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Anesth Analg 2003;96:999-1003
© 2003 International Anesthesia Research Society

ANESTHETIC PHARMACOLOGY

Isoflurane Action in Spinal Cord Indirectly Depresses Cortical Activity Associated with Electrical Stimulation of the Reticular Formation

Joseph F. Antognini, MD*, Richard Atherley, BS*, and Earl Carstens, PhD{dagger}

*Department of Anesthesiology and Pain Medicine and {dagger}Section of Neurobiology, Physiology and Behavior, University of California, Davis, Davis, California

Address correspondence and reprint requests to Joseph F. Antognini, MD, Department of Anesthesiology, TB-170, University of California, Davis, Davis, CA 95616. Address e-mail to jfantognini{at}ucdavis.edu


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Anesthetics act in the spinal cord to ablate both movement and the ascending transmission of nociceptive information. We investigated whether a spinal cord action of isoflurane affected cortical activity as determined by the electroencephalogram desynchronization that occurs after electrical stimulation of the midbrain reticular formation (MRF). Six goats were anesthetized with isoflurane, and neck dissections were performed to permit differential isoflurane delivery to the head and torso. The electroencephalogram was recorded before, during, and after focal electrical stimulation (0.05, 0.1, 0.2, 0.3, and 0.4 mA) in the MRF; in each animal, the brain isoflurane was maintained constant ({approx}1%). When the torso isoflurane was 0.3% ± 0.1%, the spectral edge frequency after MRF electrical stimulation (15.3 ± 1.7 Hz, averaged across all stimulus currents) was more than the spectral edge frequency when the torso isoflurane was 1.2% ± 0.2% (12.9 ± 1.0 Hz, averaged across all stimulus currents; P < 0.05). Bispectral index values were similarly affected: 60 ± 6 when torso isoflurane was low versus 53 ± 7 at high torso isoflurane (P < 0.05). These results suggest that a spinal depressant action of isoflurane on ascending somatosensory transmission can modulate reticulo-thalamocortical arousal mechanisms, hence possibly reducing anesthetic requirements for unconsciousness and amnesia.

IMPLICATIONS: Isoflurane action in the spinal cord indirectly reduces the cortical activity associated with electrical stimulation of the reticular formation, an effect that might contribute to anesthetic-induced amnesia and unconsciousness.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
The spinal cord is an important site of anesthetic action. Movement initiated by noxious stimulation is abolished primarily as a result of anesthetic action in the spinal cord (1–3) . This holds true for isoflurane, halothane, and, to a lesser extent, thiopental (1–3) . It is unclear whether other anesthetic end points (amnesia and unconsciousness) are affected by the spinal cord actions of anesthetics (4). Any such effect would be indirect, inasmuch as the neural structures responsible for memory and consciousness reside in the brain. Neuroaxial blockade, however, decreases sedative requirements (5,6) , presumably by decreasing ascending somatosensory transmission to the brain. We have shown that isoflurane action in the spinal cord can affect the cortical activity that follows supramaximal noxious stimulation (7,8) . This apparently results from isoflurane’s ability to decrease the level of nociceptive somatosensory information that reaches the brain. It is unclear whether isoflurane’s spinal cord action affects ascending transmission of nonnoxious somatosensory impulses.

The midbrain reticular formation (MRF) is a collection of neurons with diffuse thalamocortical projections that encompasses the classic reticular activating system thought to be involved in consciousness (9). Moruzzi and Magoun (10) first reported that electrical stimulation of the reticular formation resulted in electroencephalogram (EEG) desynchronization, which is associated (but not synonymous) with consciousness. In this study, we were interested in determining whether a spinal action of isoflurane might affect cortical activity. We hypothesized that cortical activity, as assessed by MRF stimu-lation-evoked EEG desynchronization, would be facilitated when the torso (and hence spinal cord) isoflurane concentration was decreased to enhance ascending nonnociceptive somatosensory transmission.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
This study was approved by the University of California, Davis animal care and use committee. Six female goats weighing 45 ± 8 kg were anesthetized with isoflurane via mask, intubated, and mechanically ventilated. An IV catheter was inserted into a forelimb vein for infusion of lactated Ringer’s solution. Rectal and nasopharyngeal temperatures were measured and maintained at 37.5°C ± 1.5°C and 37.8°C ± 1.6°C, respectively. A craniotomy was performed to permit insertion of stimulating electrodes.

