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Anesth Analg 2004;98:471-476
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000099755.97885.3C

NEUROSURGICAL ANESTHESIA

Intravenous Administration of Flurbiprofen Does Not Affect Cerebral Blood Flow Velocity and Cerebral Oxygenation Under Isoflurane and Propofol Anesthesia

Kenji Yoshitani, MD, Masahiko Kawaguchi, MD, Kazuyuki Tatsumi, MD{dagger}, Noriyuki Sasaoka, MD, Norio Kurumatani, MD*, and Hitoshi Furuya, MD

From the Departments of Anesthesiology and *Hygiene, Nara Medical University, Nara, Japan, and the {dagger}Department of Anesthesia, Seikeikai Hospital, Osaka, Japan

Address correspondence and reprint requests to Kenji Yoshitani, MD, Department of Anesthesiology, Nara Medical University, Nara, Japan, 840 Shijo-cho, Kashihara, Nara, 634–8522, Japan. Address email to ykenji{at}leto.eonet.ne.jp


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Flurbiprofen, a nonsteroidal antiinflammatory drug (NSAID), has been used to treat rheumatic and osteoarthritic pain and to reduce postoperative pain. Although other NSAIDs, such as indomethacin, reduce cerebral blood flow (CBF), the effect of flurbiprofen on CBF is unknown. In the present study, we investigated the effects of flurbiprofen on cerebral blood flow velocity (CBFV) and cerebral oxygenation under isoflurane or propofol anesthesia. Forty-eight patients undergoing orthopedic or abdominal surgery were enrolled. Patients were randomly allocated to receive either propofol (target control infusion: target site effect concentration 3 µg/mL) or isoflurane (1 MAC) for maintenance of anesthesia. In each group (n = 12), 1 mg/kg of flurbiprofen (PROP-F and ISO-F groups) or 0.1 mL/kg saline (PROP-S and ISO-S groups) was administered IV for 5 min. During and after the administration of flurbiprofen or saline, cerebral oxygenation variables (tissue oxygen index [TOI], total hemoglobin change [{Delta}cHb], oxygenated hemoglobin changes [{Delta}O2Hb], and deoxygenated hemoglobin changes [{Delta}HHb]), and middle cerebral artery flow velocity (Vmca) were measured using a cerebral oximeter (NIRO 300) and transcranial Doppler, respectively, from 5 min before study drug administration to 60 min postadministration. Before the administration of flurbiprofen, control values of TOI in the ISO-S and ISO-F groups were significantly higher than those in the PROP-S and PROP-F groups, respectively (ISO-S versus PROP-S, 67% ± 4% versus 60% ± 7%; IOS-F versus PROP-F, 69% ± 4% versus 63% ± 8%; P < 0.05). However, values of TOI, {Delta}cHb, {Delta}O2Hb, {Delta}HHb, and Vmca did not change significantly during and after the administration of flurbiprofen under propofol or isoflurane anesthesia, and these values were similar to those during and after the administration of saline in the same anesthesia group. These data indicate that flurbiprofen does not affect CBFV and cerebral oxygenation under propofol or isoflurane anesthesia.

IMPLICATIONS: Indomethacin, a nonsteroidal antiinflammatory drug (NSAID), has been demonstrated to reduce cerebral blood flow (CBF). The CBF effects of flurbiprofen, another NSAID, are unknown. We investigated cerebral blood flow velocity (CBFV) and cerebral oxygenation during and after the administration of flurbiprofen under isoflurane and propofol anesthesia. We found that flurbiprofen had no effect on CBFV and cerebral oxygenation.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Nonsteroidal antiinflammatory drugs (NSAIDs) exert their effects by inhibiting synthesis of prostaglandin, which plays an important role in maintenance of cerebral blood flow (CBF). Therefore, a number of investigators have examined the effects of NSAIDs on CBF and metabolism. In particular, indomethacin has been shown to cause a decrease of CBF. In anesthetized baboons and rats, indomethacin reduced CBF to 38% and 50% of control, respectively, with no significant change in cerebral metabolic rate for oxygen (CMRO2) (1,2). In normocapnic normal volunteers, an indomethacin dose of 100 mg per oral and 0.4 mg/kg IV reduced CBF to 25%–40% of control values (3–6). In patients with traumatic brain injury, indomethacin infusion reduced intracranial pressure (ICP) to 22%–52% and CBF to 22%–26% of control (7–9). During brain tumor surgery, indomethacin also reduced ICP and CBF (10). However, other NSAIDs, including aspirin, sulindac, diclofenac, and ibuprofen, have been shown to have no effect on CBF.

