4 ET-1与青光眼
放射免疫测定法在临床上已经被用于测定人血浆的内皮素水平[16],它对研究内皮素的生理学、病理生理学,已证明是非常有帮助的。正常眼压青光眼病人的ET-1的血浆水平与眼压高的青光眼病人及正常对照者相比,有升高的趋势[17]。动物模型也证明了慢性缺血可产生与ET-1浓度有关的视神经的青光眼样视杯改变。同焦的扫描激光眼底立体照像结果显示视盘苍白及青光眼杯的改变[12]。ET-1诱导的视神经缺血可以有效地被低浓度的来西地平(lacidipine)或尼非地平(nipedipine)抑制,说明这可能与内皮素的受体有关。钙离子协同剂对ET-1的血管收缩作用无增强[18]。全身使用钙离子拮抗剂可以缓解低眼压性青光眼病人病情的进展,这一结果提示钙离子拮抗剂对临床上治疗低眼压性青光眼有潜在作用[19]。研究资料支持这一假说,血管功能异常与低眼压性青光眼视神经病变的发病机理有关。
青光眼的视神经损害可以更好地定义为是一种视神经病变,它可由于不同的原因包括眼压升高引起,而这些原因只是刚刚被我们认识和了解。
作者单位:孙芳娥(河北医科大学第三医院眼科 河北省石家庄市,050051)
赵大尤(河北医科大学第三医院眼科 河北省石家庄市,050051)
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