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Anesth Analg 2003;96:1155-1160
© 2003 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

Preservation of the Cortical Somatosensory-Evoked Potential During Dexmedetomidine Infusion in Rats

Bai-Han Li, MD, Jeffrey S. Lohmann, MS CCC-A, CNIM, D.ABNM, H. Gregg Schuler, BA CCRC, and Arthur J. Cronin, MD

Department of Anesthesiology, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center

Address correspondence and reprint requests to Arthur J. Cronin, MD, 500 University Dr., H187, Hershey, PA 17033. Address e-mail to acronin{at}psu.edu


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Successful somatosensory-evoked potential (SEP) monitoring has been performed during the administration of dexmedetomidine to patients, but a systematic investigation of the dose response of the SEP to dexmedetomidine has not been reported. In this study, we evaluated the effect of a range of dexmedetomidine doses on the cortical SEP in rats. Twelve rats were initially anesthetized with ketamine and the lungs were mechanically ventilated. Femoral arterial and venous catheters were placed. Anesthesia was maintained with constant infusions of remifentanil (5–15 µg · kg-1 · min-1) and vecuronium (56 µg · kg-1 · min-1). Dexmedetomidine was infused at 0.1, 0.25, 0.5, 1.0, and 2.0 µg · kg-1 · min-1 in a stepwise manner with 10-min infusion periods at each step. In eight rats, an additional large-dose infusion of dexmedetomidine at 10 µg · kg-1 · min-1 was administered for 30 min. The cortical SEPs were recorded after stimulation of the tibial nerve. At all infusion rates, there was a statistically insignificant increase in the SEP amplitude. Dexmedetomidine consistently increased the SEP latency, but these increases were not statistically significant. These data demonstrate that dexmedetomidine maintains technically adequate conditions for SEP monitoring in rats and provides support for future studies of the effect of dexmedetomidine on SEP monitoring in humans.

IMPLICATIONS: In rats, the administration of a wide range of infusion rates of dexmedetomidine did not significantly affect the somatosensory-evoked potential. These results suggest that dexmedetomidine might be a useful adjunctive drug in patients undergoing intraoperative somatosensory-evoked potential monitoring.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Dexmedetomidine, a selective {alpha}-2 receptor agonist, provides analgesia and sedation without respiratory depression (1–3) . Principally used in sedation of critically ill patients, dexmedetomidine also has a role as an adjunctive drug in general anesthesia because it reduces volatile anesthetic requirements and provides a calm and comfortable emergence from anesthesia (4,5) . These features suggest that dexmedetomidine might be useful in neuroanesthesia.

Because intraoperative somatosensory-evoked potential (SEP) monitoring has become a part of neuroanesthesia, the effect of dexmedetomidine on SEPs needs to be described before this drug can gain widespread use in this field. There are few reports describing the effect of dexmedetomidine on SEPs. An investigation has been performed in rats using medetomidine, the racemic form of dexmedetomidine (6). In that study, medetomidine obliterated the SEP. However, in a study of volunteers, it was reported that dexmedetomidine maintained good conditions for SEP monitoring (7), and a case report of two patients undergoing spinal surgery with dexmedetomidine infusion supported this claim (8).

The chief clinical question driving this study is "What dose of dexmedetomidine suppresses the SEP to the point that SEP monitoring becomes unfeasible?" Most currently used sedative or hypnotic anesthetics suppress SEP amplitude in a dose-dependant fashion (9,10) , but other drugs increase (11) or have little effect on SEPs (12). To address this question, this study quantifies the effect of dexmedetomidine on the SEP over a wide range of doses in the rat. The rat model gives us the ability to describe the SEP effect of doses of dexmedetomidine that are larger than would be intentionally administered to humans. However, the effects of more clinically relevant doses of dexmedetomidine were also studied to provide information that might be useful to clinicians performing studies in human subjects.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Approval of the study protocol was obtained from the Institutional Animal Care and Use Committee of the Pennsylvania State University, College of Medicine. Twelve male albino Sprague-Dawley rats (Charles River Laboratories, Wilmington, MA) weighing 370–550 g were used. Anesthesia was induced with intraperitoneal ketamine (110 mg/kg) and maintained with additional doses (30 mg/kg) as required to allow completion of the surgical preparation. Lidocaine (1%) was infiltrated in all of the surgical areas before the incision. A tracheostomy was performed, the trachea was cannulated with a 14-gauge catheter, and the rat was artificially ventilated using a rodent respirator (Harvard Apparatus H680). The ventilator was adjusted as required to maintain an end-tidal carbon dioxide partial pressure of 35 mm Hg (Rascal II, Ohmeda, Salt Lake City, UT). A femoral arterial and venous catheter, both of PE50 tubing, were placed for drug infusion and blood pressure monitoring. Mean arterial blood pressure (MAP) was maintained at more than 75 mm Hg with 1- to 2-mL boluses of normal saline. Rectal temperature was kept at 37°C ± 0.5°C with a heating pad.

