Sano Y, Kanematsu E H, Yoshiura M, Iwamoto T, Takizawa N, Tokuhisa T, Mizuno A
Department of Ophthalmology, Jikei University School of Medicine, Tokyo, Japan.
Jpn J Ophthalmol. 1992;36(1):76-83.
Transient retinal and optic nerve ischemia lasting for 20 minutes was produced in Wistar rats by clipping bilateral common carotid arteries and coagulating both vertebral arteries by heat. The uric acid level in the retina and optic nerve were determined by high performance liquid chromatography with electrochemical detection just before induction of ischemia, 20 minutes after induction of ischemia, and after resolution of ischemia. Uric acid content in the optic nerve (28.0 +/- 4.5 ng/mg protein) was about 5 times higher than that in the retina (5.7 +/- 0.8 ng/mg protein) in the control experiment. Ischemia lasting for 20 minutes caused a 2.7-fold increase of uric acid in the optic nerve and a 1.8-fold increase in the retina. Following reperfusion of the blood flow by unclipping of the common carotid arteries, the uric acid level decreased to the control level in both the retina and optic nerve 30 minutes after unclipping, which was followed by 3.1- and 1.6-fold increases in uric acid in the retina and the optic nerve, respectively, at 60 minutes after unclipping. Although ischemia alone causes tissue damage, there is some clinical evidence that greater injury can occur after oxygen is reintroduced to ischemic tissue. Our results indicate that the retina is more likely to be damaged by reperfusion than the optic nerve.
通过夹闭双侧颈总动脉并热凝双侧椎动脉，在Wistar大鼠中造成持续20分钟的短暂性视网膜和视神经缺血。在缺血诱导前、缺血诱导后20分钟以及缺血解除后，采用高效液相色谱电化学检测法测定视网膜和视神经中的尿酸水平。在对照实验中，视神经中的尿酸含量（28.0±4.5 ng/mg蛋白）约为视网膜（5.7±0.8 ng/mg蛋白）中的5倍。持续20分钟的缺血导致视神经中尿酸增加2.7倍，视网膜中尿酸增加1.8倍。通过松开颈总动脉恢复血流灌注后，松开后30分钟视网膜和视神经中的尿酸水平均降至对照水平，随后在松开后60分钟，视网膜和视神经中的尿酸分别增加3.1倍和1.6倍。虽然单纯缺血会导致组织损伤，但有一些临床证据表明，向缺血组织重新供氧后可能会发生更严重的损伤。我们的结果表明，视网膜比视神经更容易受到再灌注损伤。