Bilateral neck dissections were performed to permit cranial bypass, as previously described (1,3) . In brief, the carotid arteries and jugular veins were dissected and isolated. Heparin was administered, and large Y-cannulae were inserted into the jugular veins so that cranial venous blood could be diverted to a bubble oxygenator (B-10Plus; American Edwards, Irvine, CA) or allowed to flow into the superior vena cava (i.e., natural systemic flow). A cannula was inserted into a carotid artery to permit arterial blood from the oxygenator to be infused into the cranial circulation. A second catheter was placed in this carotid artery and directed toward the torso for determination of systemic blood pressure and for withdrawal of blood for gas, pH, and hematocrit analyses. An 18-gauge catheter directed toward the head was placed into the other carotid artery to determine cranial blood pressure during bypass. An isoflurane vaporizer was placed in line with the gas flow to the oxygenator (5% CO2/95% oxygen), thereby allowing differential isoflurane delivery to the cranial circulation. The neck musculature and other tissues (excluding the carotid arteries and jugular veins) were tightly ligated to minimize venous blood return via collateral circulation in the neck (11). This experimental preparation separates the systemic arterial circulation from the cranial circulation at the level of the caudal medulla and upper cervical spinal cord (12). After the surgical procedures, pancuronium (0.15–0.2 mg/kg IV) was administered and repeated every 2–3 h.

The head was secured in a stereotaxic frame, and a bipolar stimulating electrode (Frederick Haer, Inc., Bowdoinham, ME) was stereotaxically positioned in the MRF (0–3 mm rostral to the interaural line, 5–7 mm lateral to the midline, and 30–32 mm below the surface of the cortex). The stimulation site was rostral to the "watershed" area where systemic blood mixes with cranial blood in this differential anesthetic delivery model (12). The bifrontal EEG was monitored with platinum needle electrodes inserted into the periosteum overlying the frontal bones. The EEG was amplified (Model 8-10E; Grass Instruments, Quincy, MA), filtered (0.3–35 Hz), and digitized with a commercial program (PolyViewPro; Astro-Med, West Warwick, RI). In addition, we monitored the bifrontal EEG with an Aspect-1000 bispectral index (BIS) monitor (Aspect Medical Systems, Newton, MA). Processed EEG data (BIS; spectral edge frequency, 95%) were downloaded to a personal computer. These data represented averages of 5-s epochs.

Blood ({approx}500 mL) was drained from the goat into the oxygenator. Bypass was initiated by diverting cranial venous blood to the oxygenator and infusing the arterial blood via roller pump into the carotid artery. A temporary ligature was placed around the remaining carotid artery that transmitted systemic blood to the head. Cranial blood flows were 300–500 mL/min. The torso isoflurane was estimated from the end-tidal isoflurane measured with a calibrated agent analyzer (Datex, Madison, WI). Isoflurane concentration in the cranial blood was estimated from the isoflurane concentration in the oxygenator exhaust by using a calibrated agent analyzer (1,12) . During cranial bypass, the systemic mean arterial blood pressure was 117 ± 25 mm Hg, and cranial pressure was 58 ± 22 mm Hg. Glucose was infused into the oxygenator to maintain cranial glucose levels. Systemic and oxygenator arterial blood status was maintained as follows: pH, 7.45 ± 0.05; PO2, 490 ± 111 mm Hg; PCO2, 31 ± 6 mm Hg; glucose, 127 ± 61 mg/dL; and hematocrit, 25% ± 9%.

