JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Fukuda, T. Articles by Toyooka, H. Search for Related Content PubMed PubMed Citation Articles by Fukuda, T. Articles by Toyooka, H. Related Collections Neuroanesthesia Pharmacology

---

NEUROSURGICAL ANESTHESIA

The Effects of 30% and 60% Xenon Inhalation on Pial Vessel Diameter and Intracranial Pressure in Rabbits

Taeko Fukuda, MD^*, Harumi Nakayama, MD^*, Kennichi Yanagi, MD, Taro Mizutani, MD, Masayuki Miyabe, MD^*, Norio Ohshima, DEng, and Hidenori Toyooka, MD^*

*Department of Anesthesiology, Institute of Clinical Medicine; Department of Biomedical Engineering, Institute of Basic Medical Sciences; and Department of Critical Care Medicine, Institute of Clinical Medicine, Tsukuba University, Tsukuba-City, Ibaraki, Japan

Address correspondence and reprint requests to Dr. Fukuda, Department of Anesthesiology, Institute of Clinical Medicine, Tsukuba University, Tsukuba-city, Ibaraki, 305-8575, Japan. Address e-mail to taekof{at}md.tsukuba.ac.jp

	Abstract

Top Abstract Introduction Methods Results Discussion References

 
Xenon may increase cerebral blood flow and intracranial pressure (ICP). To evaluate the effects of xenon on brain circulation, we measured pial vessel diameter changes, CO₂ reactivity, and ICP during xenon inhalation in rabbits. Minimum alveolar anesthetic concentration (MAC) for xenon was established in rabbits (n = 6). By using a cranial window model, pial vessel diameters were measured at 30% and 60% xenon inhalation and in time control groups (n = 15). ICP, mean arterial blood pressure, and heart rate were recorded during 30% and 60% xenon inhalation (n = 5). Pial vessel diameters were measured during hypocapnia and hypercapnia conditions in 60% Xenon and Control groups (n = 14). MAC for xenon was 85%. Xenon (0.35 and 0.7 MAC) dilated the arterioles (10% and 18%, respectively) and venules (2% and 4%, respectively) (P < 0.05). Dilation of arterioles was more prominent than that of venules. ICP, mean arterial blood pressure, and heart rate did not change during xenon inhalation. No difference in CO₂ reactivity was observed between Xenon and Control groups (P = 0.79). Sixty percent xenon (0.7 MAC) dilated brain vessels, but venule changes were small. Xenon did not increase ICP and preserved CO₂ reactivity of the brain vessels.

Implications: Xenon might increase cerebral blood flow; however, 0.7 minimum alveolar anesthetic concentration xenon preserved both low intracranial pressure and CO₂ reactivity of the cerebral vessels in the normal rabbit.

	Introduction

Top Abstract Introduction Methods Results Discussion References

 
In 1946, xenon was reported to have a narcotic effect on mice (1). Early in the 1950s, it was known that xenon had anesthetic properties in animals and humans (2). Xenon was used at that time as an anesthetic for surgical patients. However, it costs about 2000 times as much as nitrous oxide because it is a rare gas (0.05 ppm) (3). Therefore, xenon was disused in the field of clinical anesthesia. In 1990, Lachmann et al. (4) reevaluated the safety and efficacy of xenon in routine use as an inhaled anesthetic. Xenon has many advantages over gaseous anesthetics routinely used; for example, it has a small blood-gas partition coefficient (0.14), is nontoxic, and causes no environmental pollution (5,6). Recent improvement of low-flow or closed-circuit anesthesia techniques may serve to reduce the cost of xenon use. Therefore, xenon has been proposed to replace current inhaled anesthetics such as nitrous oxide.

Xenon has been used as a contrast agent for computed tomography of the brain. This technique enables noninvasive measurement of regional cerebral blood flow (CBF). However, it was reported in the 1980s that inhalation of 30%–35% xenon itself causes an increase in CBF (7–9), and there is the possibility that intracranial pressure (ICP) could be increased in some clinical situations. There has been no study of the effects of xenon on CO₂ reactivity of brain blood vessels.

To evaluate the effect of xenon on cerebral circulation, we conducted four experiments to investigate the following: 1) xenon minimum alveolar anesthetic concentration (MAC) in rabbits; 2) responses of pial blood vessels to 30% and 60% xenon inhalation; 3) ICP, mean arterial blood pressure (mAP), and heart rate (HR) during xenon inhalation; and 4) reactivity of pial blood vessels to hypercapnia and hypocapnia during 60% xenon inhalation.

