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ABSTRACT: To determine the effect of several common general anesthetics on intraocular pressure (IOP) after experimental aqueous outflow obstruction in the rat.
A single episcleral vein injection of hypertonic saline was used to sclerose aqueous humor outflow pathways and produce elevated IOP in Brown Norway rats. Animals were housed in either standard lighting or a constant low-level light environment. Awake IOPs were determined using a TonoPen (Mentor, Norwell, MA) immediately before induction of anesthesia by either isoflurane, ketamine, or a mixture of injectable anesthetics (xylazine, ketamine, and acepromazine). For each anesthetic, IOPs were measured immediately after adequate sedation (time 0) and at 5-minute intervals, up to 20 minutes. RESULTS; Awake IOPs ranged from 18 to 52 mm Hg. All anesthetics resulted in a statistically significant (P: < 0.01) reduction in measured IOP at every duration of anesthesia when compared with the corresponding awake IOP. With increasing duration of anesthesia, measured IOP decreased approximately linearly for both the anesthetic mixture and isoflurane. However, with ketamine, IOP declined to 48% +/- 11% (standard lighting) and 60% +/- 7% (constant light) of awake levels at 5 minutes of anesthesia, where it remained stable. In fellow eyes, the SD of the mean IOP in animals under anesthesia was always greater than the corresponding SD of the awake mean. Anesthesia's effects in normal eyes and eyes with elevated IOP were indistinguishable.
All anesthetics resulted in rapid and substantial decreases in IOP in all eyes and increased the interanimal variability in IOPs. Measurement of IOP in awake animals provides the most accurate documentation of pressure histories for rat glaucoma model studies.
Investigative Ophthalmology & Visual Science 11/2000; 41(11):3415-9. · 3.60 Impact Factor
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ABSTRACT: To determine the diural intraocular pressure (IOP) response of Brown Norway rat eyes after sclerosis of the aqueous humor outflow pathways and its relationship to optic nerve damage.
Hypertonic saline was injected into a single episcleral vein in 17 animals and awake IOP measured in both the light and dark phases of the circadian cycle for 34 days. Mean IOP for light and dark phases during the experimental period were compared with the respective pressures of the uninjected fellow eyes. Optic nerve cross sections from each nerve were graded for injury by five independent masked observers.
For fellow eyes, mean light- and dark-phase IOP was 21 +/- 1 and 31 +/- 1 mm Hg, respectively. For four experimental eyes, mean IOPs for both phases were not altered. Six eyes demonstrated significant mean IOP elevations only during the dark phase. Of these, five showed persistent, large circadian oscillations, and four had partial optic nerve lesions. The remaining seven eyes experienced significant IOP elevations during both phases, and all had extensive optic nerve damage.
Episcleral vein injection of hypertonic saline is more likely to increase IOP during the dark phase than the light. This is consistent with aqueous outflow obstruction superimposed on a circadian rhythm of aqueous humor production. Because these periodic IOP elevations produced optic nerve lesions, both light- and dark-phase IOP determinations are necessary for accurate correlation of IOP history to optic nerve damage in animals housed in a light- dark environment.
Investigative Ophthalmology & Visual Science 06/2000; 41(6):1380-5. · 3.60 Impact Factor
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ABSTRACT: To determine the chronology of optic nerve head and retinal responses to elevated intraocular pressure (IOP).
After 1 to 39 days of unilaterally elevated IOP, experimental and fellow rat eyes were examined for morphology and immunohistochemical labeling alterations and for ganglion cell DNA fragmentation.
Mean IOP for the experimental eyes was 36 +/- 8 mm Hg, an approximately 15-mm Hg elevation above normal values. By 7 days of pressure elevation above 40 mm Hg, endogenous immunostaining for brain-derived neurotrophic factor and neurotrophin 4/5 was absent from the nerve head and superior retina, whereas normal labeling was present in the inferior retina and distal optic nerve of these same eyes. These changes were preceded by a loss of gap junctional connexin43 labeling and astrocytic proliferation in the nerve head and by increased retinal ganglion cell layer apoptosis in the retina. Nerve head depletion of neurotrophins coincided with evidence of axonal degeneration, loss of astrocytic glial fibrillary acidic protein staining, and spread of collagen VI vascular immunolabeling. After longer durations at these same pressures, neurotrophin labeling returned to nerve head glia and scattered retinal ganglion cells.
