- •Ocular Blood Flow
- •Contents
- •1: Anatomy of the Ocular Vasculatures
- •Core Messages
- •1.1 Limbus and Conjunctiva
- •1.1.1 Cornea
- •1.1.2 Vasculature Distribution in the Anterior Segment
- •1.1.3 The Conjunctiva
- •1.1.3.1 The Conjunctival Arterial Supply
- •1.1.3.2 The Conjunctival Veins
- •1.2 Uveal Tract
- •1.2.1 The Iris
- •1.2.1.1 The Major Arterial Circle of the Iris
- •1.2.2 Ciliary Body and Processes
- •1.2.3 Choroid and Suprachoroid
- •1.2.3.1 Development of the Choroidal Vasculature
- •1.2.3.2 Arteries
- •1.2.3.3 Choroidal Veins (Vortex Veins)
- •1.2.3.4 Choriocapillaris
- •1.3 Optic Nerve Vasculature
- •1.4 Retina
- •1.4.1 Development of the Retinal Vasculature
- •1.4.2 Adult Retinal Vasculature
- •1.4.3 Nonprimate Adult Retinal Vasculatures
- •1.5 Conclusions
- •References
- •Core Messages
- •2.1 Introduction
- •2.3 Stochastic Error in the Entrapment of Microspheres
- •2.4 Methodological Errors and Practical Advice
- •2.4.1 Size of the Microspheres
- •2.4.2 Physical Characteristics of Microspheres
- •2.4.4 Dissection
- •2.4.5 Detection of RM and NAM
- •2.4.6 Detection of CM and FM
- •2.5 Biological Variation
- •2.5.1 Blood Pressure
- •2.5.3 Arterial Blood Gases
- •2.5.4 Other Possible Causes for Biological Variability
- •2.6 Summary for the Clinician
- •References
- •3: Laser Doppler Flowmetry in Animals
- •Core Messages
- •3.1 Introduction
- •3.2 History
- •3.3 Theory
- •3.4 Validation
- •3.5 Calibration
- •3.6 Zero Offset
- •3.7 Effects of Oxygen
- •3.9 Measurement Depth and Sampling Volume
- •3.10 Caveats
- •References
- •4: Oxygen Measurements in Animals
- •Core Messages
- •4.1 Introduction
- •4.2.1 Oxygen Electrodes
- •4.2.2 Hypoxyprobe
- •4.2.3 Magnetic Resonance Imaging
- •4.2.4 Phosphorescence Decay
- •4.2.5 Oximetry
- •4.3.1 Vitreal Oxygen
- •4.3.2 Intraretinal Oxygen
- •4.4 Oxygen in Avascular Retinas
- •4.5 Analysis of Retinal Oxygen Utilization
- •4.5.1 Fick Principle Analyses
- •4.5.4 Other Diffusion Models
- •4.6 Physiological Variations in Retinal Oxygen
- •4.6.1 Light
- •4.6.2 Hypoxia
- •4.6.3 Hyperoxia
- •4.6.4 Hypercapnia
- •4.7 Pathophysiology and Retinal Oxygen
- •4.7.1 Vascular Occlusion
- •4.7.2 Diabetes
- •4.7.3 Retinal Detachment
- •4.7.4 Retinal Degenerative Diseases
- •4.7.5 Retinopathy of Prematurity
- •4.8 Retinal Molecular Changes Related to Oxygen
- •4.9 Oxygen in the Optic Nerve Head
- •References
- •Core Messages
- •5.1 Measuring Technique
- •5.2 Normal Values
- •5.3 Retinal Pathologies
- •5.3.1 Diabetes Mellitus
- •5.3.2 Central Retinal Vein Occlusion
- •5.4 Summary
- •References
- •Core Messages
- •6.1 Introduction
- •6.1.1 Anatomy
- •6.3 Vessel Diameter Measurements Based on Photographic and Digitally Stored Images
- •6.3.1 Basics for Measurements on Stored Images
- •6.3.1.1 Measuring Principle
- •6.3.1.4 Problems and Measuring Errors
- •6.3.1.5 Physiological Variability of Vessel Diameter
- •6.3.2 Methods
- •6.3.2.2 Microdensitometry Based on Photographic Negatives
- •6.3.2.3 Measurements Based on Digital Images
- •6.4 Diameter Assessment for Blood Flow
- •6.4.1 Assessment of Flow by Use of Doppler Technique (CLBF)
- •6.5 Retinal Vessel Analysis
