Decombe R, Bentué-Ferrer D, Allain H, Van den Driessche J
Laboratoire de Neuropharmacologie, Faculté de Médecine, Rennes, France.
Neurol Res. 1993 Jun;15(3):192-7. doi: 10.1080/01616412.1993.11740134.
This study was designed to evaluate the effects of two consecutive ischaemias on extracellular monoaminergic neurotransmitter concentrations. The data on the neuroamine changes induced by the second ischaemia could be used to assess the delay in aminergic neurotransmission subsequent to the primary injury. Dopamine (DA), serotonin (5HT) and their metabolites, homovanillic acid (HVA), dihydroxyphenyl-acetic acid (DOPAC) and 5-hydroxyindolacetic acid (5-HIAA) were measured in vivo through striatal microdialysis of awake rats, using HPLC and electrochemical detection. Pulsinelli and Brierley's four-vessel occlusion model was used to induce a 20-minute global transient ischaemia in the forebrain. Two experimental groups were formed: the second ischaemic period was induced 3 h after the first one in group I (n = 5) and after 24 h in group II (n = 5). Dramatic increases in DA (150 times the baseline level) and 5HT (10 times the baseline level) were recorded during the first ischaemia, consistent with literature data. Metabolites of DA and 5HT (HVA and 5HIAA) decreased significantly. Baseline values were restored after 40 min of reperfusion. There was no significant difference between the effects of the first and second ischaemias on neurotransmitter release in group I. In group II, the second ischaemia did not significantly alter the baseline aminergic neurotransmitter content, although all the clinical signs of global ischaemia were present (in particular the loss of righting reflex). These original data could be explained by delayed impairment of release mechanisms, rather than by exhaustion of the releasable pools of these neurotransmitters one day after the first ischaemia.
本研究旨在评估连续两次缺血对细胞外单胺能神经递质浓度的影响。第二次缺血诱导的神经胺变化数据可用于评估原发性损伤后胺能神经传递的延迟情况。通过对清醒大鼠纹状体进行微透析,利用高效液相色谱法(HPLC)和电化学检测,在体内测量多巴胺(DA)、5-羟色胺(5HT)及其代谢产物高香草酸(HVA)、二羟基苯乙酸(DOPAC)和5-羟吲哚乙酸(5-HIAA)。采用普尔西内利和布里尔利的四血管闭塞模型在前脑诱导20分钟的全脑短暂缺血。形成了两个实验组:在第一组(n = 5)中,第一次缺血3小时后诱导第二次缺血期;在第二组(n = 5)中,第一次缺血24小时后诱导第二次缺血期。在第一次缺血期间,记录到DA(为基线水平的150倍)和5HT(为基线水平的10倍)显著增加,这与文献数据一致。DA和5HT的代谢产物(HVA和5HIAA)显著减少。再灌注40分钟后基线值恢复。在第一组中,第一次和第二次缺血对神经递质释放的影响之间没有显著差异。在第二组中,尽管存在全脑缺血的所有临床体征(特别是翻正反射消失),但第二次缺血并未显著改变基线胺能神经递质含量。这些原始数据可以通过释放机制的延迟损伤来解释,而不是通过第一次缺血一天后这些神经递质可释放池的耗尽来解释。