Optic nerve head and retinal responses, including the depletion of endogenous neurotrophins, are readily identified in the rat eye after experimental IOP elevation. However, the apparent chronology of these responses suggests that the withdrawal of neurotrophic support was not the only determinant of retinal ganglion cell apoptosis and axonal degeneration in response to pressure.
Investigative Ophthalmology & Visual Science 03/2000; 41(2):431-42. · 3.60 Impact Factor
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ABSTRACT: To describe the arterial blood supply, capillary bed, and venous drainage of the rat optic nerve head.
Ocular microvascular castings from 6 Wistar rats were prepared by injection of epoxy resin through the common carotid arteries. After polymerization, tissues were digested with 6 M KOH, and the castings washed, dried, and coated for scanning electron microscopy.
Immediately posterior to the globe, the ophthalmic artery trifurcates into the central retinal artery and two posterior ciliary arteries. The central retinal artery directly provides capillaries to the nerve fiber layer and only contributes to capillary beds in the neck of the nerve head. The remainder is supplied by branches of the posterior ciliary arteries that are analogous to the primate circle of Zinn-Haller. Arterioles arising from these branches supply the capillaries of the transitional, or laminar, region of the optic nerve head. These capillaries are continuous with those of the neck and retrobulbar optic nerve head. All optic nerve head capillaries drain into the central retinal vein and veins of the optic nerve sheath. A flat choroidal sinus communicates with the central retinal vein, the choriocapillaris, and with large veins of the optic nerve sheath.
The microvasculature of the rat optic nerve head bears several similarities to that of the primate, with a centripetal blood supply from posterior ciliary arteries and drainage into the central retinal and optic nerve sheath veins. Association of nerve sheath veins with the choroid represents an important difference from the primate.
Investigative Ophthalmology & Visual Science 08/1999; 40(8):1702-9. · 3.60 Impact Factor
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International Ophthalmology Clinics 02/1999; 39(3):29-41.
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ABSTRACT: Recent advances in glaucoma genetics hold potential for dramatically changing the clinical care of glaucoma patients. To date, 5 primary open-angle glaucoma genes and 2 congenital glaucoma genes have been mapped. As more glaucoma genes are identified, earlier diagnosis for glaucoma should become more readily available. Progress in molecular genetics holds considerable promise for both current and future therapy of glaucoma. Glaucoma classification will be tailored to each individual based upon that person's family history, i.e. family glaucoma genotype. In the future, the optimum treatment for a specific glaucoma patient might rely on the knowledge of the phenotype of that person's causal gene, without having to resort to 'trial and error'. At this time, glaucoma treatment is restricted to lowering intraocular pressure. In the near future, with the knowledge of the pathophysiology caused by the defective glaucoma gene, more traditional drug treatments may be used to bypass the gene defect. Ultimately, gene therapy would replace the mutant gene with a normal one before visual loss has occurred as has been done with a model for retinitis pigmentosa, the retinal degeneration mouse.
Drugs & Aging 12/1998; 13(5):333-40. · 2.67 Impact Factor
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ABSTRACT: To determine whether chronic topical glaucoma therapy can control intraocular pressure (IOP) and protect nerve fibers in a rat model of pressure-induced optic nerve damage.
Sixteen adult Brown Norway rats were-administered unilateral episcleral vein injections of hypertonic saline to produce scarring of the aqueous humor outflow pathways. Twice daily applications of either artificial tears (n = 6), 0.5% betaxolol (n = 5), or 0.5% apraclonidine (n = 5) were delivered to both eyes, and awake pressures were monitored with a TonoPen XL tonometer for 17 days before the rats were killed.
For animals administered artificial tears, the mean IOP of the experimental eyes was 39 +/- 2 mm Hg compared with 29 +/- 1 mm Hg for the control eyes. This difference was statistically significant (P < 0.001). Mean IOPs in the experimental eyes of animals administered betaxolol and apraclonidine were 29 +/- 7 and 29 +/- 4 mm Hg, respectively, whereas the mean IOP in the control eyes was 28 +/- 1 mm Hg for both groups. There was no statistically significant difference among these values. The mean IOP for the experimental eyes in the betaxolol and apraclonidine groups was lower than that in animals administered artificial tears (P = 0.003). Quantitative histologic analysis of optic nerve damage in experimental eyes showed that four of the six animals administered artificial tears had damage involving 100% of the neural area. This degree of damage appeared in only 3 of 10 animals administered glaucoma therapy. Optic nerve protection was closely correlated with IOP history because damage was limited to less than 10% of the cross-sectional area in all animals in which the maximal IOP was less than or equal to 39 mm Hg, more than 2 SD below the mean value for eyes administered artificial tears.
