PRIMATE BRAIN TOLERANCE TO TEMPORARY FOCAL CEREBRAL-ISCHEMIA DURING ISOFLURANE-INDUCED OR SODIUM NITROPRUSSIDE-INDUCED HYPOTENSION
PRIMATE BRAIN TOLERANCE TO TEMPORARY FOCAL CEREBRAL-ISCHEMIA DURING ISOFLURANE-INDUCED OR SODIUM NITROPRUSSIDE-INDUCED HYPOTENSION
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DOI：
10.1097/00000542-198904000-00023
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发表时间：
1989-04-01
期刊：
影响因子：
8.8
通讯作者：
MIELKE, BW
中科院分区：
文献类型：
--
作者：
GELB, AW;BOISVERT, DP;MIELKE, BW
异氟烷的特性表明它可以提供脑缺血保护。这项研究在灵长类动物中比较了异氟烷或硝普钠 (SNP) 引起的低血压期间 45 分钟暂时性局灶性缺血后的神经系统结果。研究人员对十四只猕猴进行了研究。七只动物在手术准备期间接受氟烷麻醉和七只异氟烷麻醉。经眼眶暴露大脑中动脉（MCA）后，氟烷组通过输入SNP，吸入的氟烷浓度降低至0.75%，平均血压（BP）降低至50 mmHg。在异氟烷组中，滴定异氟烷以将平均血压降低至 50 mmHg。稳定的低血压维持90分钟，其中包括45分钟的MCA闭塞期。监测包括动脉血压、动脉血气、脑电图、体感诱发电位（SEP）和温度。手术后让动物醒来并每 8 小时进行一次神经学评估。术后第三天，他们被重新麻醉并接受磁共振成像（MRI）和SEP记录。此后，用静脉注射氯化钾处死它们，并固定大脑进行神经病理学检查。所有动物均在手术过程中存活下来，但接受氟烷的两只动物和接受异氟烷的动物均未过早死亡（P < 0.02）。所有动物的 SEP 在 MCA 闭塞后 10 分钟内消失，然后部分或完全恢复。各组之间的神经系统评分、MRI 评估的病变大小（异氟烷 15.7 .+-. 6%，氟烷/SNP 10.5 .+-. 4%）或神经病理学病变的范围或严重程度没有差异。如果在诱发性低血压期间发生严重到足以导致 SEP 完全丧失的局灶性脑缺血，与氟烷麻醉和 SNP 诱发性低血压相比，异氟烷不能提供脑保护作用。
Isoflurane has properties that suggest it may provide cerebral protection from ischemia. This study compared, in primates, neurologic outcome after a 45-min period of temporary focal ischemia during hypotension induced with either isoflurane or sodium nitroprusside (SNP). Fourteen macaque monkeys were studied. Seven animals received halothane and seven isoflurane anesthesia during surgical preparation. After transorbital exposure of the middle cerebral artery (MCA), in the halothane group, the inspired halothane was reduced to 0.75% and the mean blood pressure (BP) reduced to 50 mmHg by the infusion of SNP. In the isoflurane group, the isoflurane was titrated to reduce mean BP to 50 mmHg. Stable hypotension was maintained for 90 min, which included a 45-min period of MCA occlusion. Monitoring included intraarterial blood pressure, arterial blood gases, EEG, somatosensory evoked potentials (SEP), and temperature. After the procedure the animals were allowed to awaken and were assessed neurologically every 8 h. On the third postoperative day, they were reanesthetized and underwent magnetic resonance imaging (MRI) and SEP recording. Thereafter, they were killed with iv KCl and the brains fixed for neuropathology. All animals survived the surgical procedure, but two animals receiving halothane and none receiving isoflurane died prematurely (P < 0.02). The SEP disappeared in all animals within 10 min of MCA occlusion and then returned partially or completely. There was no difference between groups in neurologic scores, in the size of the lesion as assessed by MRI (isoflurane 15.7 .+-. 6%, halothane/SNP 10.5 .+-. 4%), or in the extent or severity of the neuropathologic lesions. If focal cerebral ischemia severe enough to cause complete loss of the SEP occurs during induced hypotension, isoflurane offers no cerebral protection when compared with that of halothane anesthesia with SNP-induced hypotension.