Verhaegen M, Todd M M, Warner D S
Department of Anesthesia, University of Iowa College of Medicine, Iowa City.
Anesthesiology. 1994 Oct;81(4):965-73. doi: 10.1097/00000542-199410000-00024.
Isoflurane-N2O anesthesia (as compared with halothane-N2O) reduces the cerebral blood flow (CBF) at which electroencephalographic changes occur in humans subjected to carotid occlusion. In contrast, no differences were seen in rats when cortical depolarization (instead of the electroencephalogram) was used as the ischemic marker during equi-MAC isoflurane-N2O and halothane-N2O anesthesia. To extend these findings, we used laser-Doppler flowmetry to continuously examine CBF (CBFLDF) and attempted to better define the relation between CBF and the time to depolarization (as a measure of the rate of energy depletion after ischemia).
Cortical CBFLDF was measured in normothermic, normocarbic rats, and the cortical direct-current potential was recorded using glass microelectrodes. Animals were anesthetized with 0.75 MAC halothane or 0.75 MAC isoflurane, both in 60% N2O. After baseline recordings, both carotid arteries were occluded. Five minutes later mean arterial pressure was rapidly reduced to and held at target values of 50, 45, 40, 30 or 0 mmHg. This mean arterial pressure was maintained (and CBFLDF was continually monitored) until depolarization occurred, or for a maximum of 20 min.
CBFLDF values before and after carotid occlusion (but before hypotension) were similar in the two groups. As intended, CBFLDF decreased as postocclusion mean arterial pressure was reduced and the incidence of cortical depolarization increased. The delay until depolarization, defined as the interval between the moment CBFLDF reached 25% of the preocclusion baseline until depolarization occurred, decreased as CBFLDF was reduced. However, there were no intergroup differences except after a circulatory arrest (CBF = 0), where cortical depolarization was seen approximately 30 s later in isoflurane-N2O-anesthetized rats.
The CBF threshold for cortical depolarization as measured by laser-Doppler flowmetry did not differ significantly between halothane-N2O- and isoflurane-N2O-anesthetized rats. There were also no important differences in the times until depolarization, other than a small difference when flow = 0. If the time to depolarization is reflects the potential ischemic injury, the it is unlikely that isoflurane-N2O conveys any protective advantage relative to halothane-N2O.
异氟烷 - N₂O 麻醉（与氟烷 - N₂O 相比）可降低人类在颈动脉闭塞时出现脑电图变化的脑血流量（CBF）。相比之下，在等效最低肺泡有效浓度（MAC）的异氟烷 - N₂O 和氟烷 - N₂O 麻醉期间，当使用皮层去极化（而非脑电图）作为缺血标志物时，大鼠未见差异。为扩展这些发现，我们使用激光多普勒血流仪持续检测脑血流量（CBFLDF），并试图更好地界定脑血流量与去极化时间（作为缺血后能量耗竭速率的一种度量）之间的关系。
在体温正常、二氧化碳分压正常的大鼠中测量皮层 CBFLDF，并使用玻璃微电极记录皮层直流电位。动物用 0.75 MAC 的氟烷或 0.75 MAC 的异氟烷麻醉，均吸入 60%的 N₂O。在进行基线记录后，双侧颈动脉均被阻断。5 分钟后，平均动脉压迅速降至并维持在 50、45、40、30 或 0 mmHg 的目标值。维持此平均动脉压（并持续监测 CBFLDF）直至出现去极化，或最长持续 20 分钟。
两组在颈动脉闭塞前及闭塞后（但在低血压前）的 CBFLDF 值相似。正如预期，随着闭塞后平均动脉压降低，CBFLDF 下降，皮层去极化发生率增加。去极化延迟时间（定义为 CBFLDF 降至闭塞前基线的 25%时刻至去极化发生的时间间隔）随着 CBFLDF 降低而缩短。然而，除了循环停止（CBF = 0）后，异氟烷 - N₂O 麻醉的大鼠皮层去极化大约晚出现 30 秒外，两组之间没有差异。
通过激光多普勒血流仪测量，氟烷 - N₂O 麻醉和异氟烷 - N₂O 麻醉大鼠的皮层去极化脑血流量阈值无显著差异。去极化时间也没有重要差异，除了血流 = 0 时有微小差异。如果去极化时间反映潜在的缺血性损伤，那么异氟烷 - N₂O 相对于氟烷 - N₂O 不太可能具有任何保护优势。
