THE RESPONSE OF THE FELINE CEREBRAL-CIRCULATION TO PACO2 DURING ANESTHESIA WITH ISOFLURANE AND HALOTHANE AND DURING SEDATION WITH NITROUS-OXIDE
THE RESPONSE OF THE FELINE CEREBRAL-CIRCULATION TO PACO2 DURING ANESTHESIA WITH ISOFLURANE AND HALOTHANE AND DURING SEDATION WITH NITROUS-OXIDE
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DOI：
10.1097/00000542-198503000-00010
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发表时间：
1985-01-01
期刊：
影响因子：
8.8
通讯作者：
TODD, MM
中科院分区：
文献类型：
--
作者：
DRUMMOND, JC;TODD, MM
低碳酸血症引起的脑血流量(CBF)减少是神经麻醉技术的重要组成部分。虽然在氟烷给药期间大脑循环的二氧化碳反应(CO2.cntdot.R)增强(即更大的差值CBF/差值PaCO2[部分动脉二氧化碳分压])，但异氟醚对CO2.cntdot.R的影响尚未完全评估。测定猫在1.0MAC异氟醚(含75%N2O)麻醉时的CO2.cntdot.R，并与1.0MAC氟烷(含75%N2O)麻醉时的CO2.cntdot.R及单独使用75%N2O时的CO2.cntdot.R进行比较。与氟烷-N2O(P<；0.025)和单独使用N2O(P<；0.001)相比，异氟烷-N2O麻醉时的CO2.cntdot.R明显增加。氟烷-N2O麻醉时的CO2.cntdot.R又大于单独使用N2O时的CO2.cntdot.R(P<；0.025)。在相同水平的低碳酸血症(PaCO2 18-20 mm Hg)下，给予异氟醚-N2O(29.0±-)时，CBF显著降低(P<；0.01)。4.5毫升.cntdot。100g.cntdo.Min)，而不是在任一N2O(40.6.+-.5.5毫升.cntdot。100g.cntdo.Min)或氟烷-N2O(39.6±-.7.8毫升.cntdot。100g.cntdo.Min)。低碳酸血症时，单独应用N2O和氟烷-N2O的CBF值无明显差异。猫的CO2.cntdot.R不仅在注射1.0MAC异氟醚(含75%N2O)时被保留，而且相对于在1.0MAC氟烷麻醉(含75%N2O)和仅用N2O镇静时观察到的增强。异氟醚-N2O诱导的低碳酸血症(PaCO2 18-20 mm Hg)使脑血流量下降到低于氟烷-N2O或单独给N2O的水平。如果麻醉人的脑循环反应与猫相似，这些结果表明，在异氟醚(含N2O)麻醉期间诱导低碳酸血症可能比在氟烷(含N2O)麻醉期间或仅用N2O时在同等PaCO2下更容易降低脑血流量，从而可能更大程度地降低颅内压。
The reduction in cerebral blood flow (CBF) caused by hypocapnia is an important element of neuroanesthesic techniques. While the CO2 response of the cerebral circulation (CO2.cntdot.R) is enhanced (i.e., greater .DELTA.CBF/.DELTA.PaCO2 [partial arterial CO2 tension]) during halothane administration, the effect of isoflurane on CO2.cntdot.R has not been evaluated completely. The CO2.cntdot.R was examined in cats during anesthesia with 1.0 MAC [mimimum alveolar concentration] isoflurane (with 75% N2O) and compared it with CO2.cntdot.R during anesthesia with 1.0 MAC halothane (with 75% N2O) and with CO2.cntdot.R during the administration of 75% N2O alone. CO2.cntdot.R during anesthesia with isoflurane-N2O was enhanced relative to that observed during administration of both halothane-N2O (P < 0.025) and N2O alone (P < 0.001). CO2.cntdot.R during anesthesia with halothane-N2O was, in turn, greater than that observed during the administration of N2O alone (P < 0.025). At similar levels of hypocapnia (PaCO2 18-20 mm Hg), CBF was significantly lower (P < 0.01) during administration of isoflurane-N2O (29.0 .+-. 4.5 ml .cntdot. 100 g .cntdot. min) than during administration of either N2O (40.6 .+-. 5.5 ml .cntdot. 100 g .cntdot. min) or halothane-N2O (39.6 .+-. 7.8 ml .cntdot. 100 g .cntdot. min). CBF values during administration of the N2O alone and halothane-N2O were not different during hypocapnia. CO2.cntdot.R in cats not only is preserved during administration of 1.0 MAC isoflurane (with 75% N2O) but is enhanced relative to that observed during anesthesia with 1.0 MAC halothane (with 75% N2O) and during sedation with N2O alone. The induction hypocapnia (PaCO2 18-20 mm Hg) resulted in a reduction of CBF to lower levels during the administration of isoflurane-N2O than during administration of halothane-N2O or N2O alone. If the cerebral circulation of anesthetized humans responds similarly to that of the cat, these results suggest that the induction of hypocapnia during the administration of isoflurane (with N2O) may facilitate a greater reduction in CBF, and therefore perhaps ICP [intercranial pressure], than will occur at a comparable PaCO2 during anesthesia with halothane (with N2O) or during the administration of N2O alone.