- •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
230 |
J.W. Kiel |
|
|
Flux (PU) IOP (mmHg) MAP (mmHg)
120
100
80
60
40
20
0
160
120
80
40
0
800
600
400
200
0
Cat retina |
|
|
Cat choroid |
|
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Rabbit choroid |
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|
80 |
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(mmHg) |
60 |
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|
40 |
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MAP |
20 |
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0 |
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80 |
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(mmHg) |
60 |
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20 |
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40 |
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IOP |
0 |
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1,000 |
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|
800 |
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(PU) |
600 |
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|
400 |
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Flux |
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200 |
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0 |
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4:10:56 |
4:14:16 |
4:17:36 |
4:32:16 |
4:35:36 |
4:38:56 |
4:42:16 |
12:33:43 |
12:34:33 |
12:35:23 |
Fig. 11.29 Lack of choroidal reactive hyperemia in cat and rabbit [5]
Simulation
12 . 50
2140.00
3100.00
11 . 88
2105.00
375.00
11 . 25
270.00
350.00
10.625
235.00
325.00
10.0
20.0
30.0
Experiment
flux |
|
8 |
Choroid |
(V) |
4 |
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MAP |
(mmHg) |
120 |
80 |
||
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40 |
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0 |
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(mmHg) |
40 |
IOP |
20 |
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0 |
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Simulation |
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1 |
2 |
. 50 |
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2 |
140 |
. 00 |
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3 |
100 |
. 00 |
1: FLOW |
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1: FLOW |
1 |
1 . 88 |
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2 |
105 |
. 00 |
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3 |
75 |
. 00 |
2: MAP |
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2: MAP |
1 |
1 . 25 |
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2 |
70 |
. 00 |
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3 |
50 |
. 00 |
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1 |
0 . 625 |
3: Pch |
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2 |
35 |
. 00 |
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3 |
25 |
. 00 |
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3: Pch |
1 |
0 . 0 |
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2 |
0 . 0 |
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3 |
0 . 0 |
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Experiment
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flux |
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8 |
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(V) |
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Choroid |
4 |
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MAP |
(mmHg) |
0 |
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80 |
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40 |
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0 |
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(mmHg) |
80 |
30 s |
IOP |
40 |
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0 |
Fig. 11.30 Evidence of choroidal myogenic local control [51]
with IOP at 20 mmHg suggests that choroidal blood ßow does a poor job of stabilizing retinal temperature. Indeed, some of that increase in temperature may have been a light-induced reßex, since Parver et al. found that light applied to the contralateral eye increased ipsilateral retinachoroid and scleral temperature as well as an index of choroidal blood ßow; the reßex presumably also works when the ipsilateral eye is lightexposed [61]. Such a reßex suggests that choroidal
blood ßow is not regulated to maintain retinal temperature.
11.4.3 Retina
Evidence of retinal autoregulation comes from different species using various blood ßow measuring techniques and methods of perfusion pressure manipulation (Fig. 11.33). Retinal
11 Local Determinants |
231 |
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IOP (mmHg) MAP (mmHg) IOP (mmHg) MAP (mmHg)
120
100
80
60
40
20
0
30
20
10 |
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0 |
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12:09:35 |
12:11:15 |
1:20:00 |
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100 |
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80 |
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60 |
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40 |
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40 |
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0 |
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30 |
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20 |
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10 |
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0 |
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11:12:04 |
11:12:54 11:13:44 12:06:34 12:07:24 |
12:08:14 |
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(mmHg) |
120 |
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100 |
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80 |
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60 |
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MAP |
40 |
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20 |
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0 |
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(mmHg) |
30 |
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20 |
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IOP |
10 |
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0 |
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1:40 |
3:20 |
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5:00 |
6:40 |
(mmHg) |
120 |
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100 |
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80 |
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60 |
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MAP |
40 |
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20 |
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0 |
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(mmHg) |
30 |
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20 |
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IOP |
10 |
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0 |
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0 |
3:20 |
6:40 |
10:00 |
13:20 |
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Fig. 11.31 Choroidal myogenic mechanism may protect the eye from arterial pressure-dependent changes in IOP (time in seconds) [57]
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40 |
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(°c) |
a |
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7.5 V |
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b |
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7.5 V |
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temp. |
39 |
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Macula |
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- choroidal |
38 |
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0.0 V |
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37 |
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Retinal |
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0.0 V |
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36 |
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20 |
40 |
60 |
80 |
100 |
20 |
40 |
60 |
80 |
100 |
120 |
Intra-ocular pressure (mmHg)
Control response |
Response of nonstimulated eye |
|
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after lidocaine hydrochloride injection |
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TC |
0.5°C |
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ΔΤΒ |
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150 |
mm |
BP |
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Hg |
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50 |
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20 s
Light on contralateral eye
40 |
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Cool |
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Hot |
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Toes |
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18–20°C |
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40°C |
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200 |
39 |
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HR |
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160 |
38 |
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Temperature(°C) |
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120 |
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Heart(beats/min)rate |
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37 |
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80 |
0 |
10 |
20 |
30 0 |
10 |
20 |
30 |
40 |
50 |
60 |
Time (min)
Fig. 11.32 Choroidal thermoregulation. (Upper left) Retinal temperature increases as choroidal blood ßow is reduced by raising IOP in two monkey eyes when retina is illuminated with a lamp powered at 7.5 V and decreased when the lamp is off. (Upper right) Core body temperature range during walking in a cool and hot environment.
