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  • 學位論文

大鼠高眼壓模式之建立-眼壓上升機制及對眼球影響的研究

The Rat Model of Chronic Intraocular Pressure (IOP) Elevation - The Mechanism of IOP Elevation and Its Related Ocular Changes

指導教授 : 王惠珠 蔡榮坤
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摘要


目的:比較兩種方法在大鼠製造慢性高眼壓和眼球內之病理變化,並釐清其機制。 材料與方法:六十二隻Lewis大鼠的一眼當成是控制組,另一眼則分別利用電燒(GC組)或是血管結紮(GT組)3條深部上鞏膜靜脈來製造高眼壓,在3個月的期間內評估眼壓,視網膜神經節細胞密度,眼球內的病理變化,並探討細胞死亡機制。利用循血綠做深部上鞏膜靜脈的血液流動研究。 結果:GC組或是GT組均可達到3個月的穩定高眼壓,並造成視網膜神經節細胞數目的逐漸減少,細胞是經由細胞凋零途徑而逐漸死亡,眼球內整體的葡萄膜組織會充血。GC組還發現有眼球內炎,隅角周邊前黏連和外側視網膜萎縮。前房內注射循血綠會出現在深部上鞏膜靜脈的遠端,注射到深部上鞏膜靜脈則會在葡萄膜組織見到其分佈。 結論:血管結紮法與電燒法都可達到類似的結果,但併發症較容易出現在電燒組,因此血管結紮法是較為理想的方法,而變得狹窄的隅角是誘發在阻塞深部上鞏膜靜脈後所致眼壓上升的原因。

並列摘要


Purpose:To compare the results and to clarify the mechanism of two different methods of inducing ocular hypertension and relating ocular damage in rats. Material and Methods:Elevated ocular intraocular pressure (IOP) was induced in one eye of 62 Lewis rats by either cautery (GC) or ligation (GT) of 3 deep episcleral vessels. In 3 months, IOP, the loss of retinal ganglion cells (RGC), and intraocular pathologic changes were evaluated. The blood flow in deep episcleral veins (DEVs) was studied by indocyanine green (ICG). Results:Elevated IOP was consistently maintained for up to 3 months in both GC and GT eyes. The density of RGC was gradually reduced, and the death of RGC was through apoptosis pathway. Uveal tissues in all GC and GT eyes were congested. intraocular inflammation, peripheral anterior synechiae, and outer retinal atrophy were found only in GC eyes. Intracameral injection of ICG was traced at the distal part of DEVs, and ICG was found in the uveal tissue by injection of ICG into the DEVs. Conclusions:Similar ocular hypertension and damage were induced by both GC and GT eyes, but more complications were found in GC eyes. So the GT method is a preferred method to induce ocular hypertension in rats. The angle-closure type of ocular hypertension plays a role in elevating IOP after occlusion of the DEVs.

參考文獻


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