	Methods

Top Abstract Introduction Methods Results Discussion References

 
All experiments were approved by the Animal Care and Use Committee of Tsukuba University. Forty female adult rabbits weighing between 2.5 and 3 kg were used in these experiments. Pregnant rabbits were not included.

Cullen et al. (10) demonstrated that the effect of halothane and xenon combined was simply additive, and MAC for the combination of xenon and halothane equaled 1.01 for the to combination and 1.04 for the to combination in humans. On the basis of their results, xenon MAC was determined in combination with 0.5 MAC halothane.

Rabbits (n = 6) were anesthetized with halothane alone (1%–2%) in a Plexiglas^® box. After tracheostomy was performed, each rabbit was connected to the xenon anesthetic circuit. We used a modified minimal-flow system developed by Luttropp et al. (11). Xenon concentration in the circuit was servocontrolled by a computer (PC-9821Xs/U7W; NEC, Tokyo, Japan), which delivered xenon or oxygen as needed via magnetic valves. Oxygen and xenon concentrations of the system were measured with an anesthetic monitor (AM-1; Acoma Medical Industry Co., Tokyo, Japan) and an exhaled xenon gas monitor (AZ-5000; Anzai Medical Co., Tokyo, Japan), respectively. Ventilation was assisted with the anesthetic circuit. The femoral artery was cannulated for sampling of blood gas analysis.

MAC was established according to methods described by Quasha et al. (12). The tail was clamped by a pair of 15-cm hemostat forceps to the first ratchet lock for 1 min. The tail was always stimulated proximal to a previous test site. Gross movements of the head, extremities, or body were taken as a positive sign, whereas no movement or small movements such as grimacing, swallowing, chewing, or tail flicking were considered negative. The end-tidal concentration of halothane was kept at 0.41% [50% of MAC for rabbits (13)] throughout the study. Xenon concentration was reduced in decrements of 10% from 70% until the negative responses became positive; 20 min of equilibration were allowed after confirming changes in the end-tidal anesthetic concentration. Xenon MAC was considered to be two times the concentration at the midpoint between the largest concentration that permitted movement in response to stimulation and the smallest concentration that prevented movement.

Rabbits (n = 15) were anesthetized with pentobarbital sodium (1–4 mg/kg IV). After tracheostomy was performed, each rabbit received pancuronium bromide (0.06–0.1 mg/kg IV), and the lungs were mechanically ventilated with 100% oxygen for denitrogenation. Tidal volume and respiratory rate were adjusted to maintain PaCO₂ between 38 and 42 mm Hg. Pentobarbital sodium (10 mg · kg^-1 · h^-1) and pancuronium bromide (0.16 mg · kg^-1 · h^-1) in lactated Ringer’s solution were infused IV at a rate of 10 mL · kg^-1 · h^-1 throughout the experiment. The femoral artery was cannulated for measurement of mAP and sampling of blood for gas analysis. An ear vein was cannulated for the administration of fluids and drugs. The mAP and HR were continuously recorded. Arterial blood pH, PaCO₂, PaO₂, and HCO₃^- were measured with a blood gas analyzer (288 Blood Gas System; Ciba-Corning Diagnostics Corp., Medfield, MA). Acidemia, when present, was corrected appropriately with IV sodium bicarbonate according to base deficit values. Rectal temperature was maintained at 38°C ± 1°C with a servoregulated heating pad.

A closed cranial window was used to observe the pial microcirculation. The head of each animal was secured in a stereotaxic frame. A midsagittal incision was made from the occiput to the forehead, and a hole 8 mm in diameter was drilled in the parietal bone. After coagulation of the dural vessels with a bipolar electrocoagulator, the dura and arachnoid membrane were removed. A plastic ring fitted with a cover glass was placed over the hole and secured with dental acrylate. The space under the window was filled with artificial cerebrospinal fluid (CSF) composed of 151 mEq/L sodium, 4 mEq/L potassium, 3 mEq/L calcium, 110 mEq/L chlorine, and 100 mg/dL glucose; pH was adjusted to 7.48.

