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氯胺酮对兔异氟烷和七氟烷诱导的脑血管舒张的影响。

Effects of ketamine on isoflurane- and sevoflurane-induced cerebral vasodilation in rabbits.

作者信息

Nagase Kiyoshi, Iida Hiroki, Dohi Shuji

机构信息

Department of Anesthesiology & Crtical Care Medicine, Gifu University School of Medicine, Gifu City, Japan.

出版信息

J Neurosurg Anesthesiol. 2003 Apr;15(2):98-103. doi: 10.1097/00008506-200304000-00006.

DOI:10.1097/00008506-200304000-00006
PMID:12657994
Abstract

Although ketamine has been reported to have little effect on the cerebral circulation when used with other anesthetics, its effect on the cerebral vascular response to volatile anesthetics, which increase cerebral blood flow in a concentration-dependent manner, remains obscure. A closed cranial window was prepared in 15 pentobarbital-anesthetized adult rabbits. The cerebral pial arteriolar alteration induced by either isoflurane (n = 8) or sevoflurane (n = 7) at 0 (before volatile anesthetic), 0.33, 0.67, and 1.0 minimum alveolar concentration (MAC) was measured under three consecutive conditions: intravenous infusion with saline, with ketamine, and with ketamine plus l-arginine. Ketamine reduced the vasodilation induced by 0.67 (120 +/- 9% versus 113 +/- 9%; P <.05) and 1.0 MAC isoflurane (136 +/- 11% versus 118 +/- 10%; P <.05), but l-arginine did not restore the isoflurane-induced cerebral vasodilation. In rabbits inhaling sevoflurane, the degree of cerebral vasodilator response was smaller than that by isoflurane, and the cerebral vasodilation was comparable whether in the presence or absence of ketamine (with or without l-arginine). In conclusion, ketamine reduces isoflurane-induced cerebral vasodilation, apparently independently of nitric oxide formation, while sevoflurane-induced cerebral vasodilation is not significantly affected by ketamine.

摘要

虽然据报道,氯胺酮与其他麻醉剂合用时对脑循环影响较小,但其对挥发性麻醉剂引起的脑血管反应的影响仍不清楚,挥发性麻醉剂会以浓度依赖的方式增加脑血流量。在15只戊巴比妥麻醉的成年兔中制备了封闭的颅骨窗口。在连续三种情况下,测量0(挥发性麻醉剂给药前)、0.33、0.67和1.0最低肺泡浓度(MAC)的异氟烷(n = 8)或七氟烷(n = 7)引起的软脑膜小动脉变化:静脉输注生理盐水、氯胺酮以及氯胺酮加L-精氨酸。氯胺酮减少了0.67 MAC(120±9%对113±9%;P<.05)和1.0 MAC异氟烷引起的血管舒张(136±11%对118±10%;P<.05),但L-精氨酸并未恢复异氟烷引起的脑血管舒张。在吸入七氟烷的兔中,脑血管舒张反应程度小于异氟烷引起的,并且无论是否存在氯胺酮(无论是否有L-精氨酸),脑血管舒张情况相当。总之,氯胺酮减少异氟烷引起的脑血管舒张,显然独立于一氧化氮的形成,而七氟烷引起的脑血管舒张不受氯胺酮的显著影响。

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