- •6.5.1 Basics of Retinal Vessel Analysis
- •6.5.2 Static Vessel Analysis
- •6.5.3 Results and Limits of Static Vessel Analysis
- •6.5.4 Results and Limits of Dynamic Vessel Analysis
- •6.5.4.1 Stimulation with Flicker Light
- •6.5.4.2 Other Provocation Tests
- •6.5.5 Systems Available for Dynamic Vessel Analysis
- •6.6 Further Perspectives
- •References
- •Core Messages
- •7.1 Introduction
- •7.2 Retinal Laser Doppler Velocimetry
- •7.2.1 The Doppler Effect
- •7.2.2 Electric Field Scattered by Singly Scattering Particles Moving in a Capillary Tube
- •7.2.5 Experimental Test of the Bidirectional LDV Technique
- •7.2.7 The DSPS for RBCs Moving in a Retinal Vessel
- •7.2.7.1 Multiple Scattering of Blood
- •7.2.7.2 DSPS from RBCs Flowing in a Glass Capillary Tube
- •7.2.7.3 DSPS from Human Retinal Vessels
- •7.2.7.4 Exploring the Scattering Process
- •7.2.9 Instrumentation
- •7.2.10 Blood Flow in Retinal Vessels
- •7.2.12 Limitations, Safety, and Future Directions of the LDV Technique
- •7.2.13 Physiologic and Clinical Applications (Brief Overview)
- •7.3.1 The DSPS for RBCs Moving in the Microvascular Bed of a Tissue
- •7.3.2 Hemodynamic Parameters Derived from the DSPS
- •7.3.3 Detection Scheme for Optic Nerve and Subfoveal Choroidal Blood Flow
- •7.3.4 Critical Questions Regarding the Application of LDF to Ocular Blood Flow
- •7.3.4.1 LDF Sample Volume
- •7.3.4.2 Linearity of LDF
- •7.3.4.3 Scattering Scheme
- •7.3.5 Reproducibility of LDF
- •7.3.6 Applications of LDF
- •7.4 Summary for the Clinician
- •References
- •8: Color Doppler Imaging
- •Core Messages
- •8.1 Principles
- •8.2 Instrumentation
- •8.3 Procedure
- •8.4 Outcome Variables
- •8.5 Reproducibility
- •8.6 Physiological and Pharmacological Stimuli
- •8.7 Results in Patients with Disease
- •8.8 Advantages and Limitations
- •References
- •9: Other Approaches
- •Core Messages
- •9.1 Blue Field Entoptic Technique
- •9.1.1 Laser Speckle Technique
- •9.1.2 Pulsatile Ocular Blood Flow
- •9.1.2.1 Laser Interferometry
- •References
- •10: Systemic Determinants
- •Core Messages
- •10.1 Introduction
- •10.1.1 Ocular and Systemic Blood Flow
- •10.2 Local Skin Cooling Effect
- •10.2.1 Choroidal Blood Flow
- •10.2.2 Retinal Blood Flow
- •10.3 Aerobic Exercise
- •10.3.1 Choroidal Blood Flow
- •10.3.2 Macular Blood Flow
- •10.3.3 Retinal Blood Flow
- •10.4 Neural Activation
- •10.4.1 Valsalva Maneuver
- •10.4.2 Nicotine
- •10.5 Blood Pressure Versus Ocular Perfusion Pressure
- •10.5.1 Increased Ocular Perfusion Pressure
- •10.5.1.1 Choroidal Blood Flow
- •10.5.2 Decreased Ocular Perfusion Pressure
- •10.5.2.1 Choroidal Blood Flow
- •10.5.2.2 Optic Nerve Head Blood Flow
- •10.5.3 Neural Retinal Function
- •10.6 Blood Gases
- •10.6.1 Hyperoxia and Blood Flow
- •10.6.3 Hypoxia and Pulsatile Choroidal Blood Flow
- •10.6.4 Hyperoxia, Hypercapnia, and Retinal Function
- •10.6.5 Hypoxia, Hyperoxia, and Retinal Function
- •10.7 Regional Choroidal Perfusion
- •10.7.1 Cones Versus Rods: Structure and Function
- •10.7.2 Choroidal Angioarchitecture
- •10.7.3 Dark Adaptation
- •10.7.4 Protracted Blue Flicker
- •10.8 Aging
- •10.8.1 Structure