Measurements of internal diameters of pial microvasculature (50 to 100 µm) were observed with an intravital epifluorescent microscope system (Model BHWI; Olympus Optical Co., Tokyo, Japan) (14). Each animal was set on a stage designed specifically for observation of the pial microvasculature of the rabbit. After IV injection of fluorescent dye (fluorescein isothiocyanate-labeled dextran with a molecular weight of 150,000; 20 mg/mL; FD-150; Sigma Chemical Co., St. Louis, MO), the microvasculature was visualized through the cranial window with a silicon intensifier target tube video camera (Model C2400; Hamamatsu Photonics, Shizuoka, Japan) and video-recorded (S-VHS, Model BR-S605B; Victor Co., Tokyo, Japan) for later analysis. To prevent damage of the microvessels, each observation was limited to <30 s. A final magnification of 200x was attained on a monitor screen (Model PVM-1445MD; Sony, Tokyo, Japan) by use of a recording lens (FK 3.3x; Olympus) and an objective lens (ULWD CDPlan 20x, numeric aperture 0.40; Olympus). A low-magnification photograph was printed with a video graphic printer (Model UP-850; Sony) to confirm the measurement sites. Three arteriole segments and three venule segments with diameters ranging from 50 to 100 µm were selected as the sites of measurement in each experiment. The measurements were performed at baseline (0 min) and after 30 min of 30% and 60% xenon inhalation in the Xenon group and at baseline (0 min) and after 30 and 60 min of 100% oxygen inhalation in the Time-Control group. The diameters of the selected microvessels were measured with an image-analysis system (ARGUS-10; Hamamatsu Photonics, Shizuoka, Japan) on individual frames of the video-recorded images. The observers were blinded to treatment group. The percentage of change of the diameter relative to the baseline value (at 0 min) was calculated.

Rabbits (n = 5) were anesthetized as described for the pial vessel diameter experiment. After placement of vascular catheters, the head of each animal was secured in a stereotaxic frame. A midsagittal scalp incision was made to expose the calvaria. A pediatric epidural needle (19-gauge, 35 mm) was inserted in the left lateral ventricle through a burr hole located 5 mm posterior to the coronal suture and 5 mm lateral to the sagittal suture. The epidural catheter (0.6 mm inner diameter, 10 cm) was inserted in the lateral ventricle via the needle. Access to the ventricle was confirmed by the appearance of CSF in the catheter. ICP was measured by connecting the catheter to a strain gauge transducer (MP5100-TW; Baxter Healthcare Co., Irvine, CA) (Polygraph; San-ei Co., Tokyo, Japan) via a short length of fine polyethylene tubing. The level of the external auditory meatus was used as the zero reference for ICP measurement.

After denitrogenation and normocapnia (PaCO₂ 40 ± 2 mm Hg) were confirmed, we measured ICP, mAP, and HR during 0%, 30%, and 60% xenon inhalation.

Rabbits (n = 14) were anesthetized and surgically prepared as described for the pial vessel diameter experiment. After denitrogenation and normocapnia (PaCO₂ 40 ± 2 mm Hg) were confirmed, we measured the diameter of the pial arteriole and of the venule at baseline (normocapnia). Afterward, PaCO₂ was decreased and then increased by changing respiratory rate. The internal diameters of the pial arteriole and of the venule (50 to 100 µm) were measured at each PaCO₂ described above. The CO₂ reactivity of pial vessel diameter (%Diameter/PaCO₂) was calculated with the following equation:

equation

We examined CO₂ reactivity during 60% xenon and 100% oxygen (control) inhalation; 30% xenon inhalation was not examined in this protocol.

The percentages of change in diameter were calculated at each segment of the arteriole and venule and were compared. All data are expressed as mean ± SD of absolute values or percentage of change from baseline values. Statistical comparisons of the absolute values were performed with two-way analysis of variance. Data presented as percentages of change were compared by nonparametric means with the Wilcoxon signed rank test and the Mann-Whitney U-test. Differences were considered significant at P < 0.05.

	Results

Top Abstract Introduction Methods Results Discussion References

 
The MAC value for xenon was 85% ± 34% in rabbits. Body temperature was kept at 38°C ± 1°C throughout the experiments. Physiologic values remained within the normal range.

Xenon produced significant dilation of arterioles and venules in a dose-dependent manner ( Fig. 1). Percentages of change in diameter of arterioles with 0.35 and 0.7 MAC xenon were 10% and 18%, respectively. Venules were slightly dilated with 0.35 and 0.7 MAC xenon (2% and 4%, respectively). In the Time-Control group, percentages of change in diameter of arterioles at 60 min were larger than those at 30 min, though no differences in percentages of change in diameter of venules were observed between 30 and 60 min.

