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Retinal Ischemia (retinal + ischemia)
Selected AbstractsEchocardiographic Findings of Patients With Retinal Ischemia or EmbolismJOURNAL OF NEUROIMAGING, Issue 3 2002Mikael Mouradian MD ABSTRACT Background and Purpose. A potential source of emboli is not detected in more than 50% of patients with retinal arterial occlusive events. Echocardiographic studies are not always included in the diagnostic workup of these patients. The authors studied the diagnostic yield of transthoracic (TTE) and/or transesophageal (TEE) echocardiography in identifying potential sources of emboli in patients with retinal ischemia or embolism. Methods. In a prospective study, 73 consecutive patients with clinically diagnosed retinal ischemia or embolism received a standardized diagnostic workup including retinal photography, echocardiography, and imaging studies of the internal carotid arteries. TTE was performed in 83.6% of patients, TEE was performed in 5.5% of patients, and both TTE and TEE were per-formed in 11.0% of patients. Ophthalmological diagnoses consisted of amaurosis fugax (n= 28), asymptomatic cholesterol embolism to the retina (n= 34), and branch or central retinal artery occlusion (n= 11). Results. Echocardiography identified a potential cardiac or proximal aortic source for embolism in 16 of 73 (21.9%) patients, including 8 who also had either atrial fibrillation or internal carotid artery stenosis of more than 50% on the side of interest. Thus, 8 of 73 (11.0%) patients had lesions detected only by echocardiography. The most commonly identified lesions were proximal aortic plaque of more than 4 mm thickness (n= 7, 9.6%) and left ventricular ejection fraction of less than 30% (n= 6, 8.2%). TEE was particularly helpful in identifying prominent aortic plaques. Conclusion. Echocardiography frequently identifies lesions of the heart or aortic arch that can act as potential sources for retinal ischemia or embolism. Further studies are needed to evaluate the prognostic and therapeutic relevance of these findings. [source] Retinal and optic nerve oxygenation and carbonic anhydrase inhibitionACTA OPHTHALMOLOGICA, Issue 2009M LA COUR Purpose To study the effects of carbonic anhydrase inhibition on porcine retinal and optic nerve oxygenation under physiological conditions and in experimental models of ischemia. Methods Polarographic oxygen electrodes were used to measure the oxygen tension in the vitreous 500 microns in front of the optic nerve and retina. Retinal ischemia was produced by diathermia of the superior arcade vein, producing a branch retinal vein occlusion, BRVO. Optic nerve ischemia was produced by intravenous administration of 100 mg Indomethacin intravenously. Results One week after induction of BRVO, the oxygen tension over BRVO affected retina was significantly decreased by 29%. Administration of the carbonic anhydrase inhibitor dorzolamide (500 mg) caused a significant increase in the oxygen tension over BRVO affected retina, and in effect restored this tension to normal values (n=5). Intravenous administration of 300 mg Indomethacin caused a decrease of optic nerve oxygen tension by 41%. Subsequent administration of 500 mg dorzolamide increased the optic nerve oxygen tension, albeit not to normal levels (n=6). Conclusion Carbonic anhydrase inhibition increases the oxygen tension in the retina and optic nerve. In BRVO affected retina, carbonic anhydrase inhibition restores oxygen tension to normal levels. [source] Inactivation of astroglial NF-,B promotes survival of retinal neurons following ischemic injuryEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2009Galina Dvoriantchikova Abstract Reactive astrocytes have been implicated in neuronal loss following ischemic stroke. However, the molecular mechanisms associated with this process are yet to be fully elucidated. In this work, we tested the hypothesis that astroglial NF-,B, a key regulator of inflammatory responses, is a contributor to neuronal death following ischemic injury. We compared neuronal survival in the ganglion cell layer (GCL) after retinal ischemia-reperfusion in wild-type (WT) and in GFAP-I,B,-dn transgenic mice, where the NF-,B classical pathway is suppressed specifically in astrocytes. The GFAP-I,B,-dn