Why we still use intravenous drugs as the basic regimen... neurosurgical anaesthesia Pol Hans and Vincent Bonhomme Introduction

Why we still use intravenous drugs as the basic regimen... neurosurgical anaesthesia Pol Hans and Vincent Bonhomme Introduction

Why we still use intravenous drugs as the basic regimen for
neurosurgical anaesthesia
Pol Hans and Vincent Bonhomme
Purpose of review
Evolution of neurosurgery mainly trends towards minimally
invasive and functional procedures including endoscopies,
small-size craniotomies, intraoperative imaging and
stereotactic interventions. Consequently, new adjustments
of anaesthesia should aim at providing brain relaxation,
minimal interference with electrophysiological monitoring,
rapid recovery, patients’ cooperation during surgery and
neuroprotection.
Recent findings
In brain tumour patients undergoing craniotomy, propofol
anaesthesia is associated with lower intracranial pressure
and cerebral swelling than volatile anaesthesia.
Hyperventilation used to improve brain relaxation may
decrease jugular venous oxygen saturation below the
critical threshold. It decreases the cerebral perfusion
pressure in patients receiving sevoflurane, but not in those
receiving propofol. The advantage of propofol over volatile
agents has also been confirmed regarding interference with
somatosensory, auditory and motor evoked potentials.
Excellent and predictable recovery conditions as well as
minimal postoperative side-effects make propofol
particularly suitable in awake craniotomies. Finally, the
potential neuroprotective effect of this drug could be
mediated by its antioxidant properties which can play a role
in apoptosis, ischaemia-reperfusion injury and inflammatoryinduced neuronal damage.
Summary
Although all the objectives of neurosurgical anaesthesia
cannot be met by one single anaesthetic agent or
technique, propofol-based intravenous anaesthesia
appears as the first choice to challenge the evolution of
neurosurgery in the third millennium.
Keywords
intravenous agents, neurosurgery, neurosurgical
anaesthesia, propofol
Introduction
Five years ago, in the Editorial Review of the Neuroanaesthesia section of Current Opinion in Anaesthesiology,
Marcel Durieux highlighted important changes in the
practice of neurosurgery, either in current progress or
foreseen in the years to come. Those changes mainly
trended towards minimally invasive and functional
surgery including endoscopic procedures, small size craniotomies, intraoperative magnetic resonance imaging
and stereotactic approaches in different pathologies.
Neurosurgery in the third millennium should aim at
preserving or restoring brain function, achieving immediate and good recovery, and avoiding as far as possible the
usual stay in the intensive care unit. Those objectives
may require long duration interventions, heavy operative
equipment, electrophysiological monitoring and patient’s
cooperation during surgery.
Such an evolution raises a question to neuroanaesthesiologists. Should new fashion neurosurgery unavoidably
cause new trends in anaesthesia practice? The answer,
which is a noncommittal one, is probably yes and no. In
the textbooks of neurosurgical anaesthesia, the classical
criteria which characterize the ideal anaesthetic agent
include a list of well-known properties such as smooth
induction, haemodynamic stability, no interference with
cerebral autoregulation, decrease of intracranial pressure
(ICP), brain relaxation, rapid emergence and neuroprotection. None of them can be discarded today, but some
should probably draw more attention than others and
additional ones should be considered. The new challenge of neurosurgical anaesthesia involves the use of
anaesthetic agents and techniques that minimally affect
brain function, are devoid of any interference with
electrophysiological monitoring, facilitate new neurosurgical procedures, allow patient’s cooperation during
surgery, and are associated with rapid and excellent
recovery.
Curr Opin Anaesthesiol 19:498–503. ß 2006 Lippincott Williams & Wilkins.
University Department of Anaesthesia and Intensive Care Medicine, CHR de la
Citadelle, Liege University Hospital, Liege, Belgium
Correspondence to Pol Hans, University Department of Anaesthesia and ICM, CHR
de la Citadelle, Boulevard du 12e de Ligne 1, 4000 Liege, Belgium
Tel: +32 4 225 6470; fax: +32 4 225 7308; e-mail: [email protected]
Current Opinion in Anaesthesiology 2006, 19:498–503
Abbreviation
ICP
intracranial pressure
ß 2006 Lippincott Williams & Wilkins
0952-7907
Neuroanaesthesia is not blind cooking and believing that
one single agent or technique can be applied to all
patients whatever the type of surgery would be naive.