- •10.8.2 Blood Flow
- •10.8.3 Retinal Function
- •References
- •11: Local Determinants
- •Core Messages
- •11.1 Introduction
- •11.2 Ocular Perfusion Pressure, IOP, and the Ocular Starling Resistor Effect
- •11.3 Types of Local Control
- •11.3.1 Myogenic Local Control
- •11.3.2 Metabolic Local Control
- •11.3.3 Flow-Mediated Vasodilation
- •11.3.4 Flow Control by Intercellular Conduction
- •11.4 Ocular Local Control
- •11.4.1 Optic Nerve Head (ONH)
- •11.4.2 Choroid
- •11.4.3 Retina
- •11.4.4 Ciliary Body
- •11.4.5 Iris
- •11.5 Caveats
- •11.6 Summary for the Clinician
- •References
- •12: Neural Control of Ocular Blood Flow
- •Core Messages
- •12.1 Overview of Ocular Blood Supplies and Their Neural Control
- •12.2 Neural Control of Optic Nerve and Retinal Blood Flow
- •12.3 Neural Control of Iridial and Ciliary Body Blood Flow
- •12.4 Neural Control of Blood Flow in Orbital Glands
- •12.5 Neural Control of Choroidal Blood Flow
- •12.5.1 Importance of the Choroid
- •12.5.2 Choroidal Innervation: Overview of Anatomy
- •12.5.3 Facial Nucleus Parasympathetic Input
- •12.5.3.4 Choroidal Autoregulation and the PPG Input to Choroid – Mammals
- •12.5.3.8 Choroidal Autoregulation and the PPG Input to Choroid – Birds
- •12.5.4 Oculomotor Nucleus Parasympathetic Input
- •12.5.4.1 Ciliary Ganglion Circuitry – Mammals
- •12.5.4.2 Function of the EW-Ciliary Ganglion Circuit – Mammals
- •12.5.4.3 Ciliary Ganglion Circuitry – Birds
- •12.5.4.4 Function of vSCN-EWM-Ciliary Ganglion Circuit – Birds
- •12.5.5 Sympathetic Superior Cervical Ganglion Input
- •12.5.6 Trigeminal Sensory Input
- •12.5.7 Intrinsic Choroidal Neurons
- •12.5.8 Disturbed Neural Control of Choroidal Blood Flow in Aging and Retinal Disease
- •12.5.8.1 Effect of Aging on Retina and Choroid
- •12.5.8.2 Effect of Disease on Retina and Choroid
- •References
- •13: Endothelial and Adrenergic Control
- •Core Messages
- •13.1 Nitric Oxide
- •13.2 Endothelins
- •13.3 Arachidonic Acid Metabolites
- •13.4 Adrenergic Control
- •13.5 Alpha Receptors
- •13.6 Topical Administration
- •13.6.1 Clonidine
- •13.6.2 Brimonidine
- •13.6.3 Beta Receptors
- •13.6.4 Timolol
- •13.6.5 Human Studies
- •13.6.6 Betaxolol
- •13.6.7 Human Studies
- •13.6.8 Levobunolol
- •13.6.9 Carteolol
- •13.6.10 Serotonin
- •13.7 Carbonic Anhydrase Inhibitors
- •13.8 Acetazolamide
- •13.9 Dorzolamide
- •13.10 Retrobulbar Blood Flow
- •13.11 Retinal Blood Flow
- •13.12 Choroidal and Optic Nerve Head Blood Flow
- •13.13 Brinzolamide
- •References
- •Core Messages
- •14.1 Introduction
- •14.2 Retinal Ischemia Basic Mechanisms
- •14.3 Oxidative Stress
- •14.6 Animal Studies Relating Ischemia, Glaucoma, and Neuroprotection
- •14.6.1 Retinal Ischemia
- •14.6.6 Role of Mitochondria (Fig. 14.6)
- •References
- •Core Messages
- •15.1 Introduction
- •15.2 Retinal Blood Flow in Diabetes
- •15.3 Retinal Hypoperfusion
- •15.3.1 Mechanisms of Hypoperfusion
- •15.3.1.1 Glycaemic Control
- •15.3.1.2 Protein Kinase C
- •15.3.1.3 Ion Channel Dysfunction
- •15.4 Retinal Hyperperfusion
- •15.4.1 Mechanisms of Hyperperfusion: A Link to Hypoperfusion, Tissue Hypoxia and Retinal Leukostasis?
