Mäepea O, Karlsson C, Alm A
Arch Ophthalmol. 1984 Sep;102(9):1366-9. doi: 10.1001/archopht.1984.01040031108035.
Edetic acid labeled with chromium 51 was injected intravenously in normal rats and in rats with streptozocin-induced diabetes. One hour after the injection the animals were killed and the concentrations of edetic acid 51Cr in vitreous body, retina, and brain were determined. No significant difference was observed between the two groups for either tissue. In a second series, a mixture of tritiated 1-glucose and aminohippuric acid tagged with carbon 14 was injected instead of edetic acid. A substantial accumulation of aminohippuric acid 14C compared with tritiated 1-glucose was observed in the vitreous body and the brain of diabetic rats in comparison with the control group. It is concluded that untreated streptozocin-induced diabetes in rats for one to two weeks will not cause a generalized increase in the permeability of the blood-ocular or the blood-brain barriers, but organic acids may accumulate in the vitreous body as well as in the brain as a consequence of reduced outward transport through these barriers.
将用铬51标记的依地酸静脉注射到正常大鼠和链脲佐菌素诱导的糖尿病大鼠体内。注射1小时后处死动物,测定玻璃体、视网膜和大脑中依地酸51Cr的浓度。两组在任何一种组织中均未观察到显著差异。在第二个系列中,注射的是氚标记的1-葡萄糖和用碳14标记的氨基马尿酸的混合物,而不是依地酸。与对照组相比,在糖尿病大鼠的玻璃体和大脑中观察到,与氚标记的1-葡萄糖相比,氨基马尿酸14C有大量蓄积。得出的结论是,未治疗的链脲佐菌素诱导的大鼠糖尿病1至2周不会导致血眼屏障或血脑屏障通透性普遍增加,但由于通过这些屏障的外向转运减少,有机酸可能会在玻璃体以及大脑中蓄积。