Kadoya F, Mitani A, Kataoka K, Arai T
Department of Anesthesia, Uwajima Municipal Hospital.
Masui. 1992 Oct;41(10):1610-6.
The xanthine derivative propentofylline (HWA 285) has been reported to show protective effects against neuronal damage induced by cerebral ischemia. In the present study, we investigated the effect of propentofylline on the hypoxia-hypoglycemia-induced intracellular calcium accumulation in gerbil hippocampal slices using microfluorometry. When slices were superfused with hypoxic-hypoglycemic medium that did not contain propentofylline, an acute increase in calcium accumulation was detected 75-200s (mean latency of 123s) after the start of hypoxic-hypoglycemia. When slices were superfused with hypoxic-hypoglycemic medium that contained 10 microM, 100 microM and 1mM propentofylline, the latency period before acute increase in calcium accumulation was prolonged in all subregions of the hippocampus in a dose-dependent manner: mean latencies in field CA 1 were 146, 168, and 197s after hypoxic-hypoglycemia, respectively. This retardation in calcium accumulation may be involved in the mechanisms by which propentofylline diminishes ischemic injury.
据报道,黄嘌呤衍生物丙戊茶碱(HWA 285)对脑缺血诱导的神经元损伤具有保护作用。在本研究中,我们使用微量荧光测定法研究了丙戊茶碱对沙土鼠海马切片中缺氧-低血糖诱导的细胞内钙积累的影响。当切片用不含丙戊茶碱的缺氧-低血糖培养基灌流时,在缺氧-低血糖开始后75-200秒(平均潜伏期123秒)检测到钙积累急性增加。当切片用含有10微摩尔、100微摩尔和1毫摩尔丙戊茶碱的缺氧-低血糖培养基灌流时,海马所有亚区钙积累急性增加前的潜伏期均呈剂量依赖性延长:缺氧-低血糖后,CA1区的平均潜伏期分别为146、168和197秒。钙积累的这种延迟可能参与了丙戊茶碱减轻缺血性损伤的机制。