Flurbiprofen, also a NSAID, is an arylpropionic acid derivative and has been mainly used as an oral treatment of rheumatoid arthritis and osteoarthritis. In addition, esterified flurbiprofen is injectable, allowing it to be used for preemptive analgesia and perioperative pain management (11,12). The effects of flurbiprofen on CBF and metabolism have not been investigated. We therefore investigated the effects of flurbiprofen on cerebral blood flow velocity (CBFV) and cerebral oxygenation under propofol (PROP) or isoflurane (ISO) anesthesia.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Forty-eight patients (ASA physical status I–II) undergoing orthopedic or abdominal surgery without epidural anesthesia were enrolled in this study. Patients with cardiac and cerebrovascular disease were excluded. After institutional approval, informed consent was obtained from each patient. All patients were randomly allocated, by selecting closed envelopes, to receive either PROP or ISO for maintenance of anesthesia. In each group (n = 12), 1 mg/kg of flurbiprofen (the PROP-F group and ISO-F group) or saline (the PROP-S group and ISO-S group) was administered IV during the operation to investigate the effect of flurbiprofen on cerebral hemodynamics.

No drug was given for preanesthetic medication. In the PROP-F and PROP-S groups, anesthesia was induced and maintained with fentanyl and PROP, using Stelpump, a target controlled infusion (TCI) system. The Stelpump program for TCI on a personal computer was used to control a Graseby 3400 syringe pump (Graseby, Watford, UK). Stelpump was written by J. F. Coetzee, MD (University of Stellenbosch Department of Anesthesiology, Tygergerg, South Africa) and is freely available from http://www.sed.sun.ac.za. Stelpump controls effect-compartment controlled infusion. We used the model of Marsh et al. (13) in Stelpump. Coetzee et al. (14) found that this model gave appropriate PROP target prediction within the range 3–6 µg/mL. For induction of anesthesia, the target effect-site concentration of PROP was set at 3 µg/mL. The trachea was intubated after the administration of vecuronium 0.2 mg/kg, and the lungs were mechanically ventilated with an air/oxygen mixture (FIO2 = 0.4). In the ISO-F and ISO-S groups, anesthesia was induced with IV fentanyl 4 µg/kg, PROP 2 mg/kg, and vecuronium 0.2 mg/kg, and the trachea was intubated. Anesthesia was maintained with 1 MAC of isoflurane 1.1 vol% (end-tidal) in oxygen and air (FIO2 = 0.4). In all groups, additional fentanyl was administered if necessary.

Routine monitoring equipment included a radial artery catheter for direct arterial blood pressure measurement, a pulse oximeter, and an electrocardiograph. Ephedrine was administered IV to maintain mean arterial blood pressure (MAP) more than 60 mm Hg. End-tidal carbon dioxide (ETCO2) tension and end-tidal concentration of ISO were measured using a CAPNOMAC multi-gas analyzer (Hewlett-Packard, Andover, MA). Tympanic membrane temperature was continuously monitored by Mon-a Therm (Mallinckrodt, St. Louis, MO) and maintained between 35.5°C and 36.5°C using a warming blanket.

