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PubMed2005

[Treatment of acute retinal necrosis: systematic review].

PURPOSE: The purpose of this study was to identify, according to an systematic review, the best treatment for acute retinal necrosis. METHODS: Following the methodologic guidance of the Cochrane Collaboration and its editorial subgroup "Eye and Vision Group", using search strategy for study identification, articles about the treatment of acute retinal necrosis were selected. RESULTS: 146 bibliographic references were selected, 13 studies were considered relevant. Among them 2 were considered to follow the inclusion criteria. The first study tested the possibility of using intravenous acyclovir associated with corticosteroids, protecting contralateral eye from being affected. Fifty-four patients who reported unilateral acute retinal necrosis have been studied, 31 treated and 23 not treated, the disease occurring in the contralateral eye in 12.9% of the patients of the treated group and in 69.5% of the patients in the non-treated group. The second study considered treatment with photocoagulation with argon laser to prevent retinal detachment, that was observed in 57.1% of the eyes. The second included study disclosed 19 eyes affected by acute retinal necrosis, considering that 12 of these eyes were treated with photocoagulation with argon laser to prevent retinal detachment. Among the 12 eyes, 2 developed retinal detachment (16.6%) while, in the non-treated group, 7 eyes, 4 developed retinal detachment (57.1%). CONCLUSION: The author concludes that both types of proposed interventions have proven to be effective. However, once the mentioned studies are methodologically considered weak, it is necessary to perform randomized clinical trials with the purpose of establishing the most suitable treatment for acute retinal necrosis.

Acyclovir↗
PubMedDate not supplied

[The surgical causes for the development of retinal detachment in experimental vitrectomy].

The operative causes of development of detachment of the retina after vitrectomy were experimentally studied. The principal causes were scleral incision outside the flat segment of the ciliary body, ciliary body injury, traction exposures, intraocular pressure differences. Specific features of the morphologic picture were detected related to exposure to a certain aggravating factor.

Animals↗
PubMed1995

The effect of litter size on normal retinal vascular development in the neonatal rat.

Many animal models of retinal disease use the neonatal rat. Raising rat pups in large litters has been shown to result in postnatal growth retardation. We investigated the effect of litter size on the normal postnatal vascularization of the neonatal rat retina. Sixty-six newborn rat pups were divided among 5 nursing mothers into 3 small litters (n = 10) and 2 large litters (n = 18). On day 6 of life the rats were sacrificed and total retinal and vascularized retinal areas analyzed. The total retinal area was reduced in the rats raised in larger litters (28.6 mm2 vs. 25.9 mm2 p < 0.001) but there was a more pronounced reduction in vascularized retinal area (67% vascularized vs. 54% vascularized, p < 0.001). Postnatal vascularization of the normal rat retina may be influenced by litter size.

Animals↗
PubMed2003

Proapoptotic bcl-2 family members, Bax and Bak, are essential for developmental photoreceptor apoptosis.

PURPOSE: Apoptosis has been implicated in retinal development and degeneration, but the specific apoptotic pathways used are incompletely understood. The purpose of this study was to characterize the roles in retinal development of the proapoptotic Bcl-2 family members Bax and Bak. METHODS: Eyes from mice at postnatal day (P)7, during the peak of developmental apoptosis in the retina, were processed for TdT-dUTP terminal nick-end labeling (TUNEL) to determine whether Bax knockout or double Bax/Bak knockout causes a defect in developmental apoptosis. Adult (>2-month-old) eyes from wild-type, Bak(-/-), Bax(-/-), and Bax(-/-)Bak(-/-) mice were analyzed by histology and immunocytochemistry to identify persistent retinal cells. RESULTS: Adult Bax(-/-)Bak(-/-) eyes showed significant increases in the number of inner retinal cells, with an almost complete absence of TUNEL-positive cell death at P7. Some of these persistent cells in the inner retina notably included rod photoreceptors that normally undergo apoptosis after failure to migrate to the outer retina. These inner nuclear layer (INL) rods contained markers of early rod differentiation: rod opsin, arrestin, and recoverin. However, they did not form ectopic outer segments or contain the associated markers ROM-1, peripherin-2, and RP1. CONCLUSIONS: Bax and Bak are important for retinal development and are the first apoptotic factors identified as essential for developmental photoreceptor apoptosis. Future studies will investigate the potential role of Bax and Bak in mediating pathologic photoreceptor death.