Topical glaucoma therapy in this model can prevent IOP elevation and protect optic nerve fibers.
Investigative Ophthalmology & Visual Science 03/1998; 39(3):526-31. · 3.60 Impact Factor
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ABSTRACT: To develop unilateral, chronically elevated intraocular pressure in rats, episcleral veins were injected with hypertonic saline and the intraocular pressure was monitored with a Tono-Pen XL tonometer. Histologic analyses of eyes with differing degrees and durations of intraocular pressure elevation were performed to ascertain the effects of these pressures on the optic nerve. Out of 20 consecutive animals, nine had elevations of intraocular pressure following a single injection, while subsequent injections raised intraocular pressure in seven others. One eye became hypotonous. In the remaining animals, subsequent injections sufficient to raise intraocular pressure were deliberately withheld, to determine the possible direct effects of injections on the optic nerve. Mean sustained pressure elevations ranged from 7 to 28 mm Hg and the retinal vasculature remained perfused in all eyes. Optic nerve cross sections from eyes without intraocular pressure elevation appeared identical to those from uninjected eyes, while nerves from eyes with the greatest intraocular pressure rise demonstrated axonal damage that involved 100% of the neural area. Eyes with either less severe pressure elevations or shorter durations showed partial damage, ranging from 0.5% to 10.4% of the neurla area. In 70% of these nerves, damage was concentrated in the superior temporal region. Within the optic nerve head, often associated with astrocytes, axons contained abnormal accumulations of membrane-bound vesicles and mitochondria. The anterior chamber angles showed sclerosis of the trabecular meshwork with anterior synechiae, but Schlemm's canal, collector channels and aqueous veins appeared patent. Unilateral sclerosis of the trabecular meshwork produces sustained elevation of intraocular pressure in rats with optic nerve damage that in many ways resembles that seen in human glaucoma. Understanding the mechanism of nerve damage in this model may provide new insights into the pathogenesis of human glaucoma.
Experimental Eye Research 02/1997; 64(1):85-96. · 3.26 Impact Factor
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ABSTRACT: The extracellular matrix of the optic nerve head is altered in both human glaucoma and in experimental primate models of this disease. However, the relationship of this change to glaucomatous optic nerve degeneration is unknown. This report describes similar matrix alterations in rats with unilateral elevated intraocular pressure. Brown Norway rats received episcleral vein injections of hypertonic saline to produce prolonged elevations of intraocular pressure. After up to 6 months of pressure elevation, optic nerve head sections from the rats were evaluated by light microscopic immunohistochemistry using antibodies to collagens I, III, IV and VI, laminin, elastin and chondroitin and dermatan sulfate proteoglycans. In experimental eyes with 11 days or more of pressure elevation, depositions of collagen IV, collagen VI and laminin were found within regions of the optic nerve head that, in normal eyes, are occupied solely by nerve bundles. Collagen I and III deposition appeared to be more dependent on the level and duration of the pressure rise. Eyes with lower mean intraocular pressures showed deposits of interstitial collagens primarily at the level of the sclera, while eyes with higher mean pressure elevations had depositions in the neck regions as well. Chondroitin and dermatan sulfate proteoglycans were deposited in a pattern similar to that of collagen I. No extracellular matrix deposition was seen in the orbital optic nerve in any experimental eye. These extracellular matrix changes in rats replicate previous findings in human glaucomatous eyes and monkey eyes with experimentally elevated pressures. They also suggest a sequence of extracellular matrix protein deposition in response to pressure elevation. The optic nerve head deposition of matrix materials in response to elevated intraocular pressures may affect the susceptibility of remaining axons to pressure by changing the physical properties of their support tissues, by affecting the support functions of astrocytes and by changing the microenvironment of injured axons. This model may be useful for studying these and other aspects of the process of axonal injury resulting from elevated intraocular pressure.