Nevertheless, we are convinced that intravenous anaesthetic agents are still the basic anaesthetic regimen in the
majority of neurosurgical procedures. In so far as synthetic opioids and other intravenous analgesics are commonly used in the operating room whatever the hypnotic
agent, this review will essentially compare propofol and
498
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Why we still use intravenous drugs Hans and Bonhomme
volatile anaesthetics at the light of the more recent data in
the literature.
Brain relaxation
Brain relaxation appears to be a cornerstone in anaesthesia for intracranial surgery, being mandatory in the case of
intracranial hypertension and of great interest for the
surgical approach of the base of the skull in the absence
of expanding lesions. It can be considered as a neuroprotective measure in so far as it may reduce surgical
compression, local hypoperfusion and cerebral ischaemia.
It is of outstanding importance in minimally invasive
surgery for the removal of brain lesions through small
size craniotomies. However, brain relaxation must be
balanced according to the degree of intracranial hypertension and the surgical approach of the lesion which
relies on preplanned navigation data.
In contrast to inhalational agents which may adversely
affect ICP, propofol plays a key role in brain relaxation. In
a randomized prospective study of patients subjected to
craniotomy for cerebral tumours, ICP and cerebral swelling at the opening of the dura have been shown to be
lower, and mean arterial blood pressure and cerebral
perfusion pressure to be higher in propofol-anaesthetized
patients compared to patients anaesthetized with isoflurane or sevoflurane [1]. It was concluded in the same study
that during craniotomy for cerebral tumours, operating
conditions would be better during propofol than isoflurane or sevoflurane anaesthesia. Indeed, sevoflurane, even
when used at subanaesthetic concentrations, increases
regional cerebral blood flow and regional cerebral blood
volume [2], and may impair dynamic cerebral autoregulation [3]. Propofol is known to reduce regional cerebral
blood flow and metabolism comparably, while sevoflurane reduces blood flow to a lesser extent, due to its own
vasodilating effect [4]. Indeed sevoflurane, such as the
other volatile anaesthetic agents, has both a direct, intrinsic dilating effect on cerebral vessels and an indirect,
extrinsic constricting effect related to brain metabolism
depression. The opposite effect of propofol and sevoflurane on cerebral vascular tone has been confirmed by
Marval et al., using transcranial Doppler ultrasonography
[5]. In that study, hypocapnia decreased the estimated
cerebral perfusion pressure and increased the zero flow
pressure under sevoflurane anaesthesia, but did not
change those parameters in propofol-anaesthetized
patients. The incidence of low jugular venous bulb oxygen saturation has been reported to be higher during
propofol than sevoflurane/nitrous oxide anaesthesia and
hyperventilation should be more cautiously applied in
propofol anaesthetized patients [6,7]. Recent results,
however, indicate that increasing propofol concentrations
do not affect jugular venous bulb oxygen saturation
in neurosurgical patients [8]. In summary, in case of
low intracranial compliance, ICP can be decreased by
499
propofol and increased by volatile anaesthetics. The use
of hyperventilation to improve intracranial relaxation,
expected to be more frequent in the case of volatile
anaesthesia, may compromise cerebral perfusion pressure. Finally, moderately deep sedation with propofol
in spontaneously breathing, nonintubated patients with
an intracranial expanding lesion does not result in a
higher ICP than the use of no sedation [9].
According to another recent study, more episodes of
arterial hypotension would be observed with sevoflurane
than with propofol anaesthesia during elective intracranial surgery [10]. In our personal practice, total intravenous anaesthesia using propofol and remifentanil for
craniotomies is well tolerated in normotensive patients,
but may be associated to some degree of arterial hypertension in hypertensive patients. Those episodes of
arterial hypertension are usually not resolved by deepening the level of anaesthesia or analgesia, impede the
neurosurgeon’s work and may favour brain bulk in case
of disturbed autoregulation. They can often be treated by
intravenous administration of hypotensive drugs, but may
also be successfully controlled by adding sevoflurane at
subanaesthetic concentrations to the basic intravenous
regimen.
