Saletu B, Grünberger J, Linzmayer L, Anderer P
Department of Psychiatry, School of Medicine, University of Vienna, Austria.
Psychopharmacology (Berl). 1992;109(1-2):30-40. doi: 10.1007/BF02245477.
In a double-blind, placebo-controlled trial, human brain function and mental performance were studied under two different degrees of hypoxia after administration of two different doses (6 mg and 9 mg) of co-dergocrine mesylate (CDM) utilizing blood gas analysis, EEG mapping and psychometry. Hypoxic hypoxidosis (i.e. impairment of cerebral metabolism due to hypoxia) was experimentally induced by a fixed gas combination of 9.8% oxygen (O2) and 90.2% nitrogen (N2) (found in 6000 m altitude), and of 8.6% O2, 91.4% N2 (found in 7000 m altitude), which was inhaled for 23 min under normobaric conditions by 18 healthy volunteers. They received randomized after an adaptation session placebo, 6 mg and 9 mg co-dergocrine mesylate (CDM). Evaluation of blood gases, brain mapping and psychometry was carried out at 0, 2, 4, 6, 8 h after oral drug administration. Blood gas analysis demonstrated a drop in PO2 to 42 and 32 mm Hg 23 min after inhalation of the 9.8% and 8.6% gas mixture, respectively, PCO2 decreased to 32 and 31 mm Hg, pH increased to 7.46 and 7.47 and base excess increased to 0.50 and 0.90 nmol/l, respectively. EEG mapping demonstrated an increase in delta and decrease of alpha power and a slowing of the centroid over almost the whole brain. 6 mg and slightly less so 9 mg CDM attenuated this deterioration of vigilance (i.e. dynamic state of the neuronal network determining adaptive behavior). At the behavioral level, moderate hypoxia induced a deterioration of noopsychic performance, which was mitigated by 6 mg, but not by 9 mg CDM. A deepening of the hypoxia resulted in a loss of these brain protective effects of both doses. Decrement of the thymopsyche increased after both doses in the moderate hypoxic condition, while under marked hypoxia 6 mg CDM attenuated and 9 mg aggravated this deterioration. Time-wise, brain protective effects reached the level of statistical difference between the 2nd and the 6th hour. Somatic complaints like feeling dazed, giddiness and headache were mitigated dose dependently by CDM in the moderate, but not in the marked hypoxic hypoxidosis.
在一项双盲、安慰剂对照试验中，利用血气分析、脑电图映射和心理测量法，研究了18名健康志愿者在常压条件下吸入两种不同浓度（9.8%氧气（O₂）和90.2%氮气（N₂），相当于海拔6000米处的气体组合；以及8.6% O₂、91.4% N₂，相当于海拔7000米处的气体组合）的混合气体23分钟，从而实验性诱导出低氧性低氧血症（即由于缺氧导致的脑代谢损害）后，给予两种不同剂量（6毫克和9毫克）的甲磺酸氢化麦角碱（CDM）时的人脑功能和心理表现。他们在适应期后随机接受安慰剂、6毫克和9毫克甲磺酸氢化麦角碱（CDM）。在口服药物后的0、2、4、6、8小时进行血气、脑图谱和心理测量评估。血气分析显示，吸入9.8%和8.6%的气体混合物23分钟后，动脉血氧分压（PO₂）分别降至42和32毫米汞柱，二氧化碳分压（PCO₂）降至32和31毫米汞柱，pH值升至7.46和7.47，碱剩余升至0.50和0.90纳摩尔/升。脑电图映射显示，几乎整个大脑的δ波功率增加，α波功率降低，质心减慢。6毫克以及稍低剂量的9毫克CDM减轻了这种警觉性的恶化（即决定适应性行为的神经网络的动态状态）。在行为层面，中度缺氧导致非精神心理表现恶化，6毫克CDM可缓解这种恶化，但9毫克则不能。缺氧程度加深导致两种剂量的脑保护作用均丧失。在中度缺氧条件下两种剂量均使胸腺心理功能减退增加，而在明显缺氧时，6毫克CDM减轻了这种恶化，9毫克则加重了这种恶化。从时间上看，脑保护作用在第2小时和第6小时之间达到统计学差异水平。在中度而非明显的低氧性低氧血症中，CDM剂量依赖性地减轻了如头晕、眩晕和头痛等躯体不适。
