Fujikura H, Kato H, Araki T, Ban H, Hasegawa Y, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Brain Res. 1994 Feb 4;636(1):103-6. doi: 10.1016/0006-8993(94)90181-3.
Effects of naftidrofuryl oxalate (naftidrofuryl), a 5-HT2 antagonist, on neuronal damage and local cerebral blood flow was examined in a gerbil model of transient forebrain ischemia. Effect of ketanserin tartrate (ketanserin), another 5-HT2 antagonist, on neuronal damage was also examined. Pretreatment with naftidrofuryl or ketanserin prevented hippocampal CA1 neuronal loss after 5 min of transient ischemia. Naftidrofuryl did not improve hippocampal blood flow during and 1 h after transient ischemia determined by [14C]iodoantipyrine autoradiography but increased blood flow in the caudate-putamen 1 h after transient ischemia. The results show that: (1) the 5-HT2 antagonists protect against hippocampal CA1 neuronal damage; and (2) the protective effect of naftidrofuryl may not be caused by a hemodynamic mechanism but by a direct inhibitory neuromodulation via 5-HT2 antagonistic action.
在沙土鼠短暂性前脑缺血模型中,研究了5-羟色胺2(5-HT2)拮抗剂草酸萘呋胺酯(萘呋胺酯)对神经元损伤和局部脑血流量的影响。还研究了另一种5-HT2拮抗剂酒石酸酮色林(酮色林)对神经元损伤的作用。萘呋胺酯或酮色林预处理可预防短暂性缺血5分钟后海马CA1区神经元丢失。通过[14C]碘安替比林放射自显影术测定,萘呋胺酯在短暂性缺血期间及缺血后1小时并未改善海马血流量,但在短暂性缺血后1小时增加了尾状核-壳核的血流量。结果表明:(1)5-HT2拮抗剂可预防海马CA1区神经元损伤;(2)萘呋胺酯的保护作用可能不是由血流动力学机制引起的,而是通过5-HT2拮抗作用产生直接抑制性神经调节作用。