Adachi M, Takahashi K, Yuge K, Miki H, Uyama M
Department of Ophthalmology, Kansai Medical University, Osaka-fu, Japan.
Nippon Ganka Gakkai Zasshi. 1997 Jan;101(1):24-9.
Brief ischemia caused by high intraocular pressure induced tolerance to subsequent ischemia-reperfusion injury in rats. Male Wistar rats were subjected to 15 minutes of ischemia. This ischemic injury did not show distinct axonal damage in the optic nerve in electron microscopy. 1, 2, 4, 7, and 14 days after the first 15 min ischemia, the rats were subjected to a second ischemia for 45 minutes (ischemic tolerance). After 1 week, the rats were perfusion fixed and the optic nerves were processed for light and electron microscopy. Samples of the axonal density in the central optic nerve 2 mm behind the lamina cribrosa were observed and counted an electron micrographs. In axonal morpometric findings, 2 days and more after brief ischemia, the damage was lessened more than after 45 minutes ischemia (control) and the difference was significant. This 'ischemic tolerance' induced by brief ischemia might be considered the same stress as brain ischemia-reperfusion injury.
高眼压引起的短暂性缺血可诱导大鼠对随后的缺血再灌注损伤产生耐受性。雄性Wistar大鼠经历15分钟的缺血。在电子显微镜下,这种缺血性损伤在视神经中未显示出明显的轴突损伤。在首次15分钟缺血后的1、2、4、7和14天,大鼠再次经历45分钟的缺血(缺血耐受性)。1周后,对大鼠进行灌注固定,并对视神经进行光镜和电镜处理。在筛板后2 mm处的中央视神经中观察轴突密度样本,并在电子显微镜照片上进行计数。在轴突形态学研究结果中,短暂缺血后2天及更长时间,损伤程度比45分钟缺血(对照组)后减轻,且差异具有统计学意义。短暂缺血诱导的这种“缺血耐受性”可能被认为与脑缺血再灌注损伤是相同的应激反应。