Matsumoto M, Zornow M H, Rabin B C, Maze M
Department of Anesthesiology, University of California at San Diego, La Jolla 92093.
Brain Res. 1993 Nov 12;627(2):325-9. doi: 10.1016/0006-8993(93)90337-m.
This study was designed to evaluate the ability of a selective alpha 2 adrenergic agonist (dexmedetomidine) to attenuate ischemia-induced increases in striatal norepinephrine, 3 methoxy-4-hydroxyphenethyleneglycol (MHPG), dopamine, and 5-hydroxyindoleacetic acid (5-HIAA). Following the induction of anesthesia with halothane and oxygen, microdialysis catheters were stereotactically inserted into the striatum of 9 New Zealand white rabbits. Monitored variables included epidural temperature, arterial blood gases and pH, mean arterial pressure, blood glucose concentrations and the electroencephalogram. Following collection of baseline samples of dialysate, animals were randomized to receive a continuous infusion of saline (n = 4) or dexmedetomidine (n = 5). Cerebral ischemia was produced by the inflation of a neck tourniquet and induction of deliberate hypotension. Dialysate collection continued during the ischemic period and for the ensuing 140 min of reperfusion. All dialysate was frozen at -80 degrees C prior to its analysis by liquid chromatography for catecholamine content. There were no significant differences between the two groups for temperature, arterial blood gases, or mean arterial pressure. Blood glucose concentrations increased in the dexmedetomidine group. The electroencephalogram became isoelectric within 30 s of tourniquet inflation in all animals. Analysis of the norepinephrine and MHPG levels revealed significantly lower values for the dexmedetomidine-treated group during and following the ischemic period. There were no differences between groups for extracellular dopamine or 5-HIAA concentrations. These results suggest that the alpha 2 agonist dexmedetomidine can selectively attenuate ischemia-induced increases in striatal norepinephrine concentrations.
本研究旨在评估一种选择性α2肾上腺素能激动剂（右美托咪定）减轻缺血诱导的纹状体去甲肾上腺素、3-甲氧基-4-羟基苯乙二醇（MHPG）、多巴胺和5-羟吲哚乙酸（5-HIAA）增加的能力。在用氟烷和氧气诱导麻醉后，将微透析导管立体定向插入9只新西兰白兔的纹状体。监测变量包括硬膜外温度、动脉血气和pH值、平均动脉压、血糖浓度和脑电图。在收集透析液基线样本后，将动物随机分为接受连续输注生理盐水（n = 4）或右美托咪定（n = 5）。通过颈部止血带充气和诱导故意低血压来产生脑缺血。在缺血期及随后140分钟的再灌注期间继续收集透析液。所有透析液在-80℃下冷冻，然后通过液相色谱法分析儿茶酚胺含量。两组在温度、动脉血气或平均动脉压方面无显著差异。右美托咪定组血糖浓度升高。所有动物在止血带充气后30秒内脑电图变为等电位。去甲肾上腺素和MHPG水平分析显示，右美托咪定治疗组在缺血期及缺血后的值显著较低。两组细胞外多巴胺或5-HIAA浓度无差异。这些结果表明，α2激动剂右美托咪定可以选择性减轻缺血诱导的纹状体去甲肾上腺素浓度增加。