Electrophysiological monitoring
Electrophysiological monitoring can be used to assess the
depth of anaesthesia as well as to localize cortical or
subcortical regions and so facilitate the surgical approach
of lesions or the placement of deep brain stimulation electrodes. It can also be of interest to control
the integrity of neural structures in patients at risk of
ischaemia.
In so far as electrophysiological effects are concerned,
propofol has a considerable advantage over volatile anaesthetics. Propofol is a potent cerebral metabolism depressor and has well established anti-convulsant properties
while the epileptogenic effects of high sevoflurane concentrations particularly in the paediatric population are
know for several years. Regarding evoked potentials,
inhalational agents significantly decrease N2O amplitude and prolong N2O latency of somatosensory evoked
potentials in a dose-dependent manner [11]. Propofol,
when compared to isoflurane in patients undergoing
spine surgery, causes less suppression of the cortical
somatosensory evoked potentials with better preservation of somatosensory evoked potential amplitude
and less variability at an equivalent depth of anaesthesia
[12,13]. Animal data have shown that sevoflurane
depresses the middle latency auditory evoked potential
waveform and suggest that sevoflurane is not the inhalant
agent of choice in a research setting where electroencephalographic measurements are to be recorded during
anaesthesia [14]. Regarding motor evoked potentials,
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
500 Neuroanaesthesia
isoflurane inhibits intraoperative neurophysiological
monitoring more than does propofol, which is recommended when motor pathway function is monitored [15].
Good conditions of motor evoked potentials recording
have also been reported in a child under ketamine-based
anaesthesia [16]. On the other hand, motor evoked
potentials can be elicited noninvasively by using transcranial magnetic stimulation, and this technique has
been recently shown to be feasible during anaesthesia
with propofol and remifentanil [17]. Propofol has also
been used successfully in spinal surgery patients subjected to double-train transcranial electrical stimulation
[18].
In summary, although intravenous and volatile anaesthetics affect evoked potential characteristics, the
significantly lower effect of propofol would incite us
to use this drug rather than inhalational agents
when electrophysiological monitoring is required. This
choice is still reinforced by the ‘anaesthetic fade’,
reflecting a progressive depression of motor transcranial
motor evoked potentials over time at a constant level of
anaesthesia [19].
Recovery and awake craniotomies
Neurosurgery is more and more focusing on neurological
function, which is best monitored by looking at the
patient directly.
After classical craniotomies, neurological function
is clinically assessed when patients emerge from
general anaesthesia and recover consciousness. A rapid
emergence will allow immediate neurological examination, early detection and efficacious management of
any potential surgical complication. In a study comparing propofol/remifentanil with propofol/sufentanil for
supratentorial craniotomy, the propofol/remifentanil
regimen was shown to provide quicker recovery [20].
On the other hand, recent studies comparing sevoflurane and propofol combined with either remifentanil or
sufentanil in patients undergoing neurosurgical procedures have shown all techniques to be comparable
in terms of time to recovery and cognitive functions
[10,21,22]. In the absence of any demonstrated difference between propofol and volatile agents regarding
the speed and quality of recovery, a lower incidence of
nausea and vomiting observed in an ambulatory anaesthesia meta-analysis with propofol is a key factor when
patient comfort in the postoperative period is concerned [23]. Referring to ambulatory anaesthesia for
neurosurgical patients could sound inappropriate, but
outpatient craniotomy for brain tumour has been
reported to be feasible [24].
