THE CEREBRAL FUNCTIONAL, METABOLIC, AND HEMODYNAMIC-EFFECTS OF DESFLURANE IN DOGS
THE CEREBRAL FUNCTIONAL, METABOLIC, AND HEMODYNAMIC-EFFECTS OF DESFLURANE IN DOGS
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DOI：
10.1097/00000542-199007000-00018
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发表时间：
1990-07-01
期刊：
影响因子：
8.8
通讯作者：
MILDE, LN
中科院分区：
文献类型：
--
作者：
LUTZ, LJ;MILDE, JH;MILDE, LN
在犬中检查了0.5-2.0 MAC（3.6-15%）地氟烷对脑功能、代谢和血流动力学以及全身代谢和血流动力学的影响。地氟烷使脑血管阻力从1.53 . ±. 0.21 mmHg. cntdot. ml-1.最小值100 g，0.5 MAC至0.50 .+-。0.03 mmHg. cntdot. ml-1.最小值100 g，2.0 MAC地氟烷。这伴随着脑血流量（CBF）从61 ± 0.5ml增加。7 ml. min-1. 100 g-1，0.5 MAC至78 .+-。3 ml. min-1. 100 g-1，1.5 MAC地氟烷。在2.0 MAC时，地氟烷CBF为52 ±。2毫升min-1. 100 g-1，但与平均动脉压（MAP）下降至43 . ±. 2毫米汞柱。当MAP增加到73 ± 0.01时，3 mmHg时，CBF增加至87 ±。3 ml. min-1. 100 g-1在此浓度下。在0.5 MAC地氟烷时，颅内压（ICP）为15 ± 0.5。5 mmHg，高于正常值，但随地氟醚浓度增加无明显变化。地氟烷浓度增加最初在EEG上产生的常见模式序列为麻醉深度增加，频率降低，振幅增加，进展为爆发抑制，然后在2.0 MAC地氟烷下，通过周期性多峰化中断规则衰减，该模式与异氟烷相似。在1.5和2.0 MAC下，在该浓度下最初观察到的EEG模式随时间变化为具有更快背景活动的模式。与EEG上观察到的变化平行，地氟烷使脑氧代谢率显著降低至2.52 ±。0.1 ml. cntdot. min-1. 100 g-1（2.0 MAC），与其他麻醉剂产生的浓度相当。研究结束时测量的脑代谢物在正常范围内。地氟醚使平均动脉压从114 ± 1.5降到114 ± 1.5，与剂量相关。在0.5 MAC至43 .+-时为5 mmHg。在2.0 MAC时> 2 mmHg，主要是由于全身血管阻力显著降低。仅在2.0 MAC时心脏指数显著降低，这也可能导致该浓度下MAP降低。增加地氟烷剂量对心率或全身耗氧量无影响。结论地氟烷是一种类似于其他挥发性麻醉药的脑血管扩张剂和类似于异氟烷的脑代谢抑制剂。它与其他麻醉剂的不同之处在于，较高浓度的地氟烷对EEG活动的影响可能随时间而有限。
The effects of 0.5-2.0 MAC (3.6-15%) desflurane on cerebral function, metabolism, and hemodynamics and on systemic metabolism and hemodymamics were examined in dogs. Desflurane produced a significant dose-related decrease in cerebral vascular resistance from 1.53 .+-. 0.21 mmHg .cntdot. ml-1 .cntdot. min .cntdot. 100 g at 0.5 MAC to 0.50 .+-. 0.03 mmHg .cntdot. ml-1 .cntdot. min .cntdot. 100 g at 2.0 MAC desflurane. This was accompanied by an increase in cerebral blood flow (CBF) from 61 .+-. 7 ml .cntdot. min-1 .cntdot. 100 g-1 at 0.5 MAC to 78 .+-. 3 ml .cntdot. min-1 .cntdot. 100 g-1 at 1.5 MAC desflurane. At 2.0 MAC desflurane CBF was 52 .+-. 2 ml .cntdot. min-1 .cntdot. 100 g-1 but was associated with a decrease in mean arterial pressure (MAP) to 43 .+-. 2 mmHg. When MAP was increased to 73 .+-. 3 mmHg with phenylephrine, CBF increased to 87 .+-. 3 ml .cntdot. min-1 .cntdot. 100 g-1 at this concentration. At 0.5 MAC desflurane, intracranial pressure (ICP) was 15 .+-. 5 mmHg, higher than normal, but did not change significanly with increasing concentrations of desflurane. Increasing concentrations of desflurane initially produced on the EEG the common pattern sequence of increasing depth of anesthesia with decreasing frequency and increasing amplitude progressing to burst suppression and then at 2.0 MAC desflurane to regular attenuation with interruption by periodic polyspiking, a pattern similar to that seen with isoflurane. At both 1.5 and 2.0 MAC the EEG pattern initially observed at that concentration changed to one with faster background activity with time. In parallel with changes observed on EEG desflurane produced a significant decrease in the cerebral metabolic rate for oxygen to 2.52 .+-. 0.1 ml .cntdot. min-1 .cntdot. 100 g-1 at 2.0 MAC, which is comparable to that produced by other anesthetics. Cerebral metabolites measure at the end of the study were within normal limits. Desflurane produced a dose-related decrease in mean arterial pressure from 114 .+-. 5 mmHg at 0.5 MAC to 43 .+-. 2 mmHg at 2.0 MACdue primarily to a significant decrease in systemic vascular resistance. Only at 2.0 MAC was there a significant decrease in cardiac index, which may also have contributed to the decreased MAP at this concentration. Increasing doses of desflurane had no effect on heart rate or whole body oxygen consumption. It is concluded that desflurane is a cerebral vasodilator similar to that of the other volatile anesthetics and a cerebral metabolic suppressant similar to isofluorane. It differs from the other anewsthetics in that the effect of higher concentrations of desflurane on EEG activity may be limited with time.