Experimental Eye Research 07/1996; 62(6):663-74. · 3.26 Impact Factor
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Microscopy Research and Technique 05/1996; 33(6):480-9. · 1.79 Impact Factor
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ABSTRACT: To define the characteristics of the diurnal variation of intraocular pressure (IOP) in eyes of awake rats, ten male brown Norway rats were entrained to a 12-hour light:12-hour dark (12L:12D) lighting schedule and were conditioned to IOP measurement with the TonoPen XL tonometer while awake, using only 0.5% proparacaine HCl anesthesia. The IOP measurements were performed in 4 experiments: Preliminary-IOP was measured at 6-hour intervals in both eyes of each animal, to determine correlation between right and left eyes; Light:Dark-lighting remained the same as in the preliminary experiment, but the measurement schedule was altered so that measurements were obtained at 4-hour intervals in alternating eyes, over two 24-hour light cycles; Dark:Dark-animals were placed in constant dark (0L:24D) and, after 72 h, measurements were obtained at 4-hour intervals in alternating eyes. Animals were then re-entrained to the previous 12L:12D schedule for 7 days, after which they were returned to constant dark and the experiment was repeated; and Dark:Light-animals were entrained to a reversed light:dark cycle (12D:12L) for 28 days, after which measurements were obtained in the same fashion as in the Light:Dark experiment. Close agreement was found between right- and left-eye IOPs. Animals on a 12L:12D schedule exhibited lowest IOP while the lights were on (19.3 +/- 1.9 mm Hg), and highest (31.3 +/- 1.3 mm Hg) while the lights were off. Pressure changes anticipated the change from light to dark and dark to light. This pattern persisted in constant dark, and was reversed when the cycle was changed to 12D:12L. Brown Norway rats possess a regular rhythm of IOP that is entrained by the cycle of light and dark, and persistence of this rhythm in constant dark establishes it as a circadian rhythm. Furthermore, our results indicate that reliable and physiologically meaningful IOP measurements can be obtained in awake rats using the TonoPen XL tonometer.
Current Eye Research 03/1996; 15(2):185-91. · 1.28 Impact Factor
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ABSTRACT: To study the optic neuropathy associated with glaucoma, a system for accurate, reliable, and non-invasive monitoring of intraocular pressure (IOP) is required. Of particular interest is the effect of sampling frequency on IOP. To address this issue, ten adult male brown Norway rats (group 1) were acclimatized to a 12-h/12-h light/dark cycle. On 20 days over a 30-day period, rats were anesthetized with short-acting isoflurane (Forane) inhalant anesthesia and IOP for each eye was determined by averaging 15 valid individual readings obtained with a TonoPen 2 tonometer. The last 12 measurement sessions were performed on a daily basis. To determine the minimum tolerable interval between IOP measurement sessions, a second group of 10 animals (group 2) was acclimatized in the same manner as group 1, and IOP was measured every 4 days over a period of 80 days. Next, IOP was measured every 4 days over a period of 28 days, and finally, every 2 days over a period of 19 days. For all group 1 measurements, there was no statistically significant difference between the right and left eye IOP, 14.75 +/- 1.08 (SEM) and 14.90 +/- 1.09 mm Hg, respectively. However, daily measurements produced a steady decrease in IOP and gradual weight loss. For group 2, overall mean right and left eye IOPs were 15.24 +/- 1.28 (SEM) and 15.12 +/- 1.26, respectively and were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)
Current Eye Research 09/1995; 14(8):711-7. · 1.28 Impact Factor
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ABSTRACT: To define the microvascular anatomy of anterior segment blood supply and aqueous drainage in the rat eye.
External limbal blood vessels were studied by direct inspection of normal, living rat eyes and eyes injected intracamerally with fluorescein dye. Intraocular connections of these vessels were then documented with scanning electron microscopy of methylmethacrylate microvascular luminal castings.
The rat limbus possesses a circumferential vascular ring consisting of a single artery and a venous plexus. The limbal artery communicates with radial anterior ciliary arteries and with perforating arterioles arising from the long posterior ciliary arteries. The venous plexus is connected to a circumferential Schlemm's canal by numerous transcleral, aqueous-containing collector channels and drains into multiple radial veins located within the episclera.