In particular situations, the neurosurgeon may require the
patient’s cooperation during surgery, either for the
removal of lesions located close to functional areas of
the brain, including vision, language and motor areas, or
to check the therapeutic efficacy of deep brain stimulations such as in surgery for Parkinson disease. In those
cases, anaesthesia relies on the concept of monitoring
anaesthesia care and should fulfil the following criteria:
sufficient depth of anaesthesia during opening and closure, full consciousness during functional testing, smooth
transition between anaesthesia and consciousness, adequate ventilation, and immobility and comfort throughout the entire procedure [25]. The drugs that are most
frequently employed for awake craniotomy patients
include local anaesthetics, sufentanil or remifentanil,
propofol, and the a2 agonists dexmedetomidine and
clonidine. Propofol is still the first choice hypnotic in
this indication. Its administration can be performed using
a target control infusion technique, guided by a depth of
anaesthesia monitor and combined to remifentanil infusion [26–28]. During propofol-based anaesthesia for excision of brain tumours located in eloquent brain areas,
patients wake up within 5–15 min after stopping propofol
infusion, and the laryngeal mask may be temporarily
removed and easily replaced [29]. In a retrospective
analysis of 98 patients undergoing craniotomy requiring
intraoperative awake functional brain mapping, combined infusion of propofol and remifentanil has been
recognized to provide satisfactory anaesthetic conditions
and allow a wake-up time of 9 min [30]. In epilepsy
surgery, propofol stopped to allow patient awakening has
not been found to interfere with electrocorticographic
recordings, and has been proposed with fentanyl as a safe
and useful regimen for awake craniotomy in selected
paediatric patients [31]. As a result of its easily titratable
sedative effect, rapid recovery with clear headedness and
antiemetic properties, propofol is a convenient agent for
awake brain surgery [32].
Neuroprotection
Neurosurgery can induce ischemic brain damage and
trigger neuronal death, the mechanisms of which vary
over time and may prolong for several weeks. Excitotoxicity appears to be a critical event in the opening
stages of ischaemia. Oxidative stress and inflammatory
response initiated afterward directly affect neurons, but
also play a key role in triggering delayed apoptotic
neuronal death.
The capacity of general anaesthesia, as compared to
the awake state, to increase neuronal tolerance
to hypoxic ischaemic insults has been established for
a long time, although this beneficial effect appears
to be transient. During the last two decades, the
ability of volatile halogenated anaesthetics to reduce
ischemic cell death through the anaesthetic preconditioning pathways has been increasingly recognized. Nevertheless, one should keep in mind that
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Why we still use intravenous drugs Hans and Bonhomme
intravenous agents such as opioids and propofol also
have potential neuroprotective properties.
Opioids such as morphine, fentanyl and remifentanil
have been demonstrated to exert some preconditioning
effect on the heart as well as on neuronal cells [11,33,34].
Propofol may affect the biochemical pathway of cell
death at different levels. During the last decade, it has
been shown to be neuroprotective in vivo, in both focal
and global models of cerebral ischaemia. First, this agent
has well-established antioxidant properties which are
partially attributed to its scavenging effect on peroxynitrite. Propofol has been reported to protect endothelial
cells exposed to a peroxynitrite donor and to increase the
expression of heme-oxygenase [35,36]. It inhibits the
protein nitration induced by activated polymorphonuclear neutrophils [37]. At clinically relevant concentrations, it attenuates the effect of oxidative stress on
astrocyte glutamate uptake and retention [38]. Propofol
also maintains the capacity of brain cells to extrude
protons during oxidative stress [39]. In an experimental
model of traumatic brain injury, it has been shown to
decrease levels of endogenous indices of oxidative stress
[40]. Its neuroprotective effect in models of cerebral
ischaemia has been related to its capacity to prevent
the increase in neuronal mitochondrial swelling [41].
In addition, one may reasonably assume that the
beneficial effect of propofol recently described on lung
endothelial injury induced by ischaemia-reperfusion and
oxidative stress could be extrapolated to the central
nervous system [42]. Second, there is a growing body
of evidence suggesting that propofol has antiapoptotic
properties. It inhibits neuronal damage after incomplete
cerebral ischaemia with reperfusion for at least 28 days
after injury [43]. It also reduces spinal cord apoptosis
associated with aortic cross-clamping in rabbits [44]. In a
rat model of cerebral ischaemia, propofol compared to
placebo has been associated with an improvement in
neurologic function still observed after 3 weeks, although
there was no difference in infarct volume [45]. That
antiapoptotic property seems to be partly mediated by
its antioxidant effect, i.e. its capacity to inhibit peroxynitrite-mediated apoptosis in astroglia cells [46], but also
implies an altered expression of apoptosis-regulating
proteins such as Bax and Bcl-2 [43,44,47,48]. Third,
several reports suggest that propofol-based anaesthesia
favourably influences the pro versus anti-inflammatory
cytokine balance when compared to isoflurane [49,50].
