Absence of abundant binding sites for anesthetics in rabbit brain: an in vivo NMR study.
Absence of abundant binding sites for anesthetics in rabbit brain: an in vivo NMR study.
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兔脑中缺乏丰富的麻醉剂结合位点：体内核磁共振研究。
DOI：
10.1097/00000542-199009000-00014
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发表时间：
1990
期刊：
影响因子：
8.8
通讯作者：
James,T
中科院分区：
文献类型：
--
作者：
Lockhart,SH;Cohen,Y;Yasuda,N;Kim,F;Litt,L;Eger2nd,EI;Chang,LH;James,T
使用磁共振波谱，作者测试了吸入麻醉剂的大脑浓度在吸入浓度超过3%时是否没有按比例增加1)因为麻醉剂结合并饱和了大脑中的特定部位，或2)因为麻醉剂引起的通风抑制限制了肺泡麻醉剂分压的增加。新西兰大白兔用甲氧己胺、70%一氧化二氮和1%利多卡因局部浸泡麻醉。脑内麻醉剂浓度由核磁共振获得的~(19)F谱测定。测量吸入、呼气末和动脉麻醉药浓度，以及呼气末和动脉二氧化碳分压。测定血/气分配系数，并将其用于将动脉麻醉剂浓度转换为分压。在7只自主呼吸的动物中，以恒定的吸入浓度给予氟烷(1%；n=5)或异氟烷(0.8%；n=2)20分钟；在10-20分钟内采集核磁共振波谱。此后，增加吸入浓度，重复这一过程，直到发生呼吸暂停。另外两只兔被异氟醚麻醉，在机械通气期间进行类似的研究，但吸入浓度更高。在自主呼吸的动物中，发生了呼吸性抑制，证明了PaCO2的显著增加，当吸入浓度超过3%时，脑内麻醉剂浓度并没有按比例增加。与自发通气时吸入浓度和大脑浓度之间没有相关性相反，动脉浓度和大脑浓度在自发和机械通气期间都呈线性相关(R2大于0.969)。这些结果与呼吸抑制是一致的，而不是结合到特定的大脑部位，作为大脑和吸入麻醉剂浓度之间的非线性关系的解释。
Using magnetic resonance spectroscopy, the authors tested whether cerebral concentrations of inhaled anesthetics do not increase proportionately at inspired concentrations exceeding 3% 1) because anesthetics bind to and saturate specific sites in the brain or 2) because anesthetic-induced depression of ventilation limits the increase in alveolar anesthetic partial pressure. New Zealand White rabbits were anesthetized with methohexital, 70% nitrous oxide, and local infiltration of 1% lidocaine. Cerebral concentrations of anesthetic were determined from 19F spectra acquired with nuclear magnetic resonance (NMR). Inspired, end-tidal, and arterial anesthetic concentrations, and end-tidal and arterial partial pressure of carbon dioxide were measured. Blood/gas partition coefficients were determined and used to convert arterial anesthetic concentration to partial pressures. In seven spontaneously breathing animals, halothane (1%; n= 5) or isoflurane (0.8%; n= 2) was administered at a constant inspired concentration for 20 min; NMR spectra were acquired between 10 and 20 min. Thereafter, the inspired concentration was increased and the process repeated until apnea occurred. Two additional rabbits were anesthetized with isoflurane and studied similarly but with higher inspired concentrations during mechanical ventilation. In spontaneously breathing animals, ventilatory depression occurred, documented by marked increases in PaCO2, and cerebral concentrations of anesthetic did not increase proportionately at inspired concentrations exceeding 3%. In contrast to an absence of a correlation of inspired and cerebral concentrations during spontaneous ventilation, arterial and cerebral concentrations correlated linearly during both spontaneous and mechanical ventilation (R2 greater than 0.969). These results are consistent with depression of ventilation, rather than binding to specific cerebral sites as an explanation for the nonlinear relationship between cerebral and inspired anesthetic concentrations.