Kassell N F, Hitchon P W, Gerk M K, Sokoll M D, Hill T R
Neurosurgery. 1980 Dec;7(6):598-603. doi: 10.1227/00006123-198012000-00011.
High dose barbiturate therapy is being used with increasing frequency in the management of a widening spectrum of neurological disorders. Accurate regulation of the barbiturate dose is essential to maximize cerebral vasoconstriction and reduce brain metabolism while avoiding the cardiovascular depressant side effects of the drug. The purpose of this study was to determine whether the electroencephalogram (EEG) could be used to regulate administration of the agent. In nine mongrel dogs cerebral blood flow (CBF) was determined using the radioactive microsphere technique. After the determination of control CBF, a slow infusion of sodium thiopental was begun. CBF determinations were repeated when the periods of burst suppression in the EEG over several minutes averaged 30, 60, 120, and 240 seconds. CBF and oxygen metabolism showed a nearly identical pattern of a precipituos drop from control levels reaching a plateau at burst suppression between 30 and 60 seconds. Changes in cerebrovascular resistance were of a similar but opposite nature. Significant increases in heart rate occurred with burst suppression of 30 seconds, whereas the arterial pressure and cardiac index decreased with burst suppression between 30 and 60 seconds. In this study cerebral metabolic depression and vasoconstriction from sodium thiopental reached a plateau when sufficient barbiturate was administered to produce EEG burst suppression of between 30 and 60 seconds. At this level there was no important cardiovascular depression. Administration of additional barbiturates significantly decreased systemic arterial pressure and cardiac output, but produced no further decrement in the cerebral metabolic rate of oxygen or the CBF. There was no predictable relationship between cerebral metabolism or cardiovascular function and blood levels of sodium thiopental.
大剂量巴比妥酸盐疗法在越来越多的神经系统疾病治疗中使用得越来越频繁。准确调节巴比妥酸盐剂量对于最大限度地实现脑血管收缩和降低脑代谢,同时避免药物的心血管抑制副作用至关重要。本研究的目的是确定脑电图(EEG)是否可用于调节该药物的给药。在9只杂种狗中,使用放射性微球技术测定脑血流量(CBF)。在测定对照CBF后,开始缓慢输注硫喷妥钠。当脑电图中持续数分钟的爆发抑制期平均为30、60、120和240秒时,重复进行CBF测定。CBF和氧代谢呈现出几乎相同的模式,即从对照水平急剧下降,在30至60秒的爆发抑制时达到平台期。脑血管阻力的变化性质相似但相反。在30秒的爆发抑制时心率显著增加,而在30至60秒的爆发抑制时动脉压和心脏指数下降。在本研究中,当给予足够的巴比妥酸盐使脑电图爆发抑制达到30至60秒时,硫喷妥钠引起的脑代谢抑制和血管收缩达到平台期。在此水平时没有重要的心血管抑制。给予额外的巴比妥酸盐显著降低了体循环动脉压和心输出量,但并未使脑氧代谢率或CBF进一步降低。脑代谢或心血管功能与硫喷妥钠血药浓度之间没有可预测的关系。