mice showed significantly increased survival of neurons in the GCL following ischemic injury as compared with WT littermates. Neuroprotection was associated with significantly reduced expression of pro-inflammatory genes, encoding Tnf-,, Ccl2 (Mcp1), Cxcl10 (IP10), Icam1, Vcam1, several subunits of NADPH oxidase and NO-synthase in the retinas of GFAP-I,B,-dn mice. These data suggest that certain NF-,B-regulated pro-inflammatory and redox-active pathways are central to glial neurotoxicity induced by ischemic injury. The inhibition of these pathways in astrocytes may represent a feasible neuroprotective strategy for retinal ischemia and stroke. [source] Cell-penetrating peptide TAT-mediated delivery of acidic FGF to retina and protection against ischemia,reperfusion injury in ratsJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 7 2010Yi Wang Abstract The development of non-invasive ocular drug delivery systems is of practical importance in the treatment of retinal disease. In this study, we evaluated the efficacy of transactivator of transcription protein transduction domain (TAT-PTD, TAT49,57) as a vehicle to deliver acidic FGF (aFGF) to retina in rats. TAT-conjugated aFGF-His (TAT-aFGF-His) exhibited efficient penetration into the retina following topical administration to the ocular surface. Immunochemical staining with anti-His revealed that TAT-aFGF-His proteins were readily found in the retina (mainly in the ganglion cell layer) at 30 min. and remained detectable for at least 8 hrs after administration. In contrast, His+ proteins were undetectable in the retina after topical administration of aFGF-His, indicating that aFGF-His cannot penetrate the ocular barrier. Furthermore, TAT-aFGF-His, but not aFGF-His, mediated significant protection against retinal ischemia,reperfusion (IR) injury. After IR injury, retina from TAT-aFGF-His-treated rats showed better-maintained inner retinal layer structure, reduced apoptosis of retinal ganglion cells and improved retinal function compared to those treated with aFGF-His or PBS. These results indicate that conjugation of TAT to aFGF-His can markedly improve the ability of aFGF-His to penetrate the ocular barrier without impairing its biological function. Thus, TAT49,57 provides a potential vehicle for efficient drug delivery in the treatment of retinal disease. [source] Echocardiographic Findings of Patients With Retinal Ischemia or EmbolismJOURNAL OF NEUROIMAGING, Issue 3 2002Mikael Mouradian MD ABSTRACT Background and Purpose. A potential source of emboli is not detected in more than 50% of patients with retinal arterial occlusive events. Echocardiographic studies are not always included in the diagnostic workup of these patients. The authors studied the diagnostic yield of transthoracic (TTE) and/or transesophageal (TEE) echocardiography in identifying potential sources of emboli in patients with retinal ischemia or embolism. Methods. In a prospective study, 73 consecutive patients with clinically diagnosed retinal ischemia or embolism received a standardized diagnostic workup including retinal photography, echocardiography, and imaging studies of the internal carotid arteries. TTE was performed in 83.6% of patients, TEE was performed in 5.5% of patients, and both TTE and TEE were per-formed in 11.0% of patients. Ophthalmological diagnoses consisted of amaurosis fugax (n= 28), asymptomatic cholesterol embolism to the retina (n= 34), and branch or central retinal artery occlusion (n= 11). Results. Echocardiography identified a potential cardiac or proximal aortic source for embolism in 16 of 73 (21.9%) patients, including 8 who also had either atrial fibrillation or internal carotid artery stenosis of more than 50% on the side of interest. Thus, 8 of 73 (11.0%) patients had lesions detected only by echocardiography. The most commonly identified lesions were proximal aortic plaque of more than 4 mm thickness (n= 7, 9.6%) and left ventricular ejection fraction of less than 30% (n= 6, 8.2%). TEE was particularly helpful in identifying prominent aortic plaques. Conclusion. Echocardiography frequently identifies lesions of the heart or aortic arch that can act as potential sources for retinal ischemia or embolism. Further studies are needed to evaluate the prognostic and therapeutic