This effect is expected to improve neurological outcome
since upregulation of pro-inflammatory cytokines such as
tumour necrosis factor-a and interleukin-6 is correlated
with increased mortality and neurological deterioration
[51,52]. Propofol has also been shown to reduce tumour
necrosis factor-a-induced human umbilical vein endothelial cell apoptosis [48]. It could therefore be
beneficial in so far as inflammation may exacerbate tissue
501
damage by increasing local metabolic demand. Indeed,
the increase in local temperature resulting from energetic
requirements further activates the inflammatory process
and worsens outcome of focal ischaemia [53].
As far as preconditioning is concerned, propofol has no
direct preconditioning effect, probably because of its
antioxidative properties. Indeed, ischaemic as well as
anaesthetic preconditioning involves activation of protein
kinase C, mitochondrial potassium ATP channels and the
transcription factor NF-kB that is at least partially triggered by activated oxygen species. In contrast, the preconditioning effect of intravenous opioids has already
been mentioned above. Nevertheless, propofol could
have a beneficial effect upstream and downstream of
the preconditioning cascade. Indeed, it inhibits activated
oxygen species responsible for damaging lipids, proteins
and DNA when produced in excess after ischaemiareperfusion. Its inhibition of NF-kB activation during
focal cerebral ischaemia-reperfusion in rats has also been
suggested to be one mechanism of neuroprotection [54].
Propofol also increases the ratio of antiapoptotic to proapoptotic proteins which partially mediates the preconditioning effect [43,44,47,48].
Conclusions
Although all the objectives of neuroanaesthesia cannot be
achieved by using one single pharmacological agent or
one single anaesthetic technique, propofol-based intravenous anaesthesia still has a promising future in the
field.
References and recommended reading
Papers of particular interest, published within the annual period of review, have
been highlighted as:
of special interest
of outstanding interest
Additional references related to this topic can also be found in the Current
World Literature section in this issue (pp. 580–581).
1
Petersen KD, Landsfeldt U, Cold GE, et al. Intracranial pressure and cerebral
hemodynamic in patients with cerebral tumors: a randomized prospective
study of patients subjected to craniotomy in propofol–fentanyl, isoflurane–
fentanyl, or sevoflurane–fentanyl anesthesia. Anesthesiology 2003; 98:
329–336.
2
Kolbitsch C, Lorenz IH, Hormann C, et al. A subanesthetic concentration of
sevoflurane increases regional cerebral blood flow and regional cerebral
blood volume and decreases regional mean transit time and regional
cerebrovascular resistance in volunteers. Anesth Analg 2000; 91:
156–162.
3
Ogawa Y, Iwasaki K, Shibata S, et al. The effect of sevoflurane on dynamic
cerebral blood flow autoregulation assessed by spectral and transfer function
analysis. Anesth Analg 2006; 102:552–559.
4
Kaisti KK, Langsjo JW, Aalto S, et al. Effects of sevoflurane, propofol,
and adjunct nitrous oxide on regional cerebral blood flow, oxygen consumption, and blood volume in humans. Anesthesiology 2003; 99:603–
613.
Marval PD, Perrin ME, Hancock SM, Mahajan RP. The effects of propofol or
sevoflurane on the estimated cerebral perfusion pressure and zero flow
pressure. Anesth Analg 2005; 100:835–840.
Propofol and sevoflurane have opposite effects on the cerebral vasculature.
Estimated cerebral perfusion pressure decreases with propofol and is maitained
with sevoflurane. In hypocapnic conditions, the zero flow pressure increases with
sevoflurane, but is maintained under propofol anaesthesia.
5
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
502 Neuroanaesthesia
6
Munoz HR, Nunez GE, de la Fuente JE, Campos MG. The effect of nitrous
oxide on jugular bulb oxygen saturation during remifentanil plus target-controlled infusion propofol or sevoflurane in patients with brain tumors. Anesth
Analg 2002; 94:389–392.
7
Kawano Y, Kawaguchi M, Inoue S, et al. Jugular bulb oxygen saturation under
propofol or sevoflurane/nitrous oxide anesthesia during deliberate mild
hypothermia in neurosurgical patients. J Neurosurg Anesthesiol 2004; 16:
6–10.
