Ocular Blood Flow in Experimentally Induced Immunogenic Uveitis

Aronson, Samuel B.; Howes, Edward L.; Fish, Mathews B.; Pollycove, Myron; O'Day, Denis N.

doi:10.1001/archopht.1974.03900060064016

Cited by 11 publications

(7 citation statements)

References 8 publications

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“…In order to develop a useful ocular inflamma tion model for antiinflammatory studies, the grading and scoring systems of Draize et al [8] and Aronson et al [9] were adapted in principle but modified to give more weight on irideal responses. When lens protein was administered intracamerally, marked con gestion and hemorrhage were observed in the iris and ciliary body region.…”

Section: Discussionmentioning

confidence: 99%

“…The eyes were anesthetized locally with 2 drops of 0.5% proparacainc hydrochloride solution instilled before intracamcral injection of 25 pi of lens protein solution (446 pg/25 pi). [9] as summarized in table I. Briefly, irideal hyperemia and hemorrhage were graded 1 through 5 depending on its severity of responses and 1 through 2 depending on the areas of iris affected.…”

Section: Ocular Inflammation Modelmentioning

confidence: 99%

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Pharmacological Prevention of Ocular Inflammation Induced by Lens Proteins

Miyano¹,

Chiou²

1984

Ophthalmic Res

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Ocular inflammation was induced by lens protein to minic the traumatic injury of the eyes. Pretreatment of the eyes with indomethacin resulted in marked reduction of this ocular inflammation in the early phase. Pretreatment of the eyes with phenidone and nordihydroguaiaretic acid (NDGA) on the other hand reduced ocular inflammation during both early and late phases. These results indicate that prostaglandins are involved in early phase of the inflammation which can be reduced with cyclooxygenase inhibitors such as indomethacin and leukotrienes are responsible primarily in the later phase because they are suppressed by lipoxygenase inhibitors such as phenidone and NDGA. Although histamine is implicated in the process of inflammation, the H₁-antagonist, pyrilamine, had very little effect on ocular inflammation, whereas the H₂-antagonist, cimetidine, exhibited no effect but rather enhanced the ocular inflammatory responses at the peak of inflammation. These results are not in accord with published findings.

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Section: Discussionmentioning

confidence: 99%

Section: Ocular Inflammation Modelmentioning

confidence: 99%

Pharmacological Prevention of Ocular Inflammation Induced by Lens Proteins

Miyano¹,

Chiou²

1984

Ophthalmic Res

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“…This indicates that circulatory disturbances are of importance in the pathogenesis of the breakdown of the blood-aqueous barrier in experimental uveitis. In immunogenic uveitis of severe grade, thrombosis of intraocular vessels has been demonstrated by several authors (Segawa & Smelser 1969 Aronson & al. 1974).…”

Section: Discussionmentioning

confidence: 84%

THE PERMEABILITY OF THE RABBIT CILIARY EPITHELIUM TO HORSERADISH PEROXIDASE IN EXPERIMENTAL UVEITIS An electron microscopic study

Pedersen

1974

Acta Ophthalmologica

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Experimental uveitis has been produced in two groups of albino rabbits by a single intravitreal injection of antigen. The animals in group I were immunized by injection of 10 mg of human serum albumin, whereas those belonging to group I1 received 50 mg of the same antigen. To study the blood-aqueous barrier to proteins in the ciliary body of these eyes, horseradish peroxidase has been used as a cytochemical tracer by electron microscopy. The tracer was injected intravenously at different time intervals (1-30 min) before enucleation.In group I, in regions of inflammatory cell infiltration in the ciliary processes, peroxidase reaction product was observed in the lateral intercellular spaces of the superficial epithelium, in the internal limiting membrane, and in the posterior chamber, as evidence of breakdown of the epithelial diffusion barrier. In areas showing moderate or no inflammatory cell infiltration, the diffusion barrier to peroxidase was found intact, although the epithelium displayed marked morphological alterations.In the more heavy inflamed eyes belonging to group 11, necrosis of the ciliary epithelium and thrombosis of the ciliary vessels were prominent. K e y words: uveitis, experimental -ciliary body -aqueous humorproteins -peroxidase -rabbits -electron microscopy.