Animals↗
PubMed2005

Ganglion cells are required for normal progenitor- cell proliferation but not cell-fate determination or patterning in the developing mouse retina.

The vertebrate retina develops from an amorphous sheet of dividing retinal progenitor cells (RPCs) through a sequential process that culminates in an exquisitely patterned neural tissue. A current model for retinal development posits that sequential cell-type differentiation is the result of changes in the intrinsic competence state of multipotent RPCs as they advance in time and that the intrinsic changes are influenced by continuous changes in the extracellular environment. Although several studies support the proposition that newly differentiated cells alter the extrinsic state of the developing retina, it is still far from clear what role they play in modifying the extracellular environment and in influencing the properties of RPCs. Here, we specifically ablate retinal ganglion cells (RGCs) as they differentiate, and we determine the impact of RGC absence on retinal development. We find that RGCs are not essential for changing the competence of RPCs, but they are necessary for maintaining sufficient numbers of RPCs by regulating cell proliferation via growth factors. Intrinsic rather than extrinsic factors are likely to play the critical roles in determining retinal cell fate.

Animals↗
PubMed2005

Symptoms and findings predictive for the development of new retinal breaks.

OBJECTIVE: To validate the conclusion of our previous prospective study of 250 patients with isolated posterior vitreous detachment: follow-up visits are only necessary if patients mention symptoms of flashes in combination with multiple floaters or a curtain or cloud at the initial examination, or an increase in number of floaters after the initial examination. METHODS: Prospective study of 270 consecutive patients with symptomatic isolated posterior vitreous detachment. All patients completed a questionnaire detailing their symptoms and had a full eye examination at the initial examination and at follow-up visits. Logistic regression with backward elimination was used for statistical analysis. We also performed pooled analysis of our previous and present study data. RESULTS: New retinal breaks developed in 10 patients (3.7%). Multiple floaters, a curtain or cloud, hemorrhages (retinal or vitreous) at the initial examination, and an increase in the number of floaters after the initial examination were found to be predictive factors for the development of new retinal breaks. These factors were also the only significant predictors after pooled analysis of both studies (520 patients, 23 breaks). CONCLUSIONS: We assume we can formulate a safe policy for scheduling patients with isolated posterior vitreous detachment: only patients with multiple floaters, a curtain or cloud, or hemorrhages (retinal or vitreous) at the initial examination should be scheduled for reexamination. All other patients should return only if the number of floaters increases.

Aged↗
PubMedDate not supplied

Susceptibility to murine cytomegalovirus retinitis during progression of MAIDS: correlation with intraocular levels of tumor necrosis factor-alpha and interferon-gamma.

PURPOSE: To correlate tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) synthesis with histopathologic disease and virus replication within murine cytomegalovirus (MCMV)-infected eyes during progression of murine acquired immunodeficiency syndrome (MAIDS). MATERIALS AND METHODS: Groups of normal mice and mice with MAIDS of 2-weeks (MAIDS-2), 4-weeks (MAIDS-4), and 12-weeks (MAIDS-12) duration were infected uniocularly with MCMV by subretinal MCMV injection. MCMV-inoculated eyes from all mice were subjected to histopathologic analysis, quantitative plaque assay, or cytometric bead array analysis for quantification of TNF-alpha and IFN-gamma. RESULTS: Whereas MCMV-inoculated eyes of normal, MAIDS-2, and MAIDS-4 mice were resistant to MCMV retinitis, all MCMV-inoculated eyes of MAIDS-12 mice developed retinitis. Surprisingly, MCMV-inoculated eyes of MAIDS-4 mice without retinitis harbored high amounts of infectious virus at a level equivalent to that of MCMV-inoculated eyes of MAIDS-12 mice that developed retinitis. Intraocular TNF-alpha levels were consistently approximately 50% greater in MCMV-inoculated eyes of MAIDS-12 mice when compared with TNF-alpha levels of normal, MAIDS-2, and MAIDS-4 mice. In contrast, intraocular INF-gamma levels within MCMV-inoculated eyes progressively declined as animals became susceptible to retinitis. CONCLUSIONS: An inverse relationship exists between TNF-alpha and INF-gamma production within MCMV-inoculated eyes during MAIDS evolution that is characterized by an increase in intraocular TNF-alpha levels and a concomitant decrease in intraocular INF-gamma levels. Susceptibility of MCMV-inoculated eyes to virus replication and development of necrotizing retinitis are independent events with susceptibility to MCMV replication preceding susceptibility to MCMV retinitis by several weeks. Time of Th1/Th2 shift in cytokine profile appears to be a crucial event in the pathogenesis of MAIDS-related MCMV retinitis.

