressure.

•This is particularly well developed in the brain since it requires

a high degree of homeostasis with respect to a balance of tissue

nutrients and fluids









Limits of Autoregulation

• Impaired Cerebral Vascular Perfusion

• Disruption of the Blood-Brain Barrier

Mechanism of Autoregulation



• Myogenic Hypothesis

– Smooth muscle in resistance

arteries

• Metabolic Influence

– O2, CO2, H+, Adenosine, K+ and

Ca2+

– A definitive role for any one of

these factors remains to be

demonstrated.

• Endothelial Factors

– Endothelium

– Endothelium derived relaxing

factor (nitric oxide), Endothelium

derived contracting factor

Regulation of Cerebral Blood Flow by O2

Regulation of Cerebral Blood Flow by CO2

Modulation of Autoregulation





• Autonomic Nerves

– Sympathetic

– Parasympathetic

– Trigeminovascular System

• The Renin-Angiotensin System

– Angiotensin

– similar to sympathetic regulation

Regulation of Cerebral Blood Flow by

The Sympathetic Nervous System

Regulation of Cerebral Blood Flow by

The Parasympathetic Nervous System



Direct stimulation of the facial nerve leads to an

increase in total cranial blood flow, however the

phsiological role is not clear. The nerves are not

directly involved in the most basic

cerebrovascular responses, such as hypoxic or

hypercapnic vasodilation, nor do thay appear to

play a role in autoregulation

Regulation of Cerebral Blood Flow by The

Trigeminovascular System



This system is the sole sensory innervation of

the cerebral vessels. Its function does not

appear to be in the maintenance of resting

cerebral flow. In situations of abnormal

physiology, this system comes into play by

mediating vasodilation.

Consequence of Chronic Hypertension

The autoregulatory plateau of the pressure-flow relation is shifted

to the right in hypertensive patients and experimental animals so

that cerebral blood flow may be normal despite very high levels of

blood pressure

Vasoactive Mediators of Cerebral Vessels

• Amines + vasoconstriction

– Norepinephrine (+) - vasorelaxation

– Serotonin (+-)

– Histamine (-)

– Dopamine (-)

– Acetylcholine (-)

• Lipid Mediators

– Eicosanoids

• Prostacyclin (-)

• Thromboxane A2 (+)

• Prostaglandins (PGD2, PGE2(-), PGF2(+))

– Leukotrienes (+)

– Platelet-Activating Factor (- +)

• Peptides

– Vasodilator Peptides (-)

• Vasoactive Intestinal Peptide (VIP)

• Calcitonin Gene-Related Peptide (CGRP)

• Adrenomedullin

• Substance P (SP)

• Bradykinin

– Vasoconstrictor Peptides (+)

• Neuropeptide-Y (NPY)

• Angiotensin-II (ATII)

• Endothelin-1 (ET1)

• Vasopressin (VP)

• Purine Nucleotides (-)

– Adenosine

– ADP and ATP

• Gases (-)

– Nitric Oxide (NO)

– Carbon Monoxide (CO)

Biology of Cerebral Vascular

Muscle

Cerebral Microcirculation

Cerebral Spinal Fluid

•Formed at the choroid plexus and drained into

the peripheral blood stream at the arachnoid villi.

•CSF volume is completely cleared via this bulk

flow process in the human brain every 4-5 hr.

Blood-Brain Barrier

Edema



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