These findings illustrate anatomic similarities between rats and primates, both in anterior segment blood supply and aqueous humor drainage. The rat limbal artery provides collateral perfusion of the anterior segment from anterior and long posterior ciliary systems. The direct communications between identifiable external aqueous-containing veins, a circumferential episcleral venous plexus, and an internal Schlemm's canal provides the anatomic basis for producing chronically elevated intraocular pressure in rats using retrograde injection of mild sclerosing agents into the aqueous humor outflow pathways, and for administering drugs and other agents to the entire trabecular meshwork and Schlemm's canal.
Investigative Ophthalmology & Visual Science 04/1995; 36(3):751-6. · 3.60 Impact Factor
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ABSTRACT: To evaluate the presence and distribution of chondroitin and dermatan sulfate-containing proteoglycans in normal human and monkey optic nerve heads by light microscopic immunohistochemistry.
Monoclonal antibodies specific for glycosaminoglycan attachment sites remaining after incubation of tissues with chondroitinase ABC and ACII were used to detect proteoglycans containing unsulfated chondroitin (OS), chondroitin-4 and/or dermatan sulfate (4S), and chondroitin-6 sulfate (6S) glycosaminoglycans.
4S antibody labeling after chondroitinase ABC was heavily and evenly distributed within the peripapillary sclera and in the core of laminar beams and optic nerve septa. Preincubation with chondroitinase AC, which exposes only chondroitin sulfate attachment sites, diminished labeling intensity in the lamina cribrosa and sclera and almost completely eliminated it in the retrolaminar optic nerve septa. In contrast, 6S antibodies demonstrated a more intermittent linear distribution throughout the laminar beams and optic nerve septa. No qualitative differences were seen between human and monkey optic nerve heads.
Chondroitin and dermatan sulfate-containing proteoglycans exist throughout the support tissues of the optic nerve head. The specific distribution patterns demonstrated by these monoclonal antibodies, and, in particular, the unique confinement of one of them to the lamina, indicate the presence of different core proteins or different functional glycosaminoglycan side chains that may influence the behavior of the lamina cribrosa.
Investigative Ophthalmology & Visual Science 04/1994; 35(3):838-45. · 3.60 Impact Factor
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ABSTRACT: The authors explored the empirical dosing requirement for administration of an alpha 2-adrenoceptor agonist, brimonidine, and determined its efficacy in decreasing elevations in intraocular pressure (IOP) after 360 degrees argon laser trabeculoplasty (ALT).
This vehicle-controlled, double-masked, multicenter trial evaluated three dosing regimens of brimonidine. Two hundred thirty-two patients for whom 360 degrees ALT was indicated were randomized into one of four treatment groups: 0.5% brimonidine both before and after ALT; brimonidine before but vehicle after ALT; vehicle before but brimonidine after ALT; or vehicle at both times.
During the first 3 hours after 360 degrees ALT, the overall incidence of IOP elevations of 5 mmHg or greater was 38% (23 of 60 eyes) in the group receiving vehicle only, and it ranged from 3% to 9% (2 of 62 to 5 of 53 eyes) in the groups receiving any brimonidine treatment. There was little difference in efficacy between the three dosing regimens of brimonidine. Brimonidine was well tolerated by the patients.
Based on this large, controlled, multicenter study, 0.5% brimonidine was an effective agent for reducing elevations in IOP after 360 degrees ALT. Only one dose, administered either before or after 360 degrees ALT, was required.
Ophthalmology 08/1993; 100(7):1083-8. · 5.45 Impact Factor
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ABSTRACT: We studied the histopathologic changes of three eyes enucleated two weeks, eight weeks, and 17 months, respectively, after noncontact Nd:YAG cyclophotocoagulation. The histologic findings at two weeks were destruction of the nonpigmented and pigmented ciliary body epithelium, occlusion of the capillaries of the ciliary processes, and ciliary body stromal necrosis in the region of the processes. Hyperplasia of the pigmented and nonpigmented epithelium, fibrosis and near total atrophy of the ciliary processes, and partial atrophy of the ciliary muscles were present at eight weeks and 17 months. We concluded that application of treatment 1.0 to 1.5 mm posterior to the corneoscleral limbus selectively destroys the pars plicata, and that, histologically, the mechanism for reducing intraocular pressure appears to be destruction of ciliary processes with reduction of aqueous formation.
American Journal of Ophthalmology 06/1993; 115(5):597-602. · 4.22 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate the Tono-Pen 2 tonometer for measuring intraocular pressure (IOP) in the living rat eye.