- •15.4.2 Retinal Autoregulation in Diabetes
- •15.5.1 Basement Membrane Thickening
- •15.5.3 Microaneurysms
- •15.5.4 Capillary Acellularity
- •15.6 Retinal Blood Flow and Vision Loss in Diabetic Retinopathy
- •15.6.1 Diabetic Macular Oedema
- •15.6.2 Proliferative Diabetic Retinopathy
- •15.7 Conclusions
- •15.8 Summary for the Clinician
- •References
- •Core Messages
- •16.1 Introduction
- •16.2 Choroidal Blood Flow
- •16.3 Systemic Vascular Factors and AMD
- •16.5 Choroidal Hemodynamic Changes in AMD
- •16.5.1 Choroidal Histopathological Vascular Changes in AMD
- •16.5.1.1 Choriocapillaris and Bruch’s Membrane in Aging and AMD
- •16.5.2 Choroidal Microcirculation in AMD
- •16.5.2.2 Choroidal Watershed Zones and Neovascularization
- •16.5.2.3 Laser Doppler Flowmetry Evaluation
- •References
- •Core Messages
- •17.1 Introduction
- •17.2 Potential Mechanisms of Ischaemic Damage in Glaucoma
- •17.2.2 Autoregulatory Disturbances
- •17.2.3 Mechanical Compression or Collapse of Vessels
- •17.2.4 Atherosclerosis
- •17.2.5 Vascular Endothelial Factors
- •17.2.6 Barriers to Nutrient Delivery
- •17.2.7 Circulating Vasoconstrictors
- •17.3 Evidence Base Supporting the Importance of Ischaemia in Glaucoma
- •17.3.1 Association and Causality
- •17.3.1.1 Reduction in Optic Nerve Head Blood Flow
- •17.3.1.2 Blood Pressure, Intraocular Pressure and Perfusion Pressure
- •17.3.1.3 Nocturnal Hypotension
- •17.3.1.4 Vasospasm
- •17.3.1.5 Endothelin and Other Circulating Peptides
- •17.3.2 Effects of Treatment
- •17.3.2.1 Calcium Channel Blockers
- •17.3.2.2 Topical Adrenergic Antagonists
- •17.3.2.4 Prostaglandin Analogues
- •17.4 Experimental Models of Ischaemia Relating to Glaucoma
- •17.4.1 Acute Ischaemia
- •17.4.2 Chronic Ischaemia
- •17.5 Summary
- •17.5.1 Diversity of Evidence
- •17.5.2 Evidence Base Compared to Intraocular Pressure
- •17.5.3 Requirements to Strengthen Evidence Base
- •References
- •Core Messages
- •18.1 Retinal Diseases
- •18.2 Uveitis
- •18.3 Optic Nerve Disorders
- •18.4 Systemic Diseases
- •References
- •Core Messages
- •19.1 Atherosclerosis
- •19.1.1 Pathogenesis of Atherosclerosis
- •19.1.2 Internal Carotid Artery Disease (ICA)
- •19.1.3 Effects on the Ocular Circulation
- •19.1.3.1 Retinal Artery Occlusion
- •Clinical Characteristics
- •Diagnosis
- •Mortality/Morbidity
- •19.1.3.2 Retinal Vein Occlusion (RVO)
- •Clinical Characteristics
- •Pathogenesis
- •Diagnosis
- •19.1.3.3 Ischemic Optic Neuropathy
- •Clinical Characteristics
- •Mortality/Morbidity
- •19.1.3.4 Asymptomatic Retinal Emboli
- •Background
- •Pathophysiology
- •19.2 Vasculitis
- •19.2.1 Takayasu’s Arteritis (Aortic Arch Syndrome)
- •19.2.1.1 Pathophysiology
- •19.2.1.2 Clinical Characteristics
- •19.2.1.3 Epidemiology
- •19.2.2 Behcet’s Disease
- •19.2.2.1 Clinical Characteristics
- •19.2.2.2 Pathogenesis
- •19.2.2.3 Diagnosis
- •19.2.2.4 Epidemiology
- •19.2.3 Thromboangiitis Obliterans
- •19.2.3.1 Diagnosis and Clinical Characteristics
- •19.2.3.2 Treatment
- •19.2.4 Temporal Arteritis
- •19.2.4.1 Epidemiology
- •19.2.4.2 Pathogenesis
- •19.2.4.3 Ocular Manifestations
- •19.2.5 Wegener’s Granulomatosis
- •19.2.5.1 Pathogenesis
- •19.2.5.2 Ocular Manifestation
- •19.2.5.3 Diagnosis
- •19.2.6 Kawasaki Disease
- •19.2.6.1 Clinical Characteristics
- •19.2.6.2 Diagnosis
- •19.3 Vascular Malformations
- •19.3.1.1 Diagnosis
- •19.3.1.2 Pathophysiology