The MRF stimulation paradigm consisted of a 2-s train of 0.1-ms pulses delivered at 300 Hz at intervals of 2–3 min. The current intensities were 0.05, 0.1, 0.2, 0.3, and 0.4 mA. Preliminary observations indicated that currents between 0.05 and 0.4 mA evoked detectable changes in EEG variables indicative of desynchronization. Additionally, the intensity of MRF stimulation required for EEG desynchronization depended on the cranial and torso isoflurane concentrations. If the cranial isoflurane concentration was too large, EEG desynchronization could not be elicited, and if it was too small, spontaneous desynchronization occurred. Thus, in each animal it was necessary to establish an initial isoflurane concentration that would permit detection of EEG desynchronization. In general, we began with cranial isoflurane concentrations of 0.8%–1.4% and torso isoflurane concentrations of 0.2%–1.4%. Once we established that EEG desynchronization could be produced, we maintained the cranial isoflurane concentration constant while we varied the torso isoflurane concentration. For example, in one animal we maintained the cranial iso-flurane at 1% while the torso isoflurane was adjusted from 0.2% to 1.2%, and the MRF electrical stimulation paradigm was repeated at each torso isoflurane concentration.

EEG data were collected for the 1-min period before and 1-min period after the onset of electrical stimulation. The BIS monitor used a rolling average with a delay. We analyzed the EEG data for the 30-s period immediately preceding the electrical stimulus and the second 30-s period after the onset of electrical stimulation. We averaged the 6 5-s epochs to determine the average value for each period. We waited 2–3 min between stimuli to permit the EEG to return to baseline. Once we had determined responses at a particular torso isoflurane concentration, the torso isoflurane was adjusted (either increased or decreased, depending on the starting concentration) and equilibrated for 15–20 min, and the stimulation paradigm was repeated. The order of torso isoflurane concentrations was counterbalanced.

After data collection, a lesion was made at the MRF stimulation site by passing direct current through the stimulating electrode, and the animal was killed with additional isoflurane and an IV KCl injection. The brains were removed, fixed in formalin, and cut in 50-µm frozen sections to verify the MRF lesion site.

Data are expressed as mean ± SD. An area under the curve analysis was used to evaluate the spectral edge frequency (SEF95) and BIS values (before and after stimulation) at each anesthetic condition (small torso isoflurane and high torso isoflurane). For example, at the low torso isoflurane concentrations, the poststimulus SEF values for each of the electrical currents were summed and compared with the summed prestimulus values and the summed values obtained at the large torso isoflurane concentrations by using analysis of variance followed by a Student-Newman-Keuls post hoc test. P < 0.05 was considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
When the cranial isoflurane concentration was maintained at 1.0% ± 0.2% and the torso isoflurane was 0.3% ± 0.1%, electrical stimulation of the MRF resulted in EEG desynchronization. In contrast, when the torso concentration was 1.1% ± 0.2%, MRF stimulation was less likely to cause EEG desynchronization. Examples of these results are shown in Figure 1. When the torso isoflurane concentration was small (0.4%), 0.1-mA stimulation evoked a delayed EEG desynchronization (left-hand panel, upper trace) and an increase in the SEF95 (thick line). Further increases in MRF stimulation intensity (Fig. 1, middle and right-hand panels) evoked greater EEG desynchronization and increases in SEF95. When the torso isoflurane concentration was large (1.0%), stimulation at 0.1 or 0.2 mA elicited no change in EEG (Fig. 1, lower EEG traces) or SEF95 (Fig. 1, thin lines), whereas stimulation at 0.3 mA resulted in a weak desynchronization and increase in SEF95 (Fig. 1, right-hand panel, lower EEG trace and thin line, respectively).



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  		Figure 1. These individual examples of the electroencephalogram (EEG) at different stimulating currents (0.1–0.3 mA) and at different anesthetic conditions demonstrate that isoflurane action in the spinal cord affected the propensity for EEG desynchronization. The thick black line represents the spectral edge frequency (SEF95) during the period before and after midbrain reticular formation (MRF) stimulation (at the 60-s mark) when the cranial and torso isoflurane concentrations were 0.8% and 0.4%, respectively. The thin black line represents the SEF95 when the cranial and torso isoflurane concentrations were 0.8% and 1.0%, respectively. The raw EEGs are shown above and below the SEF95 curves. Note that when the torso isoflurane was 0.4%, MRF stimulation desynchronized the EEG more readily than when the torso isoflurane was 1.0%.