relevance of these findings. [source] Low sensitivity of retina to AMPA-induced calcificationJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2003Noemí Andrés Abstract Glutamate is involved in most CNS neurodegenerative diseases. In particular, retinal diseases such as retinal ischemia, retinitis pigmentosa, and diabetic retinopathy are associated with an excessive synaptic concentration of this neurotransmitter. To gain more insight into retinal excitotoxicity, we carried out a dose,response study in adult rats using ,-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), a glutamate analogue. AMPA intraocular injections (between 0.27 and 10.8 nmol) caused no morphologic modification, but a 10.8 + 21 nmol double injection in a 10-day interval produced a lesion characterized by discrete neuronal loss, astroglial and microglial reactions, and calcium precipitation. Abundant calcium deposits similar to those present in rat and human brain excitotoxicity or hypoxia-ischemia neurodegeneration were detected by alizarin red staining within the retinal surface and the optic nerve. Glial reactivity, associated normally with astrocytes in the nerve fiber, was assessed in Müller cells. GABA immunoreactivity was detected not only in neuronal elements but also in Müller cells. In contrast to the high vulnerability of the brain to excitotoxin microinjection, AMPA-induced retinal neurodegeneration may provide a useful model of low central nervous system sensitivity to excitotoxicity. © 2003 Wiley-Liss, Inc. [source] 6-Formylpterin protects retinal neurons from transient ischemia,reperfusion injury in rats: A morphological and immunohistochemical studyNEUROPATHOLOGY, Issue 3 2003Taisaku Funakoshi Neuroprotective effects of 6-formylpterin (6FP) on transient retinal ischemia,reperfusion injury were evaluated in rats by means of counting the number of retinal ganglion cells, measuring the thicknesses of the inner plexiform and inner nuclear layers, and by immunohistochemical detection of apoptotic cells in the retina. Sixty-one Sprague,Dawley rats (12 weeks, male, 295,330 g) were subjected to transient retinal ischemia,reperfusion by elevated intra-ocular pressure (80 mmHg for 60 min). Intraperitoneal injection of 6FP (3.8 mg/kg) was performed before or after ischemia. The retina was histologically better preserved in rats with 6FP treatment than without 6FP treatment. 6FP showed more strong neuroprotective effects when it was administered before ischemia. The number of single-stranded DNA-positive cells in the retina also decreased remarkably in rats with 6FP treatment, especially when administered before ischemia. These results suggest that 6FP protects retinal neurons from transient ischemia,reperfusion injury, at least in part by inhibiting apoptotic cell death. [source] Assessing optic nerve pathology with diffusion MRI: from mouse to humanNMR IN BIOMEDICINE, Issue 9 2008Junqian Xu Abstract The optic nerve is often affected in patients with glaucoma and multiple sclerosis. Conventional MRI can detect nerve damage, but it does not accurately assess the underlying pathologies. Mean diffusivity and diffusion anisotropy indices derived from diffusion tensor imaging have been shown to be sensitive to a variety of central nervous system white matter pathologies. Despite being sensitive, the lack of specificity limits the ability of these measures to differentiate the underlying pathology. Directional (axial and radial) diffusivities, measuring water diffusion parallel and perpendicular to the axonal tracts, have been shown to be specific to axonal and myelin damage in mouse models of optic nerve injury, including retinal ischemia and experimental autoimmune encephalomyelitis. The progression of Wallerian degeneration has also been detected using directional diffusivities after retinal ischemia. However, translating these findings to human optic nerve is technically challenging. The current status of diffusion MRI of human optic nerve, including imaging sequences and protocols, is summarized herein. Despite the lack of a consensus among different groups on the optimal sequence or protocol, increased mean diffusivity and decreased diffusion anisotropy have been observed in injured optic nerve from patients with chronic optic neuritis. From