- •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
234 |
J.W. Kiel |
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Oxygen tension (mmHg)
Optical density
60
50
40
30
20 |
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Artery |
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10 |
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Vein |
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0 |
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0 |
2 |
4 |
6 |
8 |
10 |
12 |
14 |
16 |
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Flicker frequency (Hz) |
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Darkness |
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Flicker, 8 Hz |
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V |
C |
V |
C |
Retina |
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Retina |
1 mm. temporal of optic nerve, M and SEM, 16 sections. V = vitreous, C = choroid.
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0.07 |
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Retinal blood |
flow (g/min) |
0.06 |
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0.05 |
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0.04 |
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0.03 |
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Dark |
8 Hz |
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60 |
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index (%) |
40 |
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in capillary flow |
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20 |
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Change |
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Parafovea |
Perifovea |
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0 |
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0.2 |
0.4 |
0.6 |
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Normalized foveal eccentricity [disc-fovea distance] |
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Fig. 11.35 Flickering light stimulation increases retinal arteriovenous oxygen difference (top left) and inner retinal glucose uptake (bottom left) and elicits a retinal
functional hyperemia (right top and bottom) [69Ð71] (upper right graph data from Bill and Sperber [69])
after brief (Fig. 11.29) and long periods of ischemia (Fig. 11.37) [56]. Surprisingly, the retinal pressure-ßow relationships under lightand dark-adapted conditions have not been determined, but it seems likely that the dark-adapted curve would be shifted upward due to the heightened oxygen consumption. Similarly, reactive hyperemic responses to brief ischemic periods would be expected to be larger in the dark (Fig. 11.35).
11.4.4 Ciliary Body
While the retina has essentially one function (processing light information for the central nervous system) with a dual blood supply, the ciliary body has two functions (accommodation and aqueous secretion) with a single blood supply. Distinguishing between ciliary muscle and secretory
tissue is fairly straightforward by histology, but difÞcult in vivo, and measuring the blood ßow to the two tissue types is even harder. Microsphere measurements at normal and high IOP suggest that both ciliary muscle and ciliary processes autoregulate, but the measurements vary widely, perhaps due to the small number of spheres that can be trapped in such a small amount of tissue (Fig. 11.38).
Laser Doppler ßowmetry measurements in the rabbit also show evidence of ciliary autoregulation. However, it is also clear that the ciliary circulation is under neural control since ganglionic blockade caused an upward and leftward shift in the pressure-ßow relationship indicative of tonic neuroconstrictor tone (Fig. 11.39). This is an interesting example of the interplay between neural and local control. Ciliary blood ßow provides the oxygen and nutrient delivery to support aqueous production, and ciliary blood ßow can
11 Local Determinants |
235 |
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(%) |
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PBS |
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100 |
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120 |
Velocity |
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# |
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g) |
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100 |
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80 |
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(ml/min/100 |
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80 |
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* |
* |
* |
* |
* |
* |
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60 |
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60 |
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flow |
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120 |
Diameter |
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# |
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(n = 4) |
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100 |
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blood |
40 |
|
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(n = 10) |
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Retinal |
|
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80 |
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* |
* |
* |
* |
* |
* |
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120 |
RBF |
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# |
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20 |
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(n = 3) |
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100 |
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80 |
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* |
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0 |
50 |
100 |
150 |
200 |
250 |
300 |
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* |
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Arterial blood oxygen tension (mmHg) |
|
|||||
60 |
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|
||||||
|
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* |
|
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|
|
|
|
|
|
|
|
|
||
|
|
|
|
|
|
* |
|
|
|
|
|
|
|
|
|
|
|
||
40 |
|
|
|
* |
* |
* |
|
|
|
|
|
|
|
|
|
|
|
||
120 |
WSR |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
# |
# |
|
|
|
|
|
|
|
|
PBS |
|
|
|
|
|
|
|
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|
|
|
|
|
|
|
|
|
|
|||
|
|
|
|
|
|
|
|
|
|
(%) |
|
|
|
|
|
L-NAME |
|||
80 |
|
|
* |
|
|
|
|
|
|
|
|
|
|
|
|
||||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
D-NAME |
|||||
|
|
|
|
|
|
|
|
|
|
120 |
|
|
|
|
|
||||
60 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
−10 |
|
0 |
|
|
|
10 |
|
|
20 |
30 |
|
Diameter |
|
|
|
|
|
||
|
|
|
|
|
|
Time (min) |
|
|
110 |
|
|
|
|
|
|||||
|
|
|
|
|
|
|
|
|
|
|
|
|
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|
|||||
(%) |
|
|
|
|
|
|
|
|
|
PBS |
100 |
|
|
|
|
|
|
|
|
120 |
D |
|
|
|
|
|
|
|
|
|
150 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
L-NAME |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
Velocity |
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
125 |
|
|
|
|
|
|
|
150 |
V |
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
150 |
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
|
RBF |
|
|
|
|
|
|
200 |
RBF |
|
|
|
|
|
|
|
|
|
|
125 |
|
|
|
|
|
||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|||
|
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
120 |
WSR |
|
|
|
|
|
|
150 |
WSR |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
||
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
80 |
MABP |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
110 |
|
|
|
|
|
|||
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
120 |
MABP |
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
80 |
|
|
|
|
|
|
|
|
|
|
|
90 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
100 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
RVR |
|
|
|
|
|
|
|
|
|
|
75 |
RVR |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
40 |
|
|
|
|
|
|
|
|
|
|
|
50 |
|
|
|
|
|
|
|
|
−5 |
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
|
0 |
|
5 |
|
10 |
|
15 |
20 |
|
−10 |
−5 |
0 |
5 |
10 |
15 |
20 |
|||
|
|
|
|
Time (min) |
|
|
|
|
|
|
|
|
Time (min) |
|
|
|
|||
Fig. 11.36 Feline retinal blood ßow responses in cats consistent with metabolic local control. Retinal perfusion decreases during hyperoxia (top left and right) and
increases during hypoxia (bottom left) and hypercapnia (bottom right) [72Ð75]