(Lower left) Primate conjunctival temperature ( TC) increase during illumination of contralateral eye is unaffected by retrobulbar anesthesia, while blood pressure (BP) and core body temperature ( TB) remain unchanged [59Ð61]
232 |
J.W. Kiel |
|
|
Blood flow (mg/min)
NB ( %)
50
Retina
40
30
20
10
0 |
20 |
40 |
60 |
80 |
100 |
120 |
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Perfusion pressure (cmH2O) |
|||
100
(30 mmHg) (10 mmHg)
80
(50 mmHg)
60
(70 mmHg)
40
(80 mmHg)
20
0 |
20 |
40 |
60 |
80 |
100 |
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Ocular perfusion pressure (mmHg)
140
|
1.20 |
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units) |
1.15 |
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1.05 |
||
(arbitrary |
1.10 |
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1.00 |
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0.95 |
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RBF |
0.90 |
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0.85 |
||
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0.80 |
0.75
0.70
BI. flow (ml/min/100 g)
80 Retina
60
40
20
0
0 |
20 |
40 |
60 |
80 |
100 |
120 |
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Mean BP (mmHg) |
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Control
L-NAME
0 |
20 |
40 |
50 |
65 |
Decrease in perfusion pressure (%)
Fig. 11.33 Retinal blood ßow autoregulation in monkey (top left), piglet before (circles) and after (triangles) ibuprofen (top right), rabbit (bottom left) and cat before and after L-NAME [48, 50, 62Ð64]
autoregulation is perhaps not surprising given the lack of autonomic innervation and the metabolic needs of the retina. However, local control in the retina is by no means simple. In many species, retinal nutrient delivery and waste removal are provided by retinal and choroidal circulations, but some species have a negligible retinal circulation (e.g., rabbits) and others have none (e.g., guinea pigs), and the fovea region of primates lacks retinal vessels despite its high density of metabolically active photoreceptors. Clearly, the link between retinal perfusion and metabolism is complex and varies by species and location, which makes understanding metabolic local con-
trol difÞcult. The negative visual consequences of retinal edema underscore the likely importance of myogenic local control, but this mechanism is difÞcult to study in the in vivo retina though it is evident under in vitro conditions (Fig. 11.4). The contributions of ßow-mediated vasodilation and intercellular conduction are even harder to study and less well understood. Thus, while the evidence for retinal metabolic local control predominates, the other forms of local control may contribute as well.
A counterintuitive phenomenon in the retina is that its oxygen consumption increases in the dark due to increased Na/K ATPase activity
11 Local Determinants |
233 |
|
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|
80 |
Data |
Dark adapted |
|
70 |
Model fit |
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||
(mmHg) |
60 |
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50 |
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40 |
Outer retina |
Inner retina |
2 |
30 |
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PO |
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20 |
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10 |
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0 |
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100 |
80 |
60 |
40 |
20 |
0 |
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% Retinal depth |
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Darkness |
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Daylight |
Optical density |
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V |
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C |
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V |
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Retina |
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Retina |
2 mm temporal of optic nerve, M and SEM,
12 sections. V vitreous, C choroid.
|
80 |
Data |
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70 |
Model fit |
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(mmHg) |
60 |
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50 |
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40 |
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2 |
30 |
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PO |
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20 |
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10 |
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0 |
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100 |
80 |
60 |
40 |
% Retinal depth
|
|
0.07 |
Retinal blood |
flow (g/min) |
0.06 |
0.05 |
||
|
0.04
C
0.03
Dark
Light adapted
20 0
Light
Fig. 11.34 Retinal metabolism and blood ßow increase in darkness [68, 69] (lower right graph data from Bill and Sperber [69])
[65, 66]. In species with a dual retinal blood supply (i.e., retinal and choroidal circulations), the dark-stimulated increase in oxygen consumption is sufÞcient to lower the PO2 of the photoreceptor inner segments to near zero (Fig. 11.34) [67, 68]. There is a corresponding increase in glucose consumption in approximately same location in the dark, and retinal blood ßow is also higher in the dark [69]. This behavior appears to be an example of functional hyperemia, even though the metabolic action is occurring in the outer retina while the blood ßow action is in the inner retina.
A clearer example of functional hyperemia is the retinal response to ßickering light stimulation.
In this case, the increase in retinal blood ßow is associated with increased oxygen consumption indicated by the arteriovenous oxygen difference in paired retinal arteries and veins as well as increased glucose consumption in the inner retina [69Ð71]. Interestingly, there appears to be the greatest increase in retinal blood ßow in the area with the highest density of ganglion cells, consistent with a link between metabolic demand and perfusion [71]. Additional evidence indicating signiÞcant retinal metabolic local control include the increase in retinal blood ßow in response to hypoxia [72] and hypercapnia [73] as well as the decrease in blood ßow in response to hyperoxia [74, 75] (Fig. 11.36) and the reactive hyperemia