- •19.4 Systemic Hypertension and Treatment
- •19.4.1 Etiology
- •19.4.1.1 Primary Hypertension
- •19.4.1.2 Secondary Hypertension
- •19.4.2 Pathophysiology
- •19.4.3 Pathology and Complications
- •19.4.4 Symptoms and Signs
- •19.4.5 Diagnosis of Hypertension
- •19.4.5.1 History
- •19.4.5.2 Physical Examination
- •19.4.5.3 Testing
- •19.4.6 Prognosis
- •19.4.7 General Treatment
- •19.4.7.2 Drugs
- •19.5 Hypertensive Retinopathy
- •19.5.2 Pathophysiology
- •19.5.3 Blood Pressure
- •19.5.3.1 The Risk of Stroke
- •19.5.3.2 The Risk of Coronary Heart Disease
- •19.5.4 Treatment
- •19.5.4.1 ACE Inhibitors and the Eye
- •References
- •Index
Anatomy of the Ocular Vasculatures |
1 |
|
Gerard A. Lutty, Imran Bhutto,
and Donald Scott McLeod
Core Messages
•The human eye is an incredible assembly of unique types of tissues, each of which has its own requirements in terms of blood supply.
•The major source of blood for the anterior eye is the anterior ciliary arteries, whereas the central retinal artery and the posterior ciliary arteries, both originating from the ophthalmic artery, is the supply for the posterior eye.
•The iris receives its arterial blood supply from the major arterial circle (MAC). The iris vessels are radially oriented with slightly sinuous courses, which allow them to accommodate to the movements of the pupil. The iris venous channels roughly follow the arterial ones. The collector trunks from these
G.A. Lutty, Ph.D. (*) • D.S. McLeod
Wilmer Ophthalmological Institute, Johns Hopkins Hospital, M041 Smith Building, 400 North Broadway, Baltimore, MD 21287-9115, USA
e-mail: glutty@jhmi.edu; dmcleod1@jhmi.edu
I. Bhutto, M.D., Ph.D.
Wilmer Ophthalmological Institute, Johns Hopkins
Hospital, M041 Smith Building, 400 North Broadway,
Baltimore, MD 21287-9115, USA
Department of Ophthalmology, Wilmer Eye Institute, Johns Hopkins Hospital, M041 Smith Building, 400 North Broadway, Baltimore, MD 21287-9115, USA e-mail: ibhutto1@jhmi.edu
veins enter the ciliary body, where the blood then drains into the vortex system and the ciliary plexus.
•The ciliary body, a part of the uveal tract, is the circumferential tissue posterior to the iris composed of the ciliary muscle and ciliary processes. Its blood supply is the same as iris but the capillaries of the ciliary processes are large and fenestrated like the choriocapillaris.
•There are two sources of blood and nutrient supply for the human retina: the central retinal artery and the choroidal blood vessels. The choroid receives the greatest blood flow (65-85%), which is vital for maintenance of the outer retina. The remaining 20-30% flows to the retina through the central retinal artery in the optic nerve head to nourish the inner retinal layers.
•There are three layers of capillaries in retina: 1) the radial peripapillary capillaries (RPCs) around the optic nerve head only; 2) the inner or superficial plexus; and 3) the outer or deep layer of capillaries. The retinal vasculature is end-arterial: blood moves from artery to arteriole to capillary and precapillary venules drain into venules and then veins. A blood-retinal barrier exists.
•The only avascular area of retina is the foveal avascular zone where the foveolar
L. Schmetterer, J.W. Kiel (eds.), Ocular Blood Flow, |
3 |
DOI 10.1007/978-3-540-69469-4_1, © Springer-Verlag Berlin Heidelberg 2012 |
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