Lanier W L, Milde J H, Sharbrough F W
Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905.
Br J Anaesth. 1990 Nov;65(5):708-12. doi: 10.1093/bja/65.5.708.
We have studied the effects of suxamethonium 1.0 mg kg-1 i.v. on cerebral blood flow (CBF), cerebral metabolic rate (CMRO2), and the electroencephalogram (EEG) in dogs anaesthetized with halothane (1.0 MAC) following blood-brain barrier (BBB) disruption with intracarotid (i.c.) mannitol. The combination produced a transient increase in CBF, while CMRO2 did not change. These responses were similar to those produced by i.c. mannitol plus i.v. saline. Suxamethonium produced desynchronization of the EEG that persisted longer than that produced by saline. In only one of the six animals was the desynchronization sustained (90 min) beyond that found in dogs with a normal BBB. We conclude that disruption of the BBB did not enhance the cerebral stimulating effects of i.v. suxamethonium, and did not increase the likelihood of seizure activity following suxamethonium.
我们研究了静脉注射1.0毫克/千克琥珀胆碱对用氟烷(1.0 MAC)麻醉的犬在经颈内注射甘露醇破坏血脑屏障(BBB)后,脑血流量(CBF)、脑代谢率(CMRO2)和脑电图(EEG)的影响。该组合使CBF短暂增加,而CMRO2未改变。这些反应与颈内注射甘露醇加静脉注射生理盐水所产生的反应相似。琥珀胆碱使EEG去同步化,其持续时间比生理盐水产生的去同步化持续时间更长。在六只动物中,只有一只动物的去同步化持续(90分钟)超过了血脑屏障正常的犬的去同步化持续时间。我们得出结论,血脑屏障的破坏并未增强静脉注射琥珀胆碱的脑刺激作用,也未增加琥珀胆碱给药后癫痫活动的可能性。