Iwata M, Kawaguchi M, Inoue S, et al. Effects of increasing concentrations of
propofol on jugular venous bulb oxygen saturation in neurosurgical patients
under normothermic and mildly hypothermic conditions. Anesthesiology
2006; 104:33–38.
Changes in propofol concentrations do not affect jugular venous bulb oxygen
saturation values as long as propofol is administered in dosages commonly used in
clinical practice.
8
9
Girard F, Moumdjian R, Boudreault D, et al. The effect of propofol sedation on
the intracranial pressure of patients with an intracranial space-occupying
lesion. Anesth Analg 2004; 99:573–577.
10 Sneyd JR, Andrews CJ, Tsubokawa T. Comparison of propofol/remifentanil
and sevoflurane/remifentanil for maintenance of anaesthesia for elective
intracranial surgery. Br J Anaesth 2005; 94:778–783.
11 Zhang J, Liang WM. Effects of volatile anesthetics on cortical somatosensory
evoked potential and bispectral index. Zhonghua Yi Xue Za Zhi 2005;
85:2700–2703.
12 Clapcich AJ, Emerson RG, Roye DP, et al. The effects of propofol, small-dose
isoflurane, and nitrous oxide on cortical somatosensory evoked potential and
bispectral index monitoring in adolescents undergoing spinal fusion. Anesth
Analg 2004; 99:1334–1340.
13 Liu EH, Wong HK, Chia CP, et al. Effects of isoflurane and propofol on
cortical somatosensory evoked potentials during comparable depth of
anaesthesia as guided by bispectral index. Br J Anaesth 2005; 94:
193–197.
At comparable depth of anaesthesia guided by the bispectral index,
propofol compared to isoflurane, causes less suppression of cortical somatosensory evoked potentials with better preservation of amplitude and less
variability.
14 Murrell JC, De Groot HN, Psatha E, Hellebrekers LJ. Investigation of changes
in the middle latency auditory evoked potential during anesthesia with sevoflurane in dogs. Am J Vet Res 2005; 66:1156–1161.
15 Chen Z. The effects of isoflurane and propofol on intraoperative neurophysiological monitoring during spinal surgery. J Clin Monit Comput 2004;
18:303–308.
16 Erb TO, Ryhult SE, Duitmann E, et al. Improvement of motor-evoked potentials
by ketamine and spatial facilitation during spinal surgery in a young child.
Anesth Analg 2005; 100:1634–1636.
17 Hargreaves SJ, Watt JW. Intravenous anaesthesia and repetitive transcranial
magnetic stimulation monitoring in spinal column surgery. Br J Anaesth 2005;
94:70–73.
18 Journee HL, Polak HE, de Kleuver M, et al. Improved neuromonitoring during
spinal surgery using double-train transcranial electrical stimulation. Med Biol
Eng Comput 2004; 42:110–113.
19 Lyon R, Feiner J, Lieberman JA. Progressive suppression of motor evoked
potentials during general anesthesia: the phenomenon of ‘anesthetic fade’.
J Neurosurg Anesthesiol 2005; 17:13–19.
A prolonged exposure to anaesthetic agents necessitates higher stimulation
thresholds to elicit motor evoked responses, independently of the dose-depressant effect. Recognition of anaesthetic fade is essential when interpreting motor
evoked potentials under general anaesthesia.
20 Gerlach K, Uhlig T, Huppe M, et al. Remifentanil–propofol versus sufentanil–
propofol anaesthesia for supratentorial craniotomy: a randomized trial. Eur J
Anaesthesiol 2003; 20:813–820.
25 Yamamoto F, Kato R, Sato J, Nishino T. Anaesthesia for awake craniotomy
with noninvasive positive pressure ventilation. Br J Anaesth 2003; 90:
382–385.
26 Hans P, Bonhomme V, Born JD, et al. Target-controlled infusion of propofol
and remifentanil combined with bispectral index monitoring for awake craniotomy. Anaesthesia 2000; 55:255–259.