View larger version (13K): [in this window] [in a new window]   Figure 1. Percentage of change in cerebral arteriole and venule diameter in Xenon and Time-Control groups. Cerebral arteriole and venule diameter dilated significantly during xenon inhalation (P < 0.05 or 0.01 vs Time-Control group). Open columns refer to the Time-Control group. Hatched and solid columns refer to the 30% and 60% Xenon groups, respectively.

View larger version (14K): [in this window] [in a new window]   Figure 2. CO2 reactivity (%Diameter [D]/PaCO2) in 60% Xenon and Control groups. There was no significant difference between Xenon and Control groups. Open columns refer to the Control group, and solid columns, to the 60% Xenon group.

	Discussion

Top Abstract Introduction Methods Results Discussion References

The MAC of xenon has been measured in other mammals, and the following values were found: humans, 71%; monkeys, 95%; mice, 95%; and rats, 161% (15–18). In this study, rabbit MAC for xenon was 85%, which is close to human or monkey MAC. Cullen et al. (10) reported that a combination of xenon and halothane has an additive rather than a synergistic anesthetic effect in humans. Therefore, the MAC value for xenon was determined by ensuring additivity with 0.5 MAC halothane in our study. Not all combinations of inhaled anesthetics previously tested have shown an additive effect; for example, combinations including nitrous oxide demonstrated mild synergism or antagonism in rats (19). MAC measurement with a hyperbaric chamber may decrease the number of interfering factors and thereby increase the validity of MAC values. However, Drummond (20) reported that the ratio of MAC values of two anesthetics is often constant from species to species. This observation provides a means for assessing the validity of preexisting or newly determined MAC values. For example, xenon/halothane MAC ratios are 95 (95%/1%) in mice, 95 (71%/0.75%) in humans, and 99 (98%/0.99%) in monkeys. In this study, the xenon/halothane MAC ratio was 104 (85%/0.82%), which was very close to the ratios measured in other species.

Xenon (0.35 and 0.7 MAC) dilated arteriole diameter 10% and 18%, respectively. Venules were dilated 2% and 4% in diameter, respectively. The 10% and 18% increases in the diameter of arterioles imply about 20% and 40% increase in the cross-sectional area of the vessels. Previous studies reported that CBF increases 4%–18% with 0.4 MAC xenon in monkeys, and 13.5%–25.4% with 0.5 MAC xenon in humans (7,9). On the assumption that CBF increases in proportion to the diameter of the blood vessels, our data are in agreement with these results. However, Junck et al. (8) reported that 80% xenon (0.5 MAC) increased CBF more than twofold in the neocortex, though no remarkable change was observed in the brainstem in rats. Our observational area might be in the most sensitive part of the brain. In this study, arterioles dilated significantly with the passage of time. Our artificial CSF was made on the basis of Davson’s data (21); however, it might be slightly alkalotic because of insufficient CO₂ bubbling. Application of acidotic or alkalotic solutions to the brain dilates or constricts cerebral arteries in vivo (22). We speculated that the arterioles, which might be constricted, would return to their original size by neutralization with CSF.

Although pial artery diameter increased during inhalation of xenon, ICP remained within two to four millimeters of mercury. The cranial window technique enables direct observation of both the arterial and venous blood vessels, though the observation areas are limited to the brain surface. In contrast, the microsphere method is inadequate to investigate changes in the venous blood vessels, though it is effective for examination of CBF changes in each brain area. As previously mentioned, xenon increased CBF in the neocortex area, but not in the cerebellum, brainstem, or thalamus (8). We speculated that the stable ICP during xenon inhalation was caused by the existence of small reactive brain areas (i.e., the brainstem, etc.) in rabbits and also by a smaller increase of venule dilation. Another possible explanation might be that we examined ICP in normal rabbits. ICP increases when it exceeds a compensatory limit, and normal animals usually have sufficient compensatory ability, which attenuates an increase in ICP.

No significant difference in CO₂ reactivity of cerebral blood vessels was observed between 0.7 MAC Xenon and Control groups. A previous report found that 35% xenon increased CO₂ reactivity in monkeys (23). Some factors might affect the reactivity, for example, background anesthesia, species, xenon concentration, CBF measurement techniques, or PaCO₂ control methods. To control PaCO₂, we changed the respiratory rate, because it is difficult to add extra CO₂ to the minimal flow system without changing xenon concentration. Hyperventilation might contract cerebral blood vessels and decrease ICP during xenon inhalation. Nitrous oxide and other inhaled anesthetics in combination were found to cause a larger increase in ICP than that caused by nitrous oxide alone (24). It remains to be elucidated whether xenon causes a larger increase in ICP with other inhaled anesthetics in combination than that caused by xenon alone.