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“…16 Maymunlarda deneysel yap›lan iridosiklit ve ödematöz silier kasta üveaskleral d›fla ak›m›n belirgin bir flekilde artt›¤› tespit edilmifltir. 17 Olgumuzda da künt travma sonras› aköz hümör yap›m›n›n düflmesi ve uveoskleral d›fla ak›m›n artmas› ile hipotoni geliflti¤ini düflündük. Olgumuzda topikal steroid tedavisi ile ön kamaradaki aköz flare'in azald›¤›n› ve kan aköz bariyerinin düzeldi¤ini düflünmekteyiz.…”

Section: Tart›flmaunclassified

Künt Göz Travması Sonrası Gelişen Geçici Miyopi ve Hipotoni

Karataş¹,

Pelit²,

Akova³

2011

Tjo

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ÖzetSa¤ gözüne 1 hafta önce künt travma alm›fl hasta klini¤imize görme keskinli¤inde azalma flikayeti ile baflvurdu. Hastan›n yap›lan oftalmolojik muayenesi ve tetkikleri sonras› ayn› gözde travmatik miyopi ve hipotoni tespit edildi. T›bbi tedavi ile hastan›n flikayetleri iki hafta sonra tamamen düzeldi. Künt göz travmas› sonras›nda geliflen miyopi ve hipotoni geçi-ci olabilir. Bu hastalara ayr›nt›l› oftalmolojik muayene yap›larak, uygun tedavi uygulanmal›d›r. ( SummaryA patient whot received blunt trauma to the right eye one week ago referred to our clinic with complaints of low vision. Traumatic mMyopia and hypotonia were detected in the same eye after full ophthalmologic examination. The complaints of the patient completely disappeared after two weeks of medical treatment. Transient myopia and hypotonia after blunt ocular trauma may be temporary. After full ophthalmologic examination, proper treatment should be applied. (Turk J Ophthalmol 2011; 41: 191- GiriflNormal koflullarda dakikada 2.5 μl aköz hümör üretil-mektedir.1 Aköz hümörün ço¤u trabeküler a¤dan, %10 kadar› ise uveoskleral a¤dan gözü terk etmektedir.2 Uveoskleral d›fla ak›m büyük ölçüde göz içi bas›nc›ndan (G‹B) ba¤›m-s›zd›r. Teorik olarak hipotoni aköz hümorün yap›m›n›n azalmas›, uveoskleral d›fla ak›m›n artmas› veya episkleral venöz bas›nc›n azalmas›yla olabilir. fiiddetli hipotonide uvea, optik sinir ve retinada ödemle beraber suprasiliyer ve suprakoroidal alanlarda proteinokazeöz yap›da s›v› birikmektedir.3 Hipotoni, inflamatuar otakoidlerin etkisiyle kan-aköz bariyerinin bozulmas›na neden olmaktad›r.4 Bozulan kan-aköz bariyeri aköz hümör yap›m›n› azalt›p ve vasküler permeabiliteyi artt›rarak hipotonide bir k›s›r döngü yaratmaktad›r.Göze do¤rudan gelen künt travmalarda miyopi nadiren de olsa görülebilir. Travma sonras› de¤iflik mekanizmalarla miyopi oluflabilir. Künt göz travmas› olan hastalarda siliyer spazm ve siliyer zonüllerde zay›flama sonucu miyopi tariflenmifltir.5 Uveal effüzyon ve s›¤ ön kamara sebebiyle künt travma sonras› miyopi geliflimi de olabilmektedir. 6 Öte yandan, lens iris düzleminin öne hareketi sonucu akut aç› kapanmas› glokomu ve miyopik de¤iflim rapor edilmifltir.7 Steele 8 ise lensin ön arka çap›nda art›fla ba¤l› -4,75 ila -5,25 diyoptri de¤ifliklik gözlemlemifltir. Lensin ön arka çap›n›n artmas›, lens-iris düzleminin öne hareketi olmadan siliyer cismin ödemine ba¤l›d›r.Yaz›m›zda, künt göz travmas› sonras›nda geçici travmatik hipotoni ve miyopi geliflen bir olgu sunulmufltur.

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Ocular Blood Flow in Experimentally Induced Immunogenic Uveitis

Cited by 11 publications

References 8 publications

Pharmacological Prevention of Ocular Inflammation Induced by Lens Proteins

Pharmacological Prevention of Ocular Inflammation Induced by Lens Proteins

THE PERMEABILITY OF THE RABBIT CILIARY EPITHELIUM TO HORSERADISH PEROXIDASE IN EXPERIMENTAL UVEITIS An electron microscopic study

Künt Göz Travması Sonrası Gelişen Geçici Miyopi ve Hipotoni

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