ISCHEMIC BRAIN EDEMA--EFFECT OF Y-HYDROXYBUTYRATE ON S2-RECEPTOR BINDING SITES

我们以前的研究结果表明，缺血性水肿与 随着5-HT释放的增加， 突触体5-羟色胺（S-2）受体结合位点。 在另一项研究中， 也表明缺血前或缺血后治疗 沙鼠与γ-羟基丁酸（GHB），一种内源性中枢神经系统， 减少水肿的形成并稳定5-HT 新陈代谢. 为了进一步阐明水肿的病理机制 研究了GHB对S-2-受体的作用 结合位点在沙鼠缺血性水肿模型中进行15分钟 双侧颈动脉阻断并释放1小时。 这些研究表明，GHB诱导前，双边 沙土鼠的颈动脉阻塞阻止了缺血诱导的 使用3 H-酮色林作为配体（其 特异性标记S-2受体位点）。 因此，伽马-羟丁酸的能力， 减少缺血性水肿的形成，稳定5-HT代谢 （在以前的研究中观察到），以及防止缺血性变化， S-2受体结合位点的动力学特性，增强了 GHB对5-HT代谢途径的影响。

Our previous results demonstrated that the ischemic edema is associated with an increased release of 5-HT and kinetic changes in the properties of synaptosomal serotonin (S-2)-receptor binding sites. In another study we have also shown that either preischemic or postischemic treatment of gerbils with Gamma-hydroxybutyrate (GHB), an endogenous central nervous system depressant, reduces the formation of edema and stabilizes the 5-HT metabolism. To shed some more light on the pathomechanisms of edema formation, we investigated the preischemic GHB effect on S-2-receptor binding sites in the ischemic model of edema on gerbils subjected to 15 min bilateral carotid artery occlusion and release for 1 hr. These studies have shown that GHB given prior to the inducion of bilateral carotid artery occlusion in gerbils prevented the ischemically induced changes in S-2-receptor binding sites using 3H-ketanserin as ligand (which labels specifically S-2-receptor sites). Thus, the capability of GHB to reduce the formation of ischemic edema and stablize the 5-HT metabolism (observed in previous studies), as well as to prevent ischemic changes in the kinetic properties of S-2-receptor binding sites, reinforces the contention of GHB effect of 5-HT metabolic pathway.