Sakamoto K, Kuwagata M, Nakahara T, Ishii K
Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, 9-1 Shirokane 5-chome, Tokyo 108-8641, Minato-ku, Japan.
Eur J Pharmacol. 2001 Apr 20;418(1-2):89-93. doi: 10.1016/s0014-2999(01)00938-4.
To determine whether stimulation of adenosine receptors and opening of ATP-sensitive K(+) channels were involved in the protective effect of late preconditioning in the rat retina, rats were subjected to 60 min of retinal ischemia, and ischemic preconditioning was achieved by applying 5 min of ischemia 24 h before 60 min of ischemia. In non-preconditioned rats, cell loss in the ganglion cell layer and thinning of the inner plexiform and inner nuclear layer were observed 7 days after 60 min of ischemia. Ischemic preconditioning completely prevented the retinal tissue damage and 8-phenyltheophylline or 5-hydroxydecanoate reduced the protective effect of ischemic preconditioning. Therefore, stimulation of adenosine receptors and opening of ATP-sensitive K(+) channels might be involved in the mechanism of histological protection by late preconditioning in the retina.
为了确定腺苷受体的刺激和ATP敏感性钾通道的开放是否参与大鼠视网膜延迟预处理的保护作用,将大鼠进行60分钟的视网膜缺血,缺血预处理通过在60分钟缺血前24小时施加5分钟缺血来实现。在未预处理的大鼠中,缺血60分钟后7天观察到神经节细胞层的细胞丢失以及内网状层和内核层变薄。缺血预处理完全防止了视网膜组织损伤,而8-苯基茶碱或5-羟基癸酸降低了缺血预处理的保护作用。因此,腺苷受体的刺激和ATP敏感性钾通道的开放可能参与视网膜延迟预处理的组织学保护机制。