Ketamine, not propofol, attenuates cerebrovascular response to carbon dioxide in humans with isoflurane anesthesia

被引:10
作者
Nagase, K [1 ]
Iida, H [1 ]
Ohata, H [1 ]
Dobi, S [1 ]
机构
[1] Gifu Univ, Sch Med, Dept Anesthesiol & Crit Care Med, Gifu 5008705, Japan
关键词
anesthetics; intravenous; ketamine; propofol; volatile; isoflurane; brain : blood flow; blood flow velocity; carbon dioxide : hypercapnia; hypocapnia; carbon dioxide reactivity; monitoring : transcranial Doppler ultrasonography;
D O I
10.1016/S0952-8180(01)00328-2
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Study Objectives: To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO2) in humans during isoflurane anesthesia. Design: Randomized clinical investigation. Settings: University hospital of a medical school. Patients: 30 ASA physical status I and II adult, elective surgical patients. Interventions and Measurements: With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artel (Vmca) and pulsatitity index were measured using the transcranial Doppler method tinder hypocapnic [arterial CO2 tension (PaCO2) 28-32 mmHg], normocapnic (PaCO2 38-42 mmHg), and hypercapnic conditions (PaCO2 48-52 mmHg). PaCO2 was altered by supplementing the inspired gas with CO2 without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg . kg(-1) or propofol (2 mg . kg(-1) followed by an infusion of 6-10 mg . kg(-1) . hr(-1)) (n = 15 for each drug), and the measurements were repeated. Main Results: Ketamine reduced both absolute and relative cerebrovascular reactivity to CO2 significantly [2.9 +/- 0.8 (control) vs. 2.6 +/- 1.0 (ketamine) cm . sec(-1) . mmHg(-1): p < 0.05; and 3.5 +/- 0.7 (control) vs. 2.8 +/- 0.9 (ketamine) % . mmHg(-1): p < 0.01, respectively]. However, ketamine did not reduce Vinca during hypercapnic conditions (117 +/- 29 cm . sec(-1)) compared with controls (120 +/- 28 cm . sec(-1)). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO2 reactivity [2.5 +/- 0.8 (control) vs. 2.5 +/- 1.0 (propofol) cm . sec(-1) . mmHg(-1), and 3.3 +/- 1.3 (control) vs. 4.1 +/- 1.0 (propofol) % . mmHg(-1), respectively]. Conclusions: In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO2, but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO2. (C) 2001 by Elsevier Science Inc.
引用
收藏
页码:551 / 555
页数:5
相关论文
共 20 条
[1]   Ketamine decreases intracranial pressure and electroencephalographic activity in traumatic brain injury patients during propofol sedation [J].
Albanese, J ;
Arnaud, S ;
Rey, M ;
Thomachot, L ;
Alliez, B ;
Martin, C .
ANESTHESIOLOGY, 1997, 87 (06) :1328-1334
[2]   Carbon dioxide and the cerebral circulation [J].
Brian, JE .
ANESTHESIOLOGY, 1998, 88 (05) :1365-1386
[3]   THE NEUROPROTECTIVE ACTION OF KETAMINE AND MK-801 AFTER TRANSIENT CEREBRAL-ISCHEMIA IN RATS [J].
CHURCH, J ;
ZEMAN, S ;
LODGE, D .
ANESTHESIOLOGY, 1988, 69 (05) :702-709
[4]   Relationship between transcranial Doppler-determined pulsatility index and cerebrovascular resistance: An experimental study [J].
Czosnyka, M ;
Richards, HK ;
Whitehouse, HE ;
Pickard, JD .
JOURNAL OF NEUROSURGERY, 1996, 84 (01) :79-84
[5]   THE RESPONSE OF THE FELINE CEREBRAL-CIRCULATION TO PACO2 DURING ANESTHESIA WITH ISOFLURANE AND HALOTHANE AND DURING SEDATION WITH NITROUS-OXIDE [J].
DRUMMOND, JC ;
TODD, MM .
ANESTHESIOLOGY, 1985, 62 (03) :268-273
[6]   THE INFLUENCE OF PROPOFOL WITH AND WITHOUT NITROUS-OXIDE ON CEREBRAL BLOOD-FLOW VELOCITY AND CO2 REACTIVITY IN HUMANS [J].
ENG, C ;
LAM, AM ;
MAYBERG, TS ;
LEE, C ;
MATHISEN, T .
ANESTHESIOLOGY, 1992, 77 (05) :872-879
[7]   THE RESPONSIVENESS OF CEREBRAL BLOOD-FLOW TO CHANGES IN ARTERIAL CARBON-DIOXIDE IS MAINTAINED DURING PROPOFOL NITROUS-OXIDE ANESTHESIA IN HUMANS [J].
FOX, J ;
GELB, AW ;
ENNS, J ;
MURKIN, JM ;
FARRAR, JK ;
MANNINEN, PH .
ANESTHESIOLOGY, 1992, 77 (03) :453-456
[8]   CEREBRAL ARTERIAL DIAMETERS DURING CHANGES IN BLOOD-PRESSURE AND CARBON-DIOXIDE DURING CRANIOTOMY [J].
GILLER, CA ;
BOWMAN, G ;
DYER, H ;
MOOTZ, L ;
KRIPPNER, W ;
LOFTUS, CM ;
MUIZELAAR, JP .
NEUROSURGERY, 1993, 32 (05) :737-742
[9]   QUANTITATIVE ANALYSIS OF OCCLUSIVE PERIPHERAL ARTERIAL DISEASE BY A NON-INTRUSIVE ULTRASONIC TECHNIQUE [J].
GOSLING, RG ;
DUNBAR, G ;
KING, DH ;
NEWMAN, DL ;
SIDE, CD ;
WOODCOCK, JP ;
FITZGERALD, DE ;
KEATES, JS ;
MACMILLAN, D .
ANGIOLOGY, 1971, 22 (01) :52-+
[10]   Blood flow velocity of middle cerebral artery during prolonged anesthesia with halothane, isoflurane, and sevoflurane in humans [J].
Kuroda, Y ;
Murakami, M ;
Tsuruta, J ;
Murakawa, T ;
Sakabe, T .
ANESTHESIOLOGY, 1997, 87 (03) :527-532