Animals↗
PubMed2005

Dietary ganglioside and long-chain polyunsaturated fatty acids increase ganglioside GD3 content and alter the phospholipid profile in neonatal rat retina.

PURPOSE: During early development, the ganglioside composition of the retina changes significantly, in that GD3 becomes the primary ganglioside in the mammalian retina. Because gangliosides play an important role in neuronal cell differentiation and proliferation, this change in ganglioside profile may indicate retinal maturation. Dietary long-chain polyunsaturated fatty acids (LCPs) such as 20:4n-6 and 22:6n-3 improve visual acuity in infants. Dietary LCPs stimulate neonatal retinal development by altering membrane phospholipids, which in turn affect cell signaling pathways. It is unknown whether dietary ganglioside and LCPs affect the metabolism of phospholipids and gangliosides during retinal development. METHODS: Male Sprague-Dawley rats (18 days old) were fed semipurified diets consisting of 20% fat (control diet) for 2 weeks containing either 0.1% ganglioside enriched in GD3 (GG diet) or 1% 20:4n-6 and 0.5% 22:6n-3 (LCP diet) in the control diet. The profile of ganglioside and phospholipid was measured. RESULTS: The GG diet increased the ganglioside content by 39% in the retina, with a relative increase in GD3 (by 13%). Dietary LCPs significantly increased the relative levels of GD3 (by 19%, P < 0.01). Total phospholipid was decreased by the LCP-supplemented diet (by 28%). Phosphatidylcholine and phosphatidylserine increased with concomitant decreases in phosphatidylinositol and lyso-phosphatidylethanolamine when animals were fed either the LCP or the GG diet. CONCLUSIONS: Animals fed dietary ganglioside increased in total retinal ganglioside and GD3 content during retinal development, with a concomitant alteration of phospholipid metabolism. Feeding animals dietary LCPs also affected ganglioside metabolism in the developing retina, suggesting a new mechanism by which these dietary lipids may promote maturation of photoreceptor cells.

Animals↗
PubMed1997

The effect of raised inspired carbon dioxide on normal retinal vascular development in the neonatal rat.

PURPOSE: Raised arterial carbon dioxide levels have been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of raised inspired CO2 on normal postnatal vasculogenesis in the neonatal rat retina. METHODS: One hundred fifty newborn rat pups were divided among 15 mothers (n = 10 for each litter). Five litters were exposed to low CO2 (0.2%), 5 litters exposed to 6%, and 5 litters to 10% CO2. On day 7 of life the rats were sacrificed and the total retinal and vascularized retinal areas analyzed. RESULTS: The vascularized retinal area and ratio of vascularized to total retinal area were reduced in rats exposed to 6% and 10% CO2. CONCLUSIONS: Raised inspired CO2 was associated with retardation of normal retinal vascular development and increased peripheral avascular area in neonatal rats. Raised CO2 may be a risk factor for the development of abnormal neovascularization such as in ROP.

Animals↗
PubMed1975

Retinal tumor induction by ocular inoculation of human adneovirus in 3-day-old rats.