A remifentanil HCl (Ultiva, Abbott Laboratories, North Chicago, IL) infusion was initiated immediately after the placement of the venous catheter. The initial infusion rate of 5 µg · kg-1 · min-1 was increased in 2.5-µg · kg-1 · min-1 increments to a maximum of 15 µg · kg-1 · min-1 or until the motor response to the tail clamp was abolished. Once an appropriate dose of remifentanil was established, a bolus of 1 mg/kg of vecuronium was given followed by an infusion of vecuronium at 56 µg · kg-1 · min-1.

Dexmedetomidine HCl (Precedex, Abbott Laboratories) administration was initiated at least 30 min after remifentanil. The dexmedetomidine infusion was increased stepwise at 10-min intervals of 0.1, 0.25, 0.5, 1.0, and 2.0 µg · kg-1 · min-1 (50-min infusion time total). This regimen of dexmedetomidine administration, described by Bol et al. (13), results in plasma dexmedetomidine concentrations of 0.6, 1.5, 3.5, 7.0, and 16.0 ng/mL at 10, 20, 30, 40, and 50 min after the start of the infusion, respectively. This range of concentrations includes the 50% effective concentration for the whisker reflex (1.09 ng/mL), righting reflex (2.13 ng/mL), startle reflex (3.75 ng/mL), and motor response to tail clamp (5.49 ng/mL) but not the 50% effective concentration for the corneal reflex (24.5 ng/mL) (13).

The first two rats demonstrated little change in the SEP amplitude with increasing concentrations of dexmedetomidine. Therefore, the SEP amplitudes were followed for an additional 90-min dexmedetomidine washout period (while administering remifentanil) in the subsequent 10 rats. This increased drug exposure time was studied to address the possibility that the duration of exposure is an important variable in determining the effect of dexmedetomidine on the SEP. Again, little change in the SEP amplitude was noted after the next two rats. To determine if a large dose (much larger than that required to achieve the anesthetic state in a rat) would affect the SEP, the last eight rats also received an infusion at 10 µg · kg-1 · min-1 for 30 min after the washout period.

After the dexmedetomidine protocol was completed, eight rats were used to verify the sensitivity of our model to drugs that normally suppress the SEP in humans. The SEP was recorded in three rats after the administration of 5-mg/kg and 15-mg/kg bolus doses of propofol and in five rats after a single dose of 100 mg/kg of pentobarbital. All rats were euthanized with pentobarbital.

The tibial nerve on the lower extremity opposite the femoral catheters was stimulated by percutaneously placed needle electrodes at a supramaximal level at 15–20 mA for 0.2 ms at a frequency of 4.7 Hz (Nicolet EP System, Nicolet Biomedical Inc, Madison, WI). Using percutaneously placed needle electrodes, the cortical SEP was recorded from the midline in the frontal and parietal regions of the scalp. The ground electrode was placed at the left shoulder. The signal was filtered to exclude frequencies higher than 1500 Hz and lower than 30 Hz and was averaged over 300 repetitions. The SEP amplitude was measured as the difference in microvolts between the first negative and first positive peaks. The SEP latency was defined as the period between stimulation and the first negative peak.

The SEP was recorded during the three phases of the study and after the propofol and pentobarbital bolus doses. During the small-dose dexmedetomidine phase (12 rats), the SEP was recorded before dexmedetomidine infusion and every 10 min during dexmedetomidine infusion. During the washout phase (10 rats), SEPs were recorded 10, 40, and 90 min after the end of the small-dose dexmedetomidine infusion. During the large-dose dexmedetomidine phase (eight rats), SEPs were recorded every 10 min for 40 min.

A one-way analysis of variance for repeated measures was performed with the post hoc Dunnett test to detect the effect of each dose of dexmedetomidine on the MAP, heart rate, and cortical SEP amplitude and latency. To ensure that a significant effect was not being obscured by variability among the rats, the raw data for each rat were then transformed using a z-transformation, and the analysis was repeated. The results of the two analyses were similar. The results from the analysis using the transformed data are presented. Two-tailed paired t-tests were used to test whether the SEP amplitude or latency differed at the paired drug exposure time points estimated to represent the same plasma concentration of dexmedetomidine.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Rats tolerated the drug infusion protocol well. The mean ± SEM MAP at baseline was 126 ± 6 mm Hg. There was a significant effect of dexmedetomidine on MAP (F-ratio = 25.37; P < 0.0001). At the 0.1 and 0.25 µg · kg-1 · min-1 infusion rates, the MAP trended downwards, but it was not significantly different from baseline. At doses larger than 0.25 µg · kg-1 · min-1, the MAP increased. These increases were not statistically significant until initiation of the large dose (10 µg · kg-1 · min-1) infusion (Fig. 1). The mean ± SEM heart rate at baseline was 362 ± 15 bpm. There was a significant dexmedetomidine effect on the heart rate (F-ratio = 4.56; P < 0.0001). The heart rate was statistically significantly (P <= 0.05) slower than baseline at all points during the dexmedetomidine infusion and washout periods (Fig. 1).