 
When the torso isoflurane was 0.3% ± 0.1%, the SEF95 after MRF electrical stimulation (15.3 ± 1.7 Hz, summed and averaged across all stimulus currents) was more than the SEF95 when the torso isoflurane was 1.2% ± 0.2% (12.9 ± 1.0 Hz, summed and averaged across all stimulus currents; P < 0.05). BIS values were similarly affected: 60 ± 6 when torso isoflurane was small versus 53 ± 7 at large torso isoflurane (P < 0.05). Figure 2 plots the mean SEF95 (Fig. 2, A and B) and BIS values (Fig. 2, C and D) before and after MRF stimulation as a function of stimulus intensity, under conditions in which torso isoflurane concentration was small (0.3% ± 0.1%; Fig. 2, A and C) and large (1.1% ± 0.2%; Fig. 2, B and D). Several observations are of note. There was a tendency for mean prestimulation SEF95 and BIS values to be higher at small versus large torso isoflurane concentrations (Fig. 2, {blacksquare}), although this did not reach statistical significance. Most importantly, the mean poststimulation SEF95 and BIS values (summed across all current intensities) were larger at the small torso isoflurane concentration (Fig. 2, •). Moreover, the current threshold to elicit increased SEF95 (Fig. 2A) or BIS (Fig. 2C) tended to be lower under the condition of small torso isoflurane.



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  		Figure 2. The spectral edge frequency (SEF) and bispectral index (BIS) values before and after electrical stimulation are plotted at each electrical current applied to the midbrain reticular formation (MRF) during small (0.3% ± 0.1%; A and C) and large (1.1% ± 0.2%; B and D) torso isoflurane anesthesia. The cranial isoflurane was 1.0% ± 0.2% in both anesthetic conditions. The electrical current during small isoflurane anesthesia to the torso was associated with electroencephalogram desynchronization, as seen in the larger BIS and SEF values (*P < 0.05 compared with the prestimulus curve; #P < 0.05 compared with the curve when torso isoflurane was 1.1% ± 0.2%). During small isoflurane delivery to the torso, the SEF and BIS values increased at a smaller current (0.1 mA compared with 0.2 mA) than when the torso isoflurane was greater, although this was not statistically significant. The inset drawing shows the MRF stimulation sites; one site could not be recovered because of damage to the brain during removal. RF = reticular formation; PAG = periaqueductal gray.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The main finding of this study was that altering the torso (and hence spinal cord) concentration of isoflurane indirectly affected the EEG desynchronization response to electrical stimulation of the MRF. We take this as evidence that the arousal state of the brain during isoflurane anesthesia is dependent, at least to some extent, on the anesthetic effect in the spinal cord. In our prior studies (7,8) , we concluded that anesthetic action in the spinal cord could block the ascending transmission of noxious-evoked somatosensory transmission. Such an action would decrease cortical activity and could possibly contribute to the maintenance of unconsciousness during anesthesia, particularly at lighter anesthetic planes, when the brain is more likely to be sensitive to input arising from noxious stimulation. Our present findings extend this by showing that, in the absence of noxious stimulation, an increased spinal concentration of isoflurane reduces cortical arousability, as assessed by MRF stimulation-evoked cortical EEG desynchronization. These results support the idea that reducing nonnociceptive ascending somatosensory traffic might contribute to a reduction in anesthetic requirements for other end points, such as unconsciousness and amnesia.