A 2-MHz pulsed Doppler ultrasound device (COMPANION TCD System, EME, Überlingen, Germany) was used for transcranial measurements of CBFV in the right middle cerebral artery (MCA). Insonation of the MCA was initiated at a depth of 45 mm. Confirmation of MCA identity was achieved by increasing insonation depth to visualization of the bi-directional flow pattern typical of the bifurcation of the internal carotid artery into the MCA and anterior cerebral artery. After individual adjustment of Doppler variables such as gain, sample volume and power of ultrasound, the probe was hand-held to obtain an optimal flow velocity trace and then fixed in position for the measurement period.

A cerebral oximeter, NIRO 300 (Hamamatsu Photonics, Hamamatsu, Japan), was used to monitor brain oxygenation. The cerebral oximeter probe was placed on the right forehead with the caudal border approximately 1 cm above the eyebrow with the medial edge at the midline. NIRO 500, the earlier model of NIRO 300, monitored only changes in hemoglobin (Hb) concentration and the redox state of cytochrome oxidase with a modified Beer-Lambert equation. NIRO 300 uses a specially resolved spectrometer (15) that combines the multi-distance measurements of optical attenuation and makes it possible to calculate the absolute concentration of oxygenated Hb and deoxygenated Hb in the tissue. Then, the tissue oxygen index (TOI: %) that is the ratio of oxygenated to total tissue Hb is rapidly calculated.

At least 10 min after the beginning of surgery, while hemodynamic variables were maintained within normal ranges, CBFV in the right MCA (Vmca) and cerebral oximetry variables (oxygenated Hb change: {Delta}O2Hb, deoxygenated Hb change: {Delta}HHb, total Hb change: {Delta}cHb, and TOI) were measured as a control measurement. Arterial blood gas analysis was performed simultaneously. ETCO2 was adjusted to maintain normocapnia in reference to the value of PaCO2 at control measurement. Five minutes after the control measurement, flurbiprofen (1 mg/kg: 0.1 mL/kg) or saline (0.1 mL/kg) was administered IV for 5 min. A series of measurements was performed (Fig. 1). Hemodynamic variables were also measured at the same interval. During measurements, patients who required blood transfusion or other vasoactive drugs were excluded from the study.



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  		Figure 1. Time scheme of protocol. Five minutes after the control measurements, middle cerebral artery cerebral blood flow velocity (Vmca), tissue oxygen index (TOI), total hemoglobin change ({Delta}cHb), oxygenated hemoglobin change ({Delta}O2Hb), and deoxygenated hemoglobin change ({Delta}HHb) were measured at 0, 2, 5, 10, 20, 30, 45, and 60 min after the start of administration of flurbiprofen or saline in the four groups (propofol-flurbiprofen, propofol-saline, isoflurane-flurbiprofen, and isoflurane-saline groups).

 
Data are expressed as mean ± SD. Demographic variables were compared among groups using one-way analysis of variance and {chi}2 test. Hemodynamic variables, Vmca, and cerebral oximetry variables were analyzed using two-way analysis of variance with repeated measurement. Fisher’s protected least significant difference test was used for post hoc pairwise comparisons. P < 0.05 was considered significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Of the 48 patients who entered the study, 6 patients were excluded during measurement because of treatment with vasodilators or troubles with cerebral oximetry. Patient demographic data are shown in Table 1. There were no significant differences in demographic variables among the four groups. Physiological data are shown in Figure 2. There were no significant differences in MAP and ETCO2 between the PROP-S and PROP-F groups, and between the ISO-S and ISO-F groups. In addition, there were no significant differences in body temperature between the PROP-S and PROP-F groups or between the ISO-S and ISO-F groups during the study period (data not shown).


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  		Table 1. Demographic Data
 


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  		Figure 2. A, time course of changes of mean arterial blood pressure (MAP) during propofol anesthesia. There were no significant differences between the propofol-flurbiprofen (PROP-F) and propofol-saline (PROP-S) groups. B, time course of changes of MAP during isoflurane anesthesia. There were no significant differences between the isoflurane-flurbiprofen (ISO-F) and isoflurane-saline (ISO-S) groups. C, time course of changes of end-tidal CO2 during propofol anesthesia. There were no significant differences between the PROP-F and PROP-S groups. D, time course of changes of end-tidal CO2 during isoflurane anesthesia. There were no significant differences between the ISO-F and ISO-S groups.