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  		Figure 1. Effects of dexmedetomidine (Dex) on the mean arterial blood pressure (MAP) and heart rate. The y axis depicts the percentage of measured value in comparison to the baseline (before Dex infusion). The x axis is the time in minutes. Dex infusion is indicated by horizontal bars under the x axis. Small-dose Dex is infused with stepwise increases at 0.1, 0.25, 0.5, 1.0, and 2.0 µg · kg-1 · min-1 for 10 min. Large-dose Dex is infused at 10 µg · kg-1 · min-1 for 30 min. The number of rats involved in each condition is indicated above the x axis. *P < 0.05. Error bars represent the SE of the mean. The dashed line at 100% represents the baseline.

 
An easily recognized and measurable cortical SEP was obtained throughout the range of dexmedetomidine infusion rates (Figs. 2 and 3). The mean ± SEM SEP amplitude was 3.08 ± 0.58 µV at baseline. There was not a statistically significant difference in SEP amplitude during the course of the experiment (F-ratio = 0.91; not significant). Over the clinically relevant dexmedetomidine infusion range, 0.1–2.0 µg · kg-1 · h-1, there was a trend towards an increase (6.8% to 19.1%) in cortical SEP amplitude (Fig. 4). The mean ± SEM SEP latency was 19.52 ± 0.70 ms at baseline. There was not a statistically significant change in the SEP latency (F-ratio = 1.09; not significant). At all time points after the initiation of the dexmedetomidine infusion, the SEP latency was numerically greater than the mean SEP latency at baseline. However, because of the small sample size, this increase was never statistically significant (Fig. 4).



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  		Figure 2. Effects of the small-dose dexmedetomidine (Dex) on cortical somatosensory-evoked potentials (SEPs). Representative SEPs were recorded from a rat before the start of Dex infusion (baseline), before each change in infusion rate (0.1~2.0 µg · kg-1 · min-1, each for 10 min), and 10, 40, and 90 min after the infusion was stopped. Each division on the x axis is 10 ms. Each division on the y axis is 2.5 µV. Each trace is the average of 300 sweeps.

 


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  		Figure 4. Effects of dexmedetomidine (Dex) on the cortical somatosensory-evoked potentials (SEPs) latency and amplitude. The y axis is the percentage of the measured value in comparison to the baseline (before Dex infusion). The x axis is the time in minutes. Dex infusion is indicated by horizontal bars under the x axis. Small-dose Dex is infused with stepwise increases at 0.1, 0.25, 0.5, 1.0, and 2.0 µg · kg-1 · min-1 for 10 min. Large-dose Dex is infused at 10 µg · kg-1 · min-1 for 30 min. The number of rats involved in each condition is indicated above the x axis. Error bars represent the SE of the mean. The dashed line at 100% represents the baseline.

 


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  		Figure 3. Effects of the large-dose dexmedetomidine (Dex; 10 µg · kg-1 · min-1 for 30 min) on cortical somatosensory-evoked potentials (SEPs). Representative SEPs were recorded before the start (new baseline), 10, 20, and 30 min after the start, and 10 min after the stop of Dex infusion. The new baseline is obtained 90 min after the small-dose infusion of Dex depicted in Figure 1. Twenty minutes after the large-dose Dex infusion was completed, the rat was given a propofol bolus of 5 mg/kg, and then a propofol bolus of 15 mg/kg 10 min later. SEPs were obtained 1 min after each bolus and 10 min after the second bolus of propofol. Note that the small-dose of propofol enhanced the SEP, whereas the large-dose suppressed the SEP and that the SEP recovered quickly. Each division on the x axis is 10 ms. Each division on the y axis is 2.5 µV. Each trace is the average of 300 sweeps.

 
During the dexmedetomidine washout phase, the SEP was recorded at time points chosen to correspond to the plasma concentrations present after the 10-min infusion at 1.0 µg · kg-1 · min-1 (60 min), 0.5 µg · kg-1 · min-1 (90 min), and 0.25 µg · kg-1 · min-1 (140 min). The mean cortical SEP amplitude increased by 9.2%, 8.6%, and 26%, respectively. The mean latencies were 0.4% increased, 0.4% decreased, and 1.5% increased, respectively. None of these changes, which possibly represent the effect of increased dexmedetomidine and remifentanil exposure time as well as ketamine clearance, were statistically significant.