These findings are consistent with previous studies showing that neuroaxial blockade with local anesthetics has indirect effects on sedative requirements. Ben-David et al. (5) found that midazolam requirements were decreased in patients receiving spinal anesthesia. In an animal study, Eappen and Kissin (6) determined that spinal bupivacaine decreased thiopental requirements for sedation and for blocking responses to noxious stimuli applied above the level of the block. Spinal anesthesia by itself appears to have sedative effects (13). Hodgson and Liu (14) reported that epidural anesthesia decreased the concentration of sevoflurane that was required to achieve a BIS value of 50. These studies strongly suggest that blocking ascending somatosensory transmission alters brain activity.

Although we did not directly compare the relative abilities of isoflurane and neuroaxial blockade to alter brain arousability, it is of interest to consider the BIS data reported by Hodgson and Liu (14). The BIS number is derived from the EEG and was developed for human patients, but it appears to have value in other species, including goats (15). In this study, there was an absolute difference of approximately 7 in mean poststimulation BIS values between the small (Fig. 2C) and large (Fig. 2D) torso isoflurane conditions. Hodgson and Liu (14) reported that the sevoflurane concentration required to produce a BIS of 50 was 1% in patients without neuroaxial blockade and 0.73% in patients with neuroaxial blockade. On the basis of their linear equations, this suggests that patients who received neuroaxial blockade under 1% sevoflurane anesthesia would have had a BIS of approximately 41, i.e., a change of 9. Thus, the indirect affect of neuroaxial blockade on BIS is similar to the indirect effect of isoflurane on BIS in this study.

One limitation of the intracerebral electrical stimulation method is that both neuronal cell bodies and fibers of passage will be excited. A potential confound is MRF activation of descending fibers that might excite spinal neurons, thereby increasing ascending somatosensory traffic to supraspinal structures. Reducing the spinal isoflurane concentration might thus facilitate transmission via such a supraspinal-spinal-supraspinal loop and, hence, increase the likelihood of EEG desynchronization. However, we believe that this scenario is unlikely. Although stimulation at certain brainstem sites can facilitate spinal transmission (for reviews, see Refs. 16 and 17), stimulation in the MRF generally exerts an inhibitory effect on spinal nociceptive and nonnociceptive neurons (18–20) and reflexes (21). Assuming that descending inhibition outweighs facilitation from MRF stimulation, this would counteract the effect of decreasing the spinal isoflurane concentration, thereby underestimating the relative importance of isoflurane’s action in spinal cord to indirectly alter brain activity.

Reticular formation stimulation has been used for several decades to alter cortical activity (10). The EEG desynchronization that occurs after MRF stimulation is similar to the "awake" EEG, although this awake-like pattern does not necessarily indicate consciousness. Increased cortical activity after MRF stimulation, however, can be observed by using neurophysiological variables such as visual evoked potentials (22), which are enhanced by MRF stimulation. One report suggests that cortical activity is associated with synchronous gamma oscillations that originate in the thalamus and cortex, whereby neuronal activity is synchronized in groups of cortical cells that are far from each other, and this synchronization is enhanced during MRF stimulation (23).

In summary, we found that isoflurane action in the spinal cord indirectly altered brain cortical activity as measured by EEG changes induced by electrical stimulation of the reticular formation. This effect could indirectly affect anesthetic requirements for unconsciousness and amnesia.