different mouse models of optic nerve injuries to the emerging studies on patients with optic neuritis, directional diffusivities show great potential to be specific biomarkers for axonal and myelin injury. Copyright © 2008 John Wiley & Sons, Ltd. [source] 1263: Symptoms and signs of posterior uveitisACTA OPHTHALMOLOGICA, Issue 2010M KHAIRALLAH Purpose Posterior uveitis (PU) is an important anatomic form of uveitis in which the primary site of inflammation is the choroid or retina, with or without subsequent vitreous involvement. Methods Review of symptoms and signs of PU. Results The onset of PU can be sudden or less frequently insidious. Most common ocular symptoms include blurred vision, loss of vision, and floaters. Some patients with PU may have no symptoms, especially if inflammatory process is asymmetric. PU is usually associated with vitritis that can vary from mild to severe. Vitritis should be graded according to standardized grading systems. Other vitreous changes may include vitreous strands, vitreous hemorrhage, vitreous traction, and posterior vitreous detachment. Retinal and/or choroidal inflammation can be focal, multifocal, or more diffuse. It is important to distinguish between active and inactive chorioretinal disease. Retinal vasculitis can occur in the setting of several PU entities. It can involve retinal veins or arteries. It appears as focal, multifocal, or diffuse vascular cuffing or sheathing. Other retinal vasculitic changes include retinal hemorrhages, retinal vascular occlusion, retinal/optic disc neovascularization, and aneurysms. Maculopathy is common patients with PU. It may result from direct inflammatory infiltration, macular edema, serous retinal detachment, retinal ischemia, epiretinal membrane, or macular hole. Optic nerve involvement that can occur in association with PU include optic disc hyperemia/edema, optic neuritis, neuroretinitis, optic disc exudate, and optic disc granuloma. Conclusion Clinical examination is a key step in the diagnostic approach to PU. Clinician should be aware of the array of ocular symptoms of signs and their importance in orienting the differential diagnosis. [source] 2222: Hydrogen sulphide: a new CNS mediatorACTA OPHTHALMOLOGICA, Issue 2010N OSBORNE The recent discovery that hydrogen sulphide (H2S) is an endogenously produced gaseous secondary messenger capable of modulating many physiological processes, much like nitric oxide, prompted us to investigate the potential role of H2S as a retinal neuroprotective agent. In the current study we use dithiolethiones (kindly provided by Dr. Piero Del Soldato, Milan, Italy) as H2S donors and show that such substances attenuate the effect of retinal ischemia as well as oxidative and light-induced injury to a transformed line of cells (RGC-5 cells) in culture. Ischemia was delivered to rats by elevation of the intraocular pressure above the systolic blood pressure. Partial damage to the retina after seven days was determined by a combination of procedures which included analysis of electroretinograms, immunohistochemistry and changes in the retinal content of proteins and mRNAs known to be associated with ganglion cell function and apoptosis. Most of the changes caused by ischemia were significantly attenuated by intravitreal injection of a H2S donor directly after ischemia. Both light (400-700nm, intensity 1000 lux) and hydrogen peroxide caused death to RGC-5 cells in culture over a period of 24-48 hours in a time and dose-dependent manner, respectively. Light and hydrogen peroxide-induced RGC-5 cell death is by different forms of apoptosis but they are both attenuated by the H2S donor, ACS1. These initial findings demonstrate that donors of H2S may be value in the treatment of various retinal dysfunctions where oxidative stress, light or ischemia is implicated as causative fact [source] 2112: AO imaging of acute macular diseasesACTA OPHTHALMOLOGICA, Issue 2010M PAQUES Purpose To show clinical cases of acute macular diseases and their follow-up by adaptive optics flood imaging. Methods Cases of acute retinal ischemia, of acute macular neuroretinopathy, of photic injury and of poppers-related retinopathy have been observed by a prototypic adaptive optics flood imaging (ImagineEye corporation). Images from follow-up examinations