 
The values of pH, PaCO2, PaO2, Hb, Vmca, and TOI at baseline (control) are shown in Table 2. pH, PaCO2, PaO2, Hb, and Vmca values were similar between the PROP-S and PROP-F groups and between the ISO-S and ISO-F groups. Values of TOI in the ISO-S and ISO-F groups were significantly higher than those in the PROP-S and PROP-F groups, respectively, whereas TOI values were similar between the ISO-S and ISO-F groups and between the PROP-S and PROP-F groups. Figure 3 shows the changes in Vmca and TOI depicted as % of baseline values during the study period. %Vmca and %TOI did not change in any experimental group. There were no significant differences in {Delta}O2Hb, {Delta}HHb, and {Delta}cHb between the PROP-S and PROP-F groups or between the ISO-S and ISO-F groups during the study period (data not shown).


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  		Table 2. Data of Control Measurement
 


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  		Figure 3. A, effect of flurbiprofen on percent changes of middle cerebral artery cerebral blood flow velocity (Vmca) during propofol anesthesia. There were no significant differences between the propofol-flurbiprofen (PROP-F) and propofol-saline (PROP-S) groups. B, effect of flurbiprofen on percent change in Vmca during isoflurane anesthesia. There were no significant differences between the isoflurane-flurbiprofen (ISO-F) and isoflurane-saline (ISO-S) groups. C, effect of flurbiprofen on percent change in tissue oxygen index (%TOI) during propofol anesthesia. There were no significant differences between the PROP-F and PROP-S groups. D, effect of flurbiprofen on percent change in %TOI during isoflurane anesthesia. There were no significant differences between the ISO-F and ISO-S groups.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The results show that TOI values at baseline were significantly higher in the ISO group than in the PROP group, suggesting that cerebral oxygenation may be better under ISO anesthesia compared with that under PROP anesthesia. However, CBFV and TOI remained unchanged during and after IV administration of flurbiprofen 1 mg/kg during either ISO or PROP anesthesia. These data suggest that flurbiprofen does not affect CBF and cerebral oxygenation in anesthetized patients.

The basic mechanisms of CBF regulation have been extensively studied. Prostaglandins are involved in the control of CBF and vasodilatory response to CO2. Therefore, many investigators have focused on the effects of indomethacin and other NSAIDs, inhibitors of prostaglandin synthesis, on CBF and metabolism. Pickard and Mackenzie (1) first reported that 10 mg/kg indomethacin immediately reduced resting CBF by 38% and attenuated the response of CBF to hypercapnia by 80% in anesthetized baboons. Sakabe and Siesjo (2) demonstrated in normocapnic and hypercapnic rats that indomethacin reduced CBF to 50% and 25% of control, respectively, with no influence on CMRO2. Subsequently, the effects of indomethacin on CBF were investigated in normal volunteers. Indomethacin given as a 100-mg suppository reduced CBF to 35% and 57% of control during normocapnia and hypercapnia, respectively (3). In the presence of refractory intracranial hypertension caused by traumatic brain injury, indomethacin 30–50 mg IV infusion significantly reduced ICP to 22%–52% and CBF to 22%–26% of control without producing detectable ischemia (7–9). Bundgaard et al. (10) also documented that indomethacin reduced ICP to 77% and CBF to 49% of controls during the perioperative period of craniotomy for brain tumor resection.