   Acknowledgments
 
Supported in part by National Institutes of Health Grants GM57970 and GM61283.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Antognini JF, Schwartz K. Exaggerated anesthetic requirements in the preferentially anesthetized brain. Anesthesiology 1993; 79: 1244–9.[Web of Science][Medline]
  2. Rampil IJ. Anesthetic potency is not altered after hypothermic spinal cord transection in rats. Anesthesiology 1994; 80: 606–10.[Web of Science][Medline]
  3. Antognini JF, Carstens E, Atherley R. Does the immobilizing effect of thiopental in brain exceed that of halothane? Anesthesiology 2002; 96: 980–6.[Web of Science][Medline]
  4. Kendig JJ. Spinal cord as a site of anesthetic action. Anesthesiology 1993; 79: 1161–2.[Web of Science][Medline]
  5. Ben-David B, Vaida S, Gaitini L. The influence of high spinal anesthesia on sensitivity to midazolam sedation. Anesth Analg 1995; 81: 525–8.[Abstract]
  6. Eappen S, Kissin I. Effect of subarachnoid bupivacaine block on anesthetic requirements for thiopental in rats. Anesthesiology 1998; 88: 1036–42.[Web of Science][Medline]
  7. Antognini JF, Carstens E, Sudo M, Sudo S. Isoflurane depresses electroencephalographic and medial thalamic responses to noxious stimulation via an indirect spinal action. Anesth Analg 2000; 91: 1282–8.[Abstract/Free Full Text]
  8. Antognini JF, Wang XW, Carstens E. Isoflurane action in the spinal cord blunts electroencephalographic and thalamic-reticular formation responses to noxious stimulation in goats. Anesthesiology 2000; 92: 559–66.[Web of Science][Medline]
  9. Steriade M. Arousal: revisiting the reticular activating system. Science 1996; 272: 225–6.[Web of Science][Medline]
  10. Moruzzi G, Magoun HW. Brain stem reticular formation and activation of the EEG. Electroencephalogr Clin Neurophysiol 1949; 1: 455–73.[Medline]
  11. Antognini JF, Jinks S, Buzin V, Carstens E. A method for differential delivery of intravenous drugs to the head and torso of the goat. Anesth Analg 1998; 87: 1450–2.[Free Full Text]
  12. Antognini JF, Kien ND. A method for preferential delivery of volatile anesthetics to the in situ goat brain. Anesthesiology 1994; 80: 1148–54.[Web of Science][Medline]
  13. Pollock JE, Neal JM, Liu SS, et al. Sedation during spinal anesthesia. Anesthesiology 2000; 93: 728–34.[Web of Science][Medline]
  14. Hodgson PS, Liu SS. Epidural lidocaine decreases sevoflurane requirement for adequate depth of anesthesia as measured by the Bispectral Index monitor. Anesthesiology 2001; 94: 799–803.[Web of Science][Medline]
  15. Antognini JF, Wang XW, Carstens E. Isoflurane anaesthetic depth in goats monitored using the bispectral index of the electroencephalogram. Vet Res Commun 2000; 24: 361–70.[Web of Science][Medline]
  16. Millan MJ. Descending control of pain. Prog Neurobiol 2002; 66: 355–474.[Web of Science][Medline]
  17. Lima D, Almeida A. The medullary dorsal reticular nucleus as a pronociceptive centre of the pain control system. Prog Neurobiol 2002; 66: 81–108.[Web of Science][Medline]
  18. Peng YB, Lin Q, Willis WD. The role of 5-HT3 receptors in periaqueductal gray-induced inhibition of nociceptive dorsal horn neurons in rats. J Pharmacol Exp Ther 1996; 276: 116–24.[Abstract/Free Full Text]
  19. Gerhart KD, Yezierski RP, Wilcox TK, Willis WD. Inhibition of primate spinothalamic tract neurons by stimulation in periaqueductal gray or adjacent midbrain reticular formation. J Neurophysiol 1984; 51: 450–66.[Abstract/Free Full Text]
  20. Carstens E, Bihl H, Irvine DR, Zimmermann M. Descending inhibition from medial and lateral midbrain of spinal dorsal horn neuronal responses to noxious and nonnoxious cutaneous stimuli in the cat. J Neurophysiol 1981; 45: 1029–42.[Free Full Text]
  21. Carstens E, Douglass DK. Midbrain suppression of limb withdrawal and tail flick reflexes in the rat: correlates with descending inhibition of sacral spinal neurons. J Neurophysiol 1995; 73: 2179–94.[Abstract/Free Full Text]
  22. Steraide M, Demetrescu M. Unspecific systems of facilitation and inhibition and facilitation of potentials evoked by intermittent light. J Neurophysiol 1960; 23: 602–17.[Free Full Text]
  23. Munk MH, Roelfsema PR, Konig P, et al. Role of reticular activation in the modulation of intracortical synchronization. Science 1996; 272: 271–4.[Abstract]
Accepted for publication November 27, 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