Artru A A
Department of Anesthesiology, University of Washington School of Medicine, Seattle 98195.
Anesth Analg. 1994 Oct;79(4):751-60.
Desflurane-induced increase of intracranial pressure (ICP) does not appear to be completely explained by desflurane-induced changes in cerebral blood flow, cerebrospinal fluid (CSF) formation and reabsorption, or brain tissue water content. The present study was designed to determine whether desflurane alters intracranial volume/pressure relationships sufficiently to account for desflurane-induced increase of ICP. In 24 dogs, infusions of mock CSF were used to determine the CSF pressure increase due to increase of CSF volume, and the capacity of CSF pressure to return to baseline after a CSF pressure increase (CSF pressure normalization). CSF pressure increase was assessed by determining (a) CSF pressure prior to volume infusion (P(o)), (b) peak CSF pressure (Pp) caused by volume injection, (c) intracranial compliance (C, calculated as the ratio of change of intracranial volume [delta V] to change of CSF pressure [delta P]), (d) the volume pressure response (VPR, a measure of elastance, calculated as the ratio of delta P to delta V, (e) the pressure/volume index (PVI, calculated as the ratio of delta V to log Pp/P(o)), and (f) estimated intracranial compliance (C(e), calculated from PVI as 0.4343PVI/P(o)). CSF pressure normalization was assessed by determining the first (S1) and second (S2) phase slopes of decrease of CSF pressure from Pp, the duration of S1 (DS1), and the intersection of extrapolated S2 with the P(o) to Pp slope (delta Ps). During normocapnia (Group 1, n = 6) and hypocapnia (Group 2, n = 6), two infusions were made at each of four experimental conditions: 0.5 minimum alveolar anesthetic concentration (MAC) desflurane and normal or increased CSF pressure, and 1.0 MAC desflurane and normal or increased CSF pressure. For comparison to these two desflurane-anesthetized groups, intracranial volume/pressure values were determined at the same experimental conditions during 0.5 MAC isoflurane (Group 3, n = 6) and in controls (Group 4, n = 6) anesthetized with thiopental 12 mg/kg then 12 mg.kg-1.h-1 intravenously combined with halothane 0.5% inspired. In comparison to controls, both desflurane and isoflurane decreased Ce at normal CSF pressure but not at increased CSF pressure. However, desflurane and isoflurane had no consistent effect on the other measures of CSF pressure increase caused by increase of CSF volume. Isoflurane also decreased the capacity for CSF pressure normalization at normal CSF pressure as indicated by decreased S1 and increased delta Ps. It is concluded that, under conditions of normal ICP, desflurane may decrease Ce, favoring an increase of ICP.
地氟醚引起的颅内压(ICP)升高似乎不能完全用地氟醚引起的脑血流量、脑脊液(CSF)生成与重吸收或脑组织含水量的变化来解释。本研究旨在确定地氟醚是否充分改变颅内体积/压力关系,以解释地氟醚引起的ICP升高。在24只犬中,输注模拟脑脊液以确定由于脑脊液体积增加导致的脑脊液压力升高,以及脑脊液压力升高后恢复至基线的能力(脑脊液压力正常化)。通过确定以下各项来评估脑脊液压力升高:(a)体积输注前的脑脊液压力(P(o)),(b)体积注射引起的脑脊液峰值压力(Pp),(c)颅内顺应性(C,计算为颅内体积变化[δV]与脑脊液压力变化[δP]的比值),(d)体积压力反应(VPR,一种弹性测量指标,计算为δP与δV的比值),(e)压力/体积指数(PVI,计算为δV与log Pp/P(o)的比值),以及(f)估计颅内顺应性(C(e),根据PVI计算为0.4343PVI/P(o))。通过确定脑脊液压力从Pp下降的第一(S1)和第二(S2)阶段斜率、S1的持续时间(DS1)以及外推的S2与P(o)至Pp斜率的交点(δPs)来评估脑脊液压力正常化。在正常碳酸血症(第1组,n = 6)和低碳酸血症(第2组,n = 6)期间,在四种实验条件下各进行两次输注:0.5最低肺泡麻醉浓度(MAC)地氟醚且脑脊液压力正常或升高,以及1.0MAC地氟醚且脑脊液压力正常或升高。为了与这两个地氟醚麻醉组进行比较,在0.5 MAC异氟醚(第3组,n = 6)期间以及用硫喷妥钠12 mg/kg然后以12 mg·kg-1·h-1静脉注射并吸入0.5%氟烷麻醉的对照组(第4组,n = 6)的相同实验条件下测定颅内体积/压力值。与对照组相比,地氟醚和异氟醚在脑脊液压力正常时均降低C(e),但在脑脊液压力升高时则不然。然而,地氟醚和异氟醚对因脑脊液体积增加引起的脑脊液压力升高的其他测量指标没有一致的影响。异氟醚还降低了脑脊液压力在正常脑脊液压力下正常化的能力,表现为S1降低和δPs增加。得出的结论是,在ICP正常的情况下,地氟醚可能降低C(e),从而有利于ICP升高。