Department of Anaesthesiology, Odense University Hospital, Odense C, Denmark.
Acta Anaesthesiol Scand. 2013 Feb;57(2):229-35. doi: 10.1111/j.1399-6576.2012.02783.x. Epub 2012 Sep 28.
In patients with traumatic brain injury as well as stroke, impaired cerebral oxidative energy metabolism may be an important factor contributing to the ultimate degree of tissue damage. We hypothesize that mitochondrial dysfunction can be diagnosed bedside by comparing the simultaneous changes in brain tissue oxygen tension (PbtO(2)) and cerebral cytoplasmatic redox state. The study describes cerebral energy metabolism during mitochondrial dysfunction induced by sevoflurane in piglets.
Ten piglets were included, seven in the experimental group (anesthetized with sevoflurane) and three in the control group (anesthetized with midazolam). PbtO(2) and cerebral levels of glucose, lactate, and pyruvate were monitored bilaterally. The biochemical variables were obtained by intracerebral microdialysis.
All global variables were within normal range and did not differ significantly between the groups except for blood lactate that was slightly higher in the experimental group. Mitochondrial dysfunction was observed in the group of animals initially anesthetized with sevoflurane. Cerebral glucose was significantly lower in the experimental group than in the control group whereas lactate and lactate/pyruvate ratio were significantly higher. Pyruvate and tissue oxygen tension remained within normal range in both groups. Changes of intracerebral variables indicating mitochondrial dysfunction were present already from the very start of the monitoring period.
Intracerebral microdialysis revealed mitochondrial dysfunction by marked increases in cerebral lactate and lactate/pyruvate ratio simultaneously with normal levels of pyruvate and a normal PbtO(2). This metabolic pattern is distinctively different from cerebral ischemia, which is characterized by simultaneous decreases in PbtO(2) and intracerebral pyruvate.
在创伤性脑损伤和中风患者中，受损的脑氧化能量代谢可能是导致组织损伤最终程度的重要因素。我们假设通过比较脑组织氧张力（PbtO2）和脑细胞质还原状态的同时变化，可以在床边诊断线粒体功能障碍。本研究描述了七氟醚诱导的幼猪线粒体功能障碍期间的脑能量代谢。
纳入 10 头幼猪，7 头在实验组（七氟醚麻醉），3 头在对照组（咪达唑仑麻醉）。双侧监测 PbtO2 和脑葡萄糖、乳酸和丙酮酸水平。通过颅内微透析获得生化变量。
除实验组的血乳酸略高外，所有全局变量均在正常范围内，两组间无显著差异。最初用七氟醚麻醉的动物组观察到线粒体功能障碍。实验组脑葡萄糖明显低于对照组，而乳酸和乳酸/丙酮酸比值明显升高。两组的丙酮酸和组织氧张力均在正常范围内。表明线粒体功能障碍的颅内变量变化从监测开始就已经存在。
颅内微透析通过脑乳酸和乳酸/丙酮酸比值的显著增加以及丙酮酸和 PbtO2 的正常水平揭示了线粒体功能障碍。这种代谢模式与脑缺血明显不同，脑缺血的特征是 PbtO2 和颅内丙酮酸同时降低。