27 Berkenstadt H, Perel A, Hadani M, et al. Monitored anesthesia care using
remifentanil and propofol for awake craniotomy. J Neurosurg Anesthesiol
2001; 13:246–249.
28 Sarang A, Dinsmore J. Anaesthesia for awake craniotomy – evolution of a
technique that facilitates awake neurological testing. Br J Anaesth 2003; 90:
161–165.
29 Fukaya C, Katayama Y, Yoshino A, et al. Intraoperative wake-up procedure
with propofol and laryngeal mask for optimal excision of brain tumour in
eloquent areas. J Clin Neurosci 2001; 8:253–255.
30 Keifer JC, Dentchev D, Little K, et al. A retrospective analysis of a remifentanil/
propofol general anesthetic for craniotomy before awake functional brain
mapping. Anesth Analg 2005; 101:502–508.
This retrospective study considers continuous infusion of remifentanil/propofol
as a satisfactory anaesthetic technique in patients undergoing awake craniotomy, but emphasizes the risk of brief episodes of apnea and transient arterial
hypertension.
31 Soriano SG, Eldredge EA, Wang FK, et al. The effect of propofol on
intraoperative electrocorticography and cortical stimulation during awake
craniotomies in children. Paediatr Anaesth 2000; 10:29–34.
32 Himmelseher S, Pfenninger E. Anaesthetic management of neurosurgical
patients. Curr Opin Anaesthesiol 2001; 14:483–490.
33 Lim YJ, Zheng S, Zuo Z. Morphine preconditions Purkinje cells against cell
death under in vitro simulated ischemia-reperfusion conditions. Anesthesiology 2004; 100:562–568.
34 Kato R, Ross S, Foex P. Fentanyl protects the heart against ischaemic injury
via opioid receptors, adenosine A1 receptors and KATP channel linked
mechanisms in rats. Br J Anaesth 2000; 84:204–214.
35 Mathy-Hartert M, Mouithys-Mickalad A, Kohnen S, et al. Effects of propofol on
endothelial cells subjected to a peroxynitrite donor (SIN-1). Anaesthesia
2000; 55:1066–1071.
36 Acquaviva R, Campisi A, Murabito P, et al. Propofol attenuates peroxynitrite-mediated DNA damage and apoptosis in cultured astrocytes: an
alternative protective mechanism. Anesthesiology 2004; 101:1363–
1371.
37 Thiry JC, Hans P, Deby-Dupont G, et al. Propofol scavenges reactive oxygen
species and inhibits the protein nitration induced by activated polymorphonuclear neutrophils. Eur J Pharmacol 2004; 499:29–33.
38 Peters CE, Korcok J, Gelb AW, Wilson JX. Anesthetic concentrations of
propofol protect against oxidative stress in primary astrocyte cultures: comparison with hypothermia. Anesthesiology 2001; 94:313–321.
39 Daskalopoulos R, Korcok J, Farhangkhgoee P, et al. Propofol protection of
sodium–hydrogen exchange activity sustains glutamate uptake during oxidative stress. Anesth Analg 2001; 93:1199–1204.
40 Ozturk E, Demirbilek S, Kadir BA, et al. Antioxidant properties of propofol and
erythropoietin after closed head injury in rats. Prog Neuropsychopharmacol
Biol Psychiatry 2005; 29:922–927.
41 Adembri C, Venturi L, Tani A, et al. Neuroprotective effects of propofol in
models of cerebral ischemia: inhibition of mitochondrial swelling as a possible
mechanism. Anesthesiology 2006; 104:80–89.
This experimental study shows that propofol, at clinically relevant concentrations, is neuroprotective in models of cerebral ischaemia in vitro and in vivo,
and that it could act by preventing the increase in neuronal mitochondrial
swelling.
21 Magni G, Baisi F, La Rosa I, et al. No difference in emergence time and early
cognitive function between sevoflurane–fentanyl and propofol–remifentanil
in patients undergoing craniotomy for supratentorial intracranial surgery.
J Neurosurg Anesthesiol 2005; 17:134–138.
42 Balyasnikova IV, Visintine DJ, Gunnerson HB, et al. Propofol attenuates lung
endothelial injury induced by ischemia-reperfusion and oxidative stress.
Anesth Analg 2005; 100:929–936.