However, the effects of other NSAIDs on CBF and metabolism are different from indomethacin. Markus et al. (16) investigated the effects of a single dose of indomethacin and other NSAIDs (aspirin and sulindac) on cerebral circulation using transcranial Doppler ultrasonography in healthy normal volunteers and demonstrated that indomethacin significantly reduced Vmca, but Vmca was unchanged after aspirin or sulindac administration. Eriksson et al. (17) examined the effects of indomethacin and other prostaglandin inhibitors (naproxen and aspirin) on CBF in normal adults and reported that naproxen and aspirin had no effect on CBF, whereas indomethacin reduced CBF. Chemtob et al. (18) investigated the effects of indomethacin, aspirin, ibuprofen, and naproxen on CBF in newborn piglets. Although all NSAIDs reduced prostaglandin to a similar extent, the effects of these drugs on CBF were diverse. CBF increased after the administration of aspirin, decreased to almost the same extent after both small and large doses of indomethacin, and did not change after the administration of ibuprofen or naproxen. Other investigators have shown that ibuprofen had no effects on CBF during normocapnia, hypercapnia, and hypocapnia (18,19–22), although Leffer and Busija (23) found that ibuprofen increased CBF in the newborn pig. Diclofenac has no effects on CBF at rest or during hypercapnia (24–26). Taken together, NSAIDs other than indomethacin seem to have little effect on CBF.

This is the first report to investigate the effects of flurbiprofen on the cerebral circulation. ISO and PROP were documented to affect cerebral circulation and metabolism (27). ISO increases CBF, whereas PROP decreases CBF. Consequently the CBF/CMRO2 ratio increases or remains unchanged during ISO anesthesia and decreases during PROP anesthesia. In this study, TOI values in the ISO-S group were more than in the PROP-S group, as previous studies documented. The differences in cerebral oxygenation state between ISO and PROP anesthesia could affect the behavior of flurbiprofen on CBF. However, IV administration of flurbiprofen did not affect CBFV or TOI during either ISO or PROP anesthesia. In this study, we administered 1 mg/kg flurbiprofen because IV 1 mg/kg flurbiprofen has been shown to be effective for postoperative pain management (11,12). These results suggest that flurbiprofen can be used for pain management without a reduction of CBF, as noted when indomethacin was used. These results are compatible with the results in previous reports regarding the effects of other NSAIDs, except for indomethacin, on CBF. However, in the present study, we evaluated only patients without cerebrovascular disease or ICP increase. Further study is required to determine whether flurbiprofen can be used in patients with intracranial compromise.

Mechanisms by which indomethacin, but not other NSAIDs, reduces CBF are unknown. Possible mechanisms are as follows: first, both vasoconstrictive and vasodilative prostaglandins are synthesized in cerebral blood vessels. The effects of indomethacin and other NSAIDs, all cyclooxygenase inhibitors, on the balance of these prostaglandins may vary. Indomethacin may shift prostaglandins towards a predominantly vasoconstrictive balance. Second, endothelin may be involved in indomethacin-mediated CBF reduction. Therkelsen et al. (6) reported that indomethacin increased circulating levels of endothelin and decreased CBF compared with baseline values. Furthermore, cyclooxygenase products of arachidonic acid could be involved in endothelin-induced constriction and dilation (28). Finally, indomethacin may modulate CBF through the products from the lipoxygenase pathway. Indomethacin has been shown to potentiate the lipoxygenase pathway in contrast with other NSAIDs (28). However, these mechanisms are speculative. Further study is required to clarify why indomethacin has unique effects on CBF.

In summary, we investigated the effects of flurbiprofen on CBFV and cerebral oxygenation under PROP or ISO anesthesia. IV administration of flurbiprofen had no effect on CBFV and cerebral oxygenation variables. Although further study is required in cases with intracranial compromise, flurbiprofen can be used without a reduction in CBF in anesthetized patients.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication September 17, 2003.




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K. Yoshitani, M. Kawaguchi, M. Iwata, N. Sasaoka, S. Inoue, N. Kurumatani, and H. Furuya
Comparison of changes in jugular venous bulb oxygen saturation and cerebral oxygen saturation during variations of haemoglobin concentration under propofol and sevoflurane anaesthesia
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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press