In conclusion, the MAC value for xenon was 85% in rabbits. It was found that inhalation of 30% and 60% (0.35 and 0.7 MAC) xenon caused dilation of arterioles and venules in the brain, though the venular change was slight and xenon did not increase ICP in normal rabbits. CO₂ reactivity of the brain vessels was maintained during 0.7 MAC xenon inhalation.

	Acknowledgments

 
Supported, in part, by the Research for the Future Program (JSPS-RFTF 96100202), the Japan Society for the Promotion of Science (JSPS).

The authors thank Mr. Kozo Kobayashi, Ms. Yumiko Isaka, and Ms. Momoyo Ito for their technical assistance.

	References

Top Abstract Introduction Methods Results Discussion References

 

1. Lawrence JH, Loomis WF, Toblas CA, Turpin FH. Preliminary observations on the narcotic effect of xenon with a review of values for solubilities of gases in water and oils. J Physiol 1946; 105: 197–204.
2. Cullen SC, Gross EG. The anesthetic properties of xenon in animals and human beings, with additional observations on krypton. Science 1951; 113: 580–3.[Free Full Text]
3. Kennedy RR, Stokes JW, Downing P. Anaesthesia and the ‘inert’ gases with special reference to xenon [review]. Anaesth Intensive Care 1992; 20: 66–70.[ISI][Medline]
4. Lachmann B, Armbruster S, Schairer W, et al. Safety and efficacy of xenon in routine use as an inhalational anaesthetic. Lancet 1990; 335: 1413–5.[ISI][Medline]
5. Goto T, Suwa K, Uezono S, et al. The blood-gas partition coefficient of xenon may be lower than generally accepted. Br J Anaesth 1988; 80: 255–6.
6. Lane GA, Nahrwold ML, Tait AR, et al. Anesthetics as teratogens: nitrous oxide is fetotoxic, xenon is not. Science 1980; 210: 899–901.[Abstract/Free Full Text]
7. Gur D, Yonas H, Jackson DL, et al. Measurement of cerebral blood flow during xenon inhalation as measured by the microspheres method. Stroke 1985; 16: 871–4.[Abstract/Free Full Text]
8. Junck L, Dhawan V, Thaler HT, Rottenberg DA. Effects of xenon and krypton on regional cerebral blood flow in the rat. J Cereb Blood Flow Metab 1985; 5: 126–32.[ISI][Medline]
9. Hartmann A, Dettmers C, Schuier F, et al. Effect of stable xenon on regional cerebral blood flow and the electroencephalogram in normal volunteers. Stroke 1988; 22: 182–9.[Abstract/Free Full Text]
10. Cullen SC, Eger EI, Cullen BF, Gregory P. Observations on the anesthetic effect of the combination of xenon and halothane. Anesthesiology 1969; 31: 305–9.[ISI][Medline]
11. Luttropp HH, Rydgren G, Thomasson R, Werner O. A minimal-flow system for xenon anesthesia. Anesthesiology 1991; 75: 896–902.[ISI][Medline]
12. Quasha AL, Eger EI, Tinker JH. Determination and applications of MAC. Anesthesiology 1980; 53: 315–34.[ISI][Medline]
13. Davis NL, Nunnally RL, Malinin TI. Determination of the minimum alveolar concentration (MAC) of halothane in the white New Zealand rabbit. Br J Anaesth 1975; 47: 341–5.[Abstract/Free Full Text]
14. Suzuki T, Yanagi K, Ookawa K, et al. Blood flow and leukocyte adhesiveness are reduced in the microcirculation of a peritoneal disseminated colon carcinoma. Ann Biomed Eng 1998; 26: 803–11.[ISI][Medline]
15. Steward A, Allott PR, Cowles AL, Mapleson WW. Solubility coefficients for inhaled anesthetics for water, oil and biological media. Br J Anaesth 1973; 45: 282–93.[Free Full Text]
16. Whitehurst SL, Nemoto EM, Yao L, Yonas H. MAC of xenon and halothane in rhesus monkeys. J Neurosurg Anesthesiol 1994; 6: 275–9.[ISI][Medline]
17. Miller KW, Paton