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家兔6-氨基烟酰胺中毒的超微结构眼部病变

Ultrastructural ocular lesions of 6-aminonicotinamide toxicosis in rabbits.

作者信息

Render J A, Turek J J, Hinsman E J, Carlton W W

出版信息

Vet Pathol. 1985 Sep;22(5):475-82. doi: 10.1177/030098588502200507.

DOI:10.1177/030098588502200507
PMID:2931895
Abstract

6-Aminonicotinamide, given by intraperitoneal injection to male and female Dutch belted rabbits, produced swelling and vacuolation of ciliary and iridal epithelium plus vacuolation of the retinal pigment epithelial and outer plexiform layers of the retina. By transmission electron microscopy, inner and outer ciliary epithelial cells and inner iridal epithelial cells contained numerous coalescing, membrane-bound vacuoles of the cytocavitary network. These vacuoles were viewed as numerous interconnecting, intracytoplasmic cavities in scanning electron micrographs. Swelling of vacuolated epithelial cells and the presence of fibrin and proteinaceous fluid in the ciliary stroma resulted in thickening of the anterior ciliary processes with the formation of surface alterations detectable by scanning electron microscopy. In transmission electron micrographs the vacuoles in the retinal pigment epithelium were large, electron-lucent spaces and the vacuoles in the outer plexiform layer of the retina appeared to be intracytoplasmic spaces in axons of photoreceptor cells. Distention of cytocavitary structures has been reported in glial cells of animals given 6-aminonicotinamide and this change was apparently due to alterations in ion and water movement across cellular membranes that resulted in intracellular edema.

摘要

给雄性和雌性荷兰带兔腹腔注射6-氨基烟酰胺,可导致睫状体和虹膜上皮肿胀、空泡化,以及视网膜色素上皮和视网膜外丛状层空泡化。通过透射电子显微镜观察,睫状体内外上皮细胞和虹膜内上皮细胞含有大量融合的、与细胞腔网络膜结合的空泡。在扫描电子显微镜照片中,这些空泡被视为大量相互连接的胞质内腔。空泡化上皮细胞的肿胀以及睫状体基质中纤维蛋白和蛋白质液体的存在导致睫状突前部增厚,并形成可通过扫描电子显微镜检测到的表面改变。在透射电子显微镜照片中,视网膜色素上皮中的空泡是大的、电子透明的空间,而视网膜外丛状层中的空泡似乎是光感受器细胞轴突中的胞质内空间。已有报道称,给动物注射6-氨基烟酰胺后,神经胶质细胞中的细胞腔结构会扩张,这种变化显然是由于跨细胞膜的离子和水运动改变导致细胞内水肿所致。

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Ultrastructural ocular lesions of 6-aminonicotinamide toxicosis in rabbits.家兔6-氨基烟酰胺中毒的超微结构眼部病变
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