Kaisti Kaike K, Långsjö Jaakko W, Aalto Sargo, Oikonen Vesa, Sipilä Hannu, Teräs Mika, Hinkka Susanna, Metsähonkala Liisa, Scheinin Harry
Department of Anesthesiology, Turku University Hospital, Finland.
Anesthesiology. 2003 Sep;99(3):603-13. doi: 10.1097/00000542-200309000-00015.
Anesthetic agents, especially volatile anesthetics and nitrous oxide (N2O), are suspected to perturb cerebral homeostasis and vascular reactivity. The authors quantified the effects of sevoflurane and propofol as sole anesthetics and in combination with N2O on regional cerebral blood flow (rCBF), metabolic rate of oxygen (rCMRO2), and blood volume (rCBV) in the living human brain using positron emission tomography.
15O-labeled water, oxygen, and carbon monoxide were used as positron emission tomography tracers to determine rCBF, rCMRO2 and rCBV, respectively, in eight healthy male subjects during the awake state (baseline) and at four different anesthetic regimens: (1) sevoflurane alone, (2) sevoflurane plus 70% N2O (S+N), (3) propofol alone, and (4) propofol plus 70% N2O (P+N). Sevoflurane and propofol were titrated to keep a constant hypnotic depth (Bispectral Index 40) throughout anesthesia. End-tidal carbon dioxide was strictly kept at preinduction level.
The mean +/- SD end-tidal concentration of sevoflurane was 1.5 +/- 0.3% during sevoflurane alone and 1.2 +/- 0.3% during S+N (P < 0.001). The measured propofol concentration was 3.7 +/- 0.7 microg/ml during propofol alone and 3.5 +/- 0.7 microg/ml during P+N (not significant). Sevoflurane alone decreased rCBF in some (to 73-80% of baseline, P < 0.01), and propofol in all brain structures (to 53-70%, P < 0.001). Only propofol reduced also rCBV (in the cortex and cerebellum to 83-86% of baseline, P < 0.05). Both sevoflurane and propofol similarly reduced rCMRO2 in all brain areas to 56-70% and 50-68% of baseline, respectively (P < 0.05). The adjunct N2O counteracted some of the rCMRO2 and rCBF reductions caused by drugs alone, and especially during S+N, a widespread reduction (P < 0.05 for all cortex and cerebellum vs. awake) in the oxygen extraction fraction was seen. Adding of N2O did not alter the rCBV effects of sevoflurane and propofol alone.
Propofol reduced rCBF and rCMRO2 comparably. Sevoflurane reduced rCBF less than propofol but rCMRO2 to an extent similar to propofol. These reductions in flow and metabolism were partly attenuated by adjunct N2O. S+N especially reduced the oxygen extraction fraction, suggesting disturbed flow-activity coupling in humans at a moderate depth of anesthesia.
麻醉剂,尤其是挥发性麻醉剂和氧化亚氮(N2O),被怀疑会扰乱脑内稳态和血管反应性。作者使用正电子发射断层扫描技术,对七氟醚和丙泊酚作为单一麻醉剂以及与N2O联合使用时,对活体人脑局部脑血流量(rCBF)、氧代谢率(rCMRO2)和血容量(rCBV)的影响进行了量化。
在8名健康男性受试者的清醒状态(基线)以及四种不同麻醉方案下,分别使用15O标记的水、氧气和一氧化碳作为正电子发射断层扫描示踪剂来测定rCBF、rCMRO2和rCBV:(1)单独使用七氟醚,(2)七氟醚加70% N2O(S+N),(3)单独使用丙泊酚,(4)丙泊酚加70% N2O(P+N)。在整个麻醉过程中,滴定七氟醚和丙泊酚以维持恒定的催眠深度(脑电双频指数40)。呼气末二氧化碳严格维持在诱导前水平。
单独使用七氟醚时,七氟醚的平均±标准差呼气末浓度为1.5±0.3%,S+N时为1.2±0.3%(P<0.001)。单独使用丙泊酚时测得的丙泊酚浓度为3.7±0.7微克/毫升,P+N时为3.5±0.7微克/毫升(无显著差异)。单独使用七氟醚会使某些脑区的rCBF降低(降至基线的73 - 80%,P<0.01),而丙泊酚会使所有脑结构的rCBF降低(降至53 - 70%,P<0.001)。只有丙泊酚还会使rCBV降低(皮质和小脑降至基线的83 - 86%,P<0.05)。七氟醚和丙泊酚均同样地使所有脑区的rCMRO2分别降至基线的56 - 70%和50 - 68%(P<0.05)。辅助使用的N2O抵消了部分由药物单独引起的rCMRO2和rCBF降低,尤其是在S+N时,氧摄取分数出现广泛降低(与清醒状态相比,所有皮质和小脑P<0.05)。添加N2O并未改变七氟醚和丙泊酚单独对rCBV的影响。
丙泊酚对rCBF和rCMRO2的降低程度相当。七氟醚对rCBF的降低幅度小于丙泊酚,但对rCMRO2的降低程度与丙泊酚相似。这些血流和代谢的降低部分被辅助使用的N2O减弱。S+N尤其降低了氧摄取分数,表明在中等麻醉深度下人体的血流 - 活性耦合受到干扰。