During the large-dose dexmedetomidine infusion, the cortical SEP amplitudes decreased by no more than 9.2% from before large-dose baseline and were not statistically different from baseline. The SEP latencies increased by no more than 13.8% and were also not significantly different from baseline.

To test the sensitivity of our model to drugs known to suppress the SEP amplitude in humans, 5-mg/kg and 15-mg/kg bolus doses of propofol (three rats) or 100 mg/kg of pentobarbital (five rats) were administered after the dexmedetomidine infusion protocol. The smaller dose of propofol increased SEP amplitude, but the larger dose temporarily decreased the amplitude (Fig. 3). Pentobarbital obliterated the SEP response.


   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The chief finding from this study is the lack of a suppressive effect of dexmedetomidine on the amplitude of cortical SEPs. In contrast to most anesthetics, dexmedetomidine tended to increase the SEP amplitude. These data support and expand the findings of Thornton et al. (7) who reported that two plasma concentrations of dexmedetomidine permitted SEP recording in intraoperative patients.

For this study, we adopted the dexmedetomidine infusion regimen used by Bol et al. (13). At each infusion rate, they measured plasma concentrations of dexmedetomidine and performed behavioral tests and then measured the plasma concentrations during the washout period. The largest plasma concentration of dexmedetomidine achieved at the end of this stepped regimen was 16 ng/mL. At this plasma concentration, rats lose the righting reflex, the startle reflex, and tail-clamp withdrawal but have preservation of the corneal reflex, which is lost at 24.5 ng/mL (2).

Differing from Bol et al. (13), we administered a large-dose dexmedetomidine infusion after the washout period. Using the pharmacokinetics described by them, this infusion should have achieved plasma levels more than 24.5 ng/mL. Even at these doses, which are much larger than required for clinical purposes, dexmedetomidine had little effect on the SEP.

To confirm that our rat SEP model was capable of showing drug-induced suppression of the SEP, we recorded the SEP after large bolus doses of propofol and pentobarbital. Both drugs suppressed the SEP amplitude, and with propofol the suppression resolved 10 minutes after the dose. Augmentation of the SEP amplitude with propofol has been reported (14) but is not well described. Suppression of the SEP with large doses of propofol and barbiturate, as demonstrated by our model, is consistent with findings in humans (15,16) , cats (17), and rats (pentobarbital only) (18). This appropriate response confirmed the validity of our model.

In addition to dexmedetomidine, the rats received ketamine during the surgical preparation and a constant infusion of remifentanil during the data collection phase. Although ketamine does increase the SEP amplitude in humans (19) and possibly in rats (6), any effect in this study is likely to be negligible because the interval between the ketamine administration and the baseline SEP recording was at least three half-lives (20). Remifentanil was chosen as the analgesic because its short half-life permits rapid establishment of a stable blood concentration. However, remifentanil does have a slight suppressive effect on SEPs (21,22) , and this effect cannot be quantified in our study. To minimize this effect in our study, the smallest dose that abolished the motor response to tail clamp was determined for each rat, and this infusion rate was maintained throughout the experiment. The data analysis, using the transformed data, uses each rat as its own control and thereby decreases the influence of remifentanil on the results.

Compared with volatile anesthetics or nitrous oxide, which cause a dose-dependant suppression of the SEP amplitude (9,10) , dexmedetomidine seems to maintain favorable conditions for SEP monitoring. Our results are consistent with previous clinical reports (7,8) but differ from the findings of Hayton et al. (6). In their study, 0.3 mg/kg of the racemic form of dexmedetomidine, medetomidine, caused a profound suppression of the SEP response in rats. A possible reason for the discrepancy between their results and the results we report is the large dose of medetomidine administered in their study.

Because of its relatively long half-life and dose-limiting cardiovascular effects, dexmedetomidine is unlikely to replace inhaled anesthetics. Rather, the role of dexmedetomidine in the operating room is likely to be as an adjunctive drug. It decreases the requirement for inhaled anesthetics (23–26) , propofol (5,27) , and fentanyl (28). Because the SEP suppression by anesthetics is dose-dependant, dexmedetomidine might improve SEP monitoring conditions by decreasing the dose of other drugs required to achieve an anesthetic state.

In conclusion, increasing plasma concentrations of dexmedetomidine more than the clinical and supraclinical range for the rat did not significantly change the cortical SEP amplitude or latency. If our findings can be confirmed in humans, these findings suggest that dexmedetomidine shows promise as an adjunctive drug in patients requiring intraoperative neurophysiologic monitoring.


   Acknowledgments
 
Supported, in part, by the Career Development Award (to AJC) from the Department of Anesthesiology, Hershey Medical Center.

The authors thank Garry Russell, MD, for guidance, De-Pei Li, MD, for assistance with surgical technique, Nicolet Biomedical Inc for use of the Nicolet EP System, and Nicole DiVittore for statistical assistance.


   References
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Accepted for publication December 3, 2002.




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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