One eye from each of 20 adult, anesthetized brown Norway rats (group 1) was cannulated and simultaneously connected to a syringe and a pressure transducer with a chart recorder. We increased IOP from 15 to 45 mmHg in 5-mmHg increments and obtained 15 consecutive readings (ignoring instrument-generated averages) at each pressure increment with a Tono-Pen 2 tonometer. To test the tonopen's ability to measure unknown IOP, transducer pressures were varied randomly in 20 additional animals (group 2), and tonopen readings were obtained in masked fashion.
Plotting the mean tonopen readings for each animal against transducer IOP produced a regression formula of y = 4.54 + 0.79x (r = 0.98). Mean group 2 tonopen values plotted against transducer IOP yielded a regression formula of y = 4.75 + 0.78x (r = 0.94). A method comparison analysis showed that the tonopen significantly overestimates pressures at low IOP (< or = 15 mmHg), and it significantly underestimates pressures at high IOP (> or = 30 mmHg). Using two-way analysis of variance, it was determined that the group 2 data did not differ significantly from the group 1 data (P > or = 0.76). Because of this consistency, we generated a correction factor with 95% prediction intervals for Tono-Pen readings.
The Tono-Pen 2 can be used reliably to measure IOP in the normal rat eye.
Investigative Ophthalmology & Visual Science 02/1993; 34(2):363-9. · 3.60 Impact Factor
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ABSTRACT: Vascular luminal castings of rabbit eyes were microdissected and studied with scanning electron microscopy to elucidate the three-dimensional angioarchitecture of the optic nerve head. Using sequential microdissection, an incomplete arterial circle was identified as terminal branches of two to three short posterior ciliary arteries around the optic nerve head. Several recurrent branches from the arterial circle form a pial arterial network. This pial system supplies the optic nerve head microvasculature and receives numerous venules from them. The only large vessel to enter the optic nerve is a central retinal artery that has few branches within the optic nerve and provides several branches at the surface of the optic disc. Moderately numerous vessels connect the retinal and ciliary vascular layers within the optic nerve head. Few arterioles to the optic nerve head arise from the choroid; however, there are a small number of capillary and numerous venous connections between them. These results indicate that the principal blood supply of the rabbit optic nerve head is derived from the short posterior ciliary arteries by the arterial circle. The retinal arteries contribute to the surface vasculature of the optic nerve head. The pial system also plays a significant role in both supply and drainage of the rabbit optic nerve head.
Investigative Ophthalmology & Visual Science 07/1992; 33(7):2251-61. · 3.60 Impact Factor
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ABSTRACT: The authors counted axons in one optic nerve from each of 28 juvenile and aged rhesus monkeys using an automated image analysis system. All nerves were fixed immediately after death and treated identically. Animals ranged in age from 1 1/2 to 29 yr, which correlates with a human age range of 4 1/2-87 yr. Mean axonal number for all specimens was 1,117,859. Large variations in axonal numbers were found, even within a subgroup of ten animals aged 1 1/2-2 yr. Although young nerves had generally more fibers than those from old animals, this difference was not quite statistically significant, translating into a yearly loss of 4319 fibers (0.45% of the total). Age did not have any significant effect on mean axonal diameter.
Investigative Ophthalmology & Visual Science 09/1990; 31(8):1623-7. · 3.60 Impact Factor
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ABSTRACT: Unilateral glaucomatous optic neuropathy and optic nerve transections were produced in cynomolgus monkeys, and the optic nerve heads were examined by light and electron microscopic immunohistochemistry. Glaucomatous nerve heads showed increased labeling for collagen type IV along the margins of beams in the lamina cribrosa, due to accumulation of basement membrane-like materials. We also noted material in the pores of the laminar beams that labeled with antibodies to collagen types I, III and IV, but not elastin. In transected eyes, increased type IV labeling of laminar beam margins resulted solely from redundant astrocyte basement membranes. Extracellular matrix deposition within laminar pores was not observed following optic nerve transection; hence this may be a selective response to elevated intraocular pressure. This response may alter the biochemical composition of the lamina cribrosa and its function in patients with elevated intraocular pressure.
Archives of Ophthalmology 08/1990; 108(7):1020-4. · 3.71 Impact Factor