A direct causal relationship between a human DNA virus, adeno serotype 12, and malignant transformation in target cells (sensory retinal neuronal precursors) was suggested by the development of a remarkably uniform retinoblastoma-like neoplasm in rats. In order to focus upon incipient photoreceptor differentiation, 27 3-day-old CD rats were selected for intraocular virus inoculation. A single injection of 0.03 ml of the virus fluid, 104.5 TCID50 HeLa cells/0.1 ml was given in the left eye. Within 73 to 167 days after the virus inoculation, 12 rats (44.4%) developed retinal tumors in the left eye. Although retinal tumors mimicking human retinoblastoma with true rosettes were anticipated, the highly uniform histopathologic appearance of all 12 eyes was virtually indistinguishable from that of 0-day-old rats. However, multiple foci of malignant cells fusing with the inner segment of relatively well-differentiated retinal layers were found haphazardly throughout the cases; such retinal remnants were not detectable in tumors of 0-day-old rats. Electron microscopy revealed poorly differentiated tumor cells that possessed a single cilium consisting of a typical ring of nine doublets with no axial pair (a 9 plus 0 pattern). Advenovirus-specific T-antigens detected in vivo by the immunofluorescein microscopic procedure in abortively infected or transformed cells clearly indicated that some neuronal precursors destined for part of the ganglioneuronic layer are selectively susceptible to viral oncogenesis. No preferential involvement of the photoreceptor cells was observed. No control animals developed retinal neoplasms.

Adenoviridae↗
PubMed2026

The Impact of PCSK9 Inhibitors on Development of Retinal Vascular Occlusions.

PURPOSE: PCSK9 inhibitors (PCSK9i) are a newer class of lipid-lowering drug that may be effective at lowering risk for retinal artery occlusion (RAO) and retinal vein occlusion (RVO). This study aims to investigate the relationship between PCSK9i use and retinal vascular occlusion among patients with hyperlipidemia. DESIGN: Retrospective, comparative clinical cohort study SUBJECTS, PARTICIPANTS, AND/OR CONTROLS: Patients with hyperlipidemia, defined as serum low-density lipoprotein level of &#x2265;130 mg/dL and total cholesterol level of &#x2265;220 mg/dL, prescribed a lipid-lowering medication were identified. Patients prescribed a PCSK9i were included in the study group and compared with control patients prescribed any other type of lipid-lowering drug. METHODS: This study was conducted using electronic health record data from health organizations in the United States through the TrinetX platform. Propensity score matching was completed based on relevant patient demographics, comorbidities, and laboratory values. Comparison of main outcomes between the PCSK9i and non-PCSK9i groups was performed using measures of association analysis to determine risk ratio (RR) with 95% CI. MAIN OUTCOME MEASURES: The outcomes measured consisted of occurrence of retinal vascular occlusion, RAO, RVO, central RAO, and central RVO at 3-year, 5-year, and 7-year time points. RESULTS: After propensity score matching, a total of 12,960 patients were included in each cohort. The analysis revealed that the PCSK9i cohort had a significantly lower risk for development of retinal vascular occlusions at multiple points, including 3-year (RR = 0.56, CI = 0.39-0.79), 5-year (RR = 0.50, CI = 0.37-0.67), and 7-year (RR = 0.46, CI 0.35-0.61) time points. This lower risk was also found in the PCSK9i group for an outcome of RVO at 5 years (RR = 0.50, CI = 0.34-0.73) and 7 years (RR = 0.47, CI = 0.33-0.67). For occurrence of RAOs (RR = 0.47, CI = 0.30-0.76) and central RVO (RR = 0.46, CI = 0.29-0.74) separately, the PCSK9i cohort had a lower risk at 7 years. CONCLUSION: These findings suggest that PCSK9i may reduce the risk of retinal vascular occlusion compared with other classes of lipid-lowering medications.

Humans↗
PubMed1982

Cell death in the mammalian visual system during normal development : I. Retinal ganglion cells.

Degenerating cells may be observed with light microscopy in the hamster retinal ganglion cell layer during early postnatal development. On the first postnatal day, degenerating cell profiles were found at a rate of 2.7 per 1,000 live cells. This rate increased to a peak of 14.7 degenerating cells per 1,000 live on postnatal day 5 and then slowed to 4.2 per 1,000 live by postnatal day 10. These rates of cell death correspond to a 49% reduction in cell number in the ganglion cell layer. Examination of the spatial pattern of cell death revealed that although on visual inspection degenerating cells appear to occur in clumps, statistical analysis demonstrated a random distribution within renal areas. Across the retina, cell death rates were higher in peripheral retina than in central retina. The timing and pattern observed correspond well with that of cell degeneration observed in the superficial layers of the superior colliculus, the major target of the retinal projection.

Age Factors↗
PubMed1997

[Local therapy in treatment of cytomegalovirus (CMV) retinitis in AIDS. The ganciclovir implant (pellet)].

BACKGROUND: Cytomegalovirus (CMV) retinitis with AIDS has been treated either systemically or locally by weekly intravitreous injections. An intraocular device now offers a new therapeutic approach. We investigated its efficacy in preventing progression of CMV retinitis without additional systemic therapy. Conversely, we also studied the risks and disadvantages of this method of drug administration. PATIENTS AND METHODS: In our study 46 devices were implanted in 28 patients. All patients were pretreated with systemic medication. Systemic treatment was stopped on the day of surgery. RESULTS: Severe perioperative complications occurred in one patient, who developed retinal detachment after surgery. Most patients showed no relapse of retinitis with the implant, though they did not receive systemic treatment for 8.1 months on average. Only 20% of our patients presented with extraocular CMV disease. Thirty-five percent (n = 17) of patients with unilateral retinitis developed CMV retinitis in the primary uninvolved fellow eye. After implantation of a device into this eye also progression could be stopped without additional systemic treatment. Two patients showed progression of retinitis due to an empty ganciclovir reservoir. A second device was implanted without removal of the first. CONCLUSIONS: The intraocular ganciclovir device appears to be an effective treatment for CMV retinitis with few disadvantages. Time to progression of retinitis tends to be prolonged compared to systemic treatment.

AIDS-Related Opportunistic Infections↗
PubMed2006

Gene expression profiles of mouse retinas during the second and third postnatal weeks.

Mouse retina undergoes crucial changes during early postnatal development. By using Affymetrix microarrays, we analyzed gene expression profiles of wild-type 129SvEv/C57BL/6 mouse retinas at postnatal days (P) 7, 10, 14, 18, and 21 and found significantly altered expression of 355 genes. Characterization of these 355 genes provided insight into physiologic and pathologic processes of mouse retinal development during the second and third postnatal weeks, a period that corresponds to human embryogenesis between weeks 12 and 28. These genes formed 6 groups with similar change patterns. Among the genes, sixteen cause retinal diseases when mutated; most of these 16 genes were upregulated in retina during this period. Using the PathArt program, we identified the biological processes in which many of the 355 gene products function. Among the most active processes in the P7-P21 retina are those involved in neurogenesis, obesity, diabetes type II, apoptosis, growth and differentiation, and protein kinase activity. We examined the expression patterns of 58 genes in P7 and adult retinas by searching the Brain Gene Expression Map database. Although most genes were present in various cell types in retinas, many displayed high levels of expression specifically in the outer nuclear, inner nuclear, and/or ganglion cell layers. By combining our 3 analyses, we demonstrated that during this period of mouse retinal development, many genes play important roles in various cell types, multiple pathways are involved, and some genes in a pathway are expressed in coordinated patterns. Our results thus provide foundation for future detailed studies of specific genes and pathways in various genetic and environmental conditions during retinal development.

Aging↗
PubMed2006

Pathological but not physiological retinal neovascularization is altered in TNF-Rp55-receptor-deficient mice.

PURPOSE: Tumor necrosis factor (TNF)-alpha is one of the major cytokines in inflammation and apoptosis. It has been demonstrated that inhibition of TNFalpha can reduce leukocyte adhesion, vascular leakage, and apoptotic endothelial cell death in diabetes. This study was conducted to investigate the effect of TNF-Rp55 and TNF-Rp75 on retinal development in oxygen-induced retinopathy. METHODS: TNF-Rp55- and TNF-Rp75-deficient mice, as well as their respective wild-type controls, were exposed to 75% oxygen from postnatal day P7 to P12. Retinal vascularization was investigated in flatmount preparations after concanavalin A labeling of endothelial cells on days P6, P14, P17, and P20. Retinal mRNA expression of VEGF, angiopoietin-1 and -2, and PDGF was examined at days P14 and P20. RESULTS: TNF-Rp55- and TNF-Rp75-deficient mice demonstrated similar retinal development and vascularization under normoxic conditions. In comparison to wild-type mice, the vascularized area remained stable during the observation time, although the gene expression of VEGF, angiopoietin (ang)-1 and -2, and PDGFb changed. Compared with that in the wild type mice, the relative expression of VEGF, ang-1, ang-2, and PDGFb changed 5.14-, 1.7-, 0.39-, and 0.36-fold in Rp55(-/-) mice and 4.1-, 9.5 x 10(-5)-, 0.12-, and 2975-fold in Rp75(-/-) mice, respectively. Treatment with oxygen resulted in a significantly reduced vascularization in Rp55(-/-) but not Rp75(-/-) mice on postnatal day (P)20. CONCLUSIONS: Inhibition of TNFalpha via TNF-Rp55 can alter retinal development and angiogenesis in a model of oxygen-induced retinopathy. The data underscore the potential effectiveness of TNF-inhibitory treatments as modulators in oxygen-induced retinopathy.

Angiopoietin-1↗
PubMed2005

Retinal blood vessels develop in response to local VEGF-A signals in the absence of blood flow.

The role of hemodynamic forces and other signals from circulating blood in guiding the development of the retinal vasculature was examined by following the growth of these vessels in organ cultures. Retinal vascular development in organ cultures was monitored by immunofluorescent staining of retinal whole-mounts using antibodies against ICAM-2, a specific marker for endothelial cells and by vascular adenosine disphosphatase activity. Under culture conditions, the retinal vasculature from mice at postnatal day 3 (P3) grew from the optic nerve area to the edge of the retina in a manner similar to that observed in vivo. Both inner and outer vascular plexuses formed in retinal explants. Within the first few days of organ culture, the initial uniform meshwork of blood vessels was reorganized into arterioles, venules, and capillaries. As in animals, the initial retinal vascular plexus contained abundant vessels, and afterward some vessels regressed leading to the formation of a mature vascular bed. Changes in vascular density due to blood vessel growth and remodeling were confirmed by RT-PCR and Western blot analyses of ICAM-2 mRNA and protein levels, respectively. In addition, during in vitro retinal vascularization, arterioles acquired mural cell coverage, as shown by positive staining for alpha-smooth muscle actin. Thus, blood flow and blood-derived signals were not required for the development and maturation of retinal vessels. In contrast, stability of blood vessels in retinal explants was tightly regulated by endogenous levels of vascular endothelial growth factor-A (VEGF-A). VEGF-A was expressed in the explants throughout the culture period, and addition of neutralizing antibodies against VEGF-A to the organ culture caused a severe regression of blood vessels from the vascular front toward the optic nerve. In contrast, addition of anti-FGF-2 antibodies had no effect on the developing vasculature. Thus, retinal vascular development is dependent on local VEGF-A signals rather than systemic signals.

Actins↗
PubMed1996

Vaso-obliteration in the canine model of oxygen-induced retinopathy.

PURPOSE: To quantify the acute constrictive response of developing retinal blood vessels to hyperoxia and to examine the vaso-obliterative phase of sustained oxygen breathing in the neonatal dog model of retinopathy of prematurity. METHODS: Seven littermates were used to examine the acute constrictive response of the developing retinal vessels to hyperoxia (30 minutes to 96 hours of 100% oxygen). ADPase retinal flatmounts were prepared, and morphometric measurements were made using computer-assisted analysis. Vaso-obliteration also was examined in three animals killed after prolonged exposure to hyperoxia (4 days of 100% oxygen) and in three room air controls using ADPase flat-embedded retinas and cross-sections. Choroids were processed for alkaline phosphatase flat-embedding. RESULTS: After 1 hour of oxygen breathing, all vascular components showed a reduction in diameter: Arteries were reduced 27%, veins 18.3%, and capillaries 27.7%. Capillary constriction peaked by 24 hours (69.4% reduction), whereas arteries and veins continued to close. Although capillary diameters did not decrease significantly after 24 hours, the number of capillaries, as determined by percent vascular area calculations, continued to decrease in all areas through the additional 3 days of oxygen breathing. In contrast, after 4 days of hyperoxia the choriocapillaris lumenal diameters and percent vascular area did not vary significantly from controls. Analysis of sections taken through various retinal regions of these animals revealed significant decreases (40%) in the volume of the extracellular spaces available for blood vessel formation. Hyperoxia also reduced in a 55.6% decrease in the total number of cells (endothelial cells, ablumenal cells, perivascular cells) within the inner retina; however, there was no significant difference in ganglion cell counts in the two groups. CONCLUSIONS: This study demonstrates that the pattern and severity of the reaction of developing retinal vessels to hyperoxia in the newborn dog is similar to that described for the kitten and the premature human. This response is unlike that exhibited by the newborn rat or mouse.

Animals↗
PubMed2005

The effect of L-thyroxine supplementation on retinal vascular development in neonatal rats.

PURPOSE: Thyroxine (T4) plays a role in neuroretinal maturation, but little is known regarding its role in retinal vascularization. The neonatal rat retina is incompletely vascularized at birth, providing a model for the human premature infant retina and for retinopathy of prematurity (ROP). We hypothesized that T4 supplementation would accelerate vascular development of normal neonatal rat retina. METHODS: Two hundred twenty Sprague-Dawley rats were raised in litters of 10 in room air and received either 0.05 microg/g, 0.5 microg/g, or 1.0 microg/g of intraperitoneal T4 or saline control beginning on day 1 of life for 3 days, 7 days, or 3 days followed by 4 days recovery. Rats were sacrificed on either day 4 or day 8 of life. Left eyes were fixed, retinae dissected and ADPase-stained. Flat mounted retinae were digitized and total retinal areas and retinal vascular density were evaluated in a masked manner. Serum T4, thyroid stimulating hormone (TSH), and insulin-like growth factor-1 (IGF-1) were measured at each time point. RESULTS: Retinal vascular density was reduced in animals receiving daily 1 microg/g T4 compared with saline controls after 3 days of T4 (16.8 +/- 1.4 vessels/mm vs. 18.3 +/- 1.3 vessels/mm, p = 0.04) and 7 days of T4 (14.4 +/- 1.3 vessels/mm vs. 16.8 +/- 1.1 vessels/mm, p < 0.0006). However, retinal vascular density returned to normal after 3 days of treatment and 4 days of recovery. Vascularized retinal area was reduced in animals receiving 1 microg/g T4 for 3 days followed by 4 days recovery compared with saline controls (85 +/- 6% vs. 92 +/- 3%, p = 0.002). At lower doses of T4 (0.05 microg/g and 0.5 microg/g for 3 or 7 days) and at 1 microg/g T4 for 7 days, there was no effect on vascularized retinal area. Serum T4 levels were increased, with corresponding TSH suppression, after T4 treatment for 3 or 7 days. Serum IGF-1 levels were unaffected by T4 supplementation. CONCLUSIONS: Systemic T4 supplementation at 1 microg/g per day was detrimental to retinal vascular development in neonatal animals. If these effects are paralleled in human neonates, T4 supplementation might increase, rather than decrease, the risk of developing ROP. Further work on the role of T4 in the pathogenesis of ROP is warranted.

Animals↗