Enlund M, Mentell O, Engström C, Horneman G, Ronquist G
Department of Anaesthesia and Intensive Care, Central Hospital, Västerås, Sweden.
Ups J Med Sci. 1996;101(1):97-111. doi: 10.3109/03009739609178916.
The study objective was, firstly, to investigate whether anaesthesia with induced arterial hypotension would cause leakage of a biochemical marker of neuronal injury, adenylate kinase (AK), into the cerebrospinal fluid (CSF). (
arterial hypotension = mean arterial pressure (MAP) 50-65 mmHg during > or = 10 min). Secondly, a subgroup of patients was examined with a limited battery of psychometric tests. Patients, scheduled for orthognathic surgery, were allocated to either hypotension (n = 20) or normotension (n = 20). Seventeen patients were subjected to psychometry. Arterial blood pressure was recorded continuously and controlled by adjustments of the administered concentration of the inhalational anaesthetic isoflurane. Fentanyl, an opioid, was given equally in both groups. A lumbar puncture was performed approximately 20 h post-operatively for a CSF sample, later analysed for AK activity. Neuropsychological tests were performed the day before surgery and the fourteenth day postoperatively. The CSF-AK value was pathologically increased ( > 0.040 U/L) in 24 patients (65%), of whom 9 were normotensive. There was no significant difference between the CSF-AK values in the hypotensive and normotensive groups, mean values were 0.082 (s.d. 0.051) and 0.066 (s.d. 0.059) U/L, respectively. The overall correlation between the 10 min MAP levels and the CSF-AK values was close to zero. In the pilot neuropsychological investigation some abnormalities were observed, indicating clinically significant adverse effects in four hypotensive patients, of whom two displayed pathologically increased CSF-AK values. At the group level, the correlation between the changes in psychometry and the measured CSF-AK values was poor. Increases in CSF-AK activities may be a non-specific occurrence in the perioperative interval, possibly indicating an adverse effect on the brain. Arterial hypotension could not be proven to explain the CSF-AK outcome.
本研究的目的，首先是调查诱导性动脉低血压麻醉是否会导致神经元损伤的生化标志物腺苷酸激酶（AK）漏入脑脊液（CSF）。（定义：动脉低血压=平均动脉压（MAP）在50 - 65 mmHg持续≥10分钟）。其次，对一组患者进行了一系列有限的心理测试。计划进行正颌手术的患者被分为低血压组（n = 20）或正常血压组（n = 20）。17名患者接受了心理测试。连续记录动脉血压，并通过调整吸入麻醉药异氟烷的给药浓度进行控制。两组均给予等量的阿片类药物芬太尼。术后约20小时进行腰椎穿刺采集脑脊液样本，随后分析AK活性。术前一天和术后第十四天进行神经心理学测试。24名患者（65%）的脑脊液AK值病理性升高（> 0.040 U/L），其中9名是正常血压患者。低血压组和正常血压组的脑脊液AK值之间无显著差异，平均值分别为0.082（标准差0.051）和0.066（标准差0.059）U/L。10分钟MAP水平与脑脊液AK值之间的总体相关性接近零。在初步的神经心理学调查中观察到一些异常，表明4名低血压患者有临床显著的不良反应，其中2名脑脊液AK值病理性升高。在组水平上，心理测试变化与测得的脑脊液AK值之间的相关性较差。脑脊液AK活性升高可能是围手术期的一种非特异性现象，可能表明对大脑有不良影响。无法证明动脉低血压可解释脑脊液AK的结果。