The capacity of propofol to attenuate the lung endothelial injury induced by
ischaemia-reperfusion is clearly related to its antioxidant properties.
22 Weninger B, Czerner S, Steude U, Weninger E. Comparison between
TCI-TIVA, manual TIVA and balanced anaesthesia for stereotactic biopsy
of the brain. Anasthesiol Intensivmed Notfallmed Schmerzther 2004; 39:
212–219.
43 Engelhard K, Werner C, Eberspacher E, et al. Influence of propofol on
neuronal damage and apoptotic factors after incomplete cerebral ischemia
and reperfusion in rats: a long-term observation. Anesthesiology 2004;
101:912–917.
23 Gupta A, Stierer T, Zuckerman R, et al. Comparison of recovery profile
after ambulatory anesthesia with propofol, isoflurane, sevoflurane and
desflurane: a systematic review. Anesth Analg 2004; 98:632–641;
table.
44 Ke QB, Hou J, Chen C, et al. Effect of propofol on spinal cord apoptosis
associated with aortic cross-clamping in rabbits. Zhongguo Wei Zhong Bing
Ji Jiu Yi Xue 2005; 17:426–429.
24 Bernstein M. Outpatient craniotomy for brain tumor: a pilot feasibility study in
46 patients. Can J Neurol Sci 2001; 28:120–124.
45 Bayona NA, Gelb AW, Jiang Z, et al. Propofol neuroprotection in cerebral
ischemia and its effects on low-molecular-weight antioxidants and skilled
motor tasks. Anesthesiology 2004; 100:1151–1159.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
Why we still use intravenous drugs Hans and Bonhomme
46 Acquaviva R, Campisi A, Raciti G, et al. Propofol inhibits caspase-3 in
astroglial cells: role of heme oxygenase-1. Curr Neurovasc Res 2005; 2:
141–148.
The beneficial effect of propofol on peroxynitrite-induced apoptosis of astroglial
cells appears to be mediated by an increase in heme oxygenase expression.
47 Engelhard K, Werner C, Eberspacher E, et al. Sevoflurane and propofol
influence the expression of apoptosis-regulating proteins after cerebral
ischaemia and reperfusion in rats. Eur J Anaesthesiol 2004; 21:
530–537.
48 Luo T, Xia Z, Ansley DM, et al. Propofol dose-dependently reduces tumor
necrosis factor-alpha-induced human umbilical vein endothelial cell apoptosis: effects on Bcl-2 and Bax expression and nitric oxide generation. Anesth
Analg 2005; 100:1653–1659.
Propofol, at clinically relevant concentrations, significantly and dose-dependently
attenuates TNF-induced increase in the apoptosis index and decrease in Bcl-2/
Bax ratio in cultured human umbilical vein endothelial cells.
49 Kotani N, Hashimoto H, Sessler DI, et al. Expression of genes for proinflammatory cytokines in alveolar macrophages during propofol and isoflurane
anesthesia. Anesth Analg 1999; 89:1250–1256.
503
50 Gilliland HE, Armstrong MA, Carabine U, McMurray TJ. The choice of
anesthetic maintenance technique influences the antiinflammatory cytokine response to abdominal surgery. Anesth Analg 1997; 85:1394–
1398.
51 Vila N, Castillo J, Davalos A, Chamorro A. Proinflammatory cytokines and
early neurological worsening in ischemic stroke. Stroke 2000; 31:2325 –
2329.
52 Kazmierski R, Guzik P, Ambrosius W, et al. Predictive value of white blood cell
count on admission for in-hospital mortality in acute stroke patients. Clin
Neurol Neurosurg 2004; 107:38–43.
53 Reith J, Jorgensen HS, Pedersen PM, et al. Body temperature in acute stroke:
relation to stroke severity, infarct size, mortality, and outcome. Lancet 1996;
347:422–425.
54 Feng CS, Ma HC, Yue Y, et al. Effect of propofol on the activation of nuclear
factor-kappa B and expression of inflammatory cytokines in cerebral cortex
during transient focal cerebral ischemia-reperfusion: experiment with rats.
Zhonghua Yi Xue Za Zhi 2004; 84:2110–2114.
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.