have been registered in order to obtain retinal monitoring at the single photoreceptor level. Iamges were compared to high resolution OCT scans. Results Precise extension and progression/regression of lesions could be documented in all cases. Acute macular neuroretinopathy showed residual cones persisting within an area devoid of any detectable cone. Minute progression and regression of lesions could be documented. Acute ischemia of the inner retina due to central retinal vein occlusion resulted in focal masking of the cone mosaic. The cone mosaic reappeared during follow-up. Photic injury showed no changes over a 1 year follow-up. Images of poppers-related retinopathy showed partial improvement over time. Conclusion Adaptive optics flood imaging allows documentation of the extension and progression of acute maculopathies of various origins. [source] Regulation of retinal ganglion cell gene expression by bHLH transcription factors in the developing and ischemic retinasACTA OPHTHALMOLOGICA, Issue 2009JM MATTER Purpose The loss of retinal ganglion cells (RGC) in the glaucomatous retina exhibits similarities to the pattern of neuronal degeneration detected after experimental ischemia. However, a short episode of retinal ischemia does not provoke damage but rather triggers an endogenous form of neuroprotection. HIFs are bHLH proteins that regulate hypoxic response in ischemic retinas and they are involved in neuroprotection. Hypoxic environments also occur in the developing embryo and create specific niches controlling cell differentiation. Genetic analyses of HIF functions have revealed the importance of oxygen as a key regulator of ontogeny. We have compared the transcriptomes of RGCs in ischemic versus developing retinas. Methods Genome-wide screens were conducted to identify genes which are expressed in newborn RGCs and growing optic nerve axons and which are up- or down-regulated after venal occlusion by photodynamic thrombosis in the rat retinas. Results Atoh7 is a bHLH protein which is central to the transcriptional network regulating the production of RGCs. Among the targets of Atoh7 there are genes involved in the general metabolism and energy supply , e.g., alpha-enolase (ENO1), glucose-6 -phosphate isomerase (GPI). These glycolytic enzymes are also targets of HIFs and they are upregulated during hypoxia. To investigate the linkage of glycolysis and mitochondrial activity in RGCs, we monitored by confocal time-lapse imaging the dynamic distribution of mitochondria in the cell bodies and axons of RGCs that express HIF/Atoh7 targets in developing and ischemic retinas. Conclusion Some gene expression programs involved in differentiating RGCs might be reinitiated in neuroprotection. [source] REVIEW: An Approach for Neuroprotective Therapies of Secondary Brain Damage after Excitotoxic Retinal Injury in MiceCNS: NEUROSCIENCE AND THERAPEUTICS, Issue 5 2010Yasushi Ito SUMMARY Background: Many current therapeutic strategies for several eye diseases, such as glaucoma, retinal ischemia, and optic neuropathy, are focused on protection of the retinal ganglion cells (RGCs). In fact, loss of visual field, including irreversible blindness, is caused by RGC damage in these diseases. However, recent evidence suggests that the RGC damage extends to visual center in brain: the visual impairment induced by these diseases may result not only from RGC loss, but also from neuronal degeneration within the visual center in brain. Objective: To protect neurons within the visual center in the brain, as well as retinal treatment, for the prevention of visual disorder in these diseases. Methods: Once considered difficult to study the visual center in brain following RGCs loss, because obtaining the human samples that are suitable for the study may be difficult. In addition, the monkey, mainly used as glaucomatous model, is relatively high cost and needs to long experiment-span. Here, we focused on mice, because of their high degree of availability, relatively low cost, and amenability to experimental and genetic manipulation. Conclusion: In this review, we describe time-dependent alterations in the visual center in brain following RGCs loss, and whether some drugs prevent the neuronal damage of the visual center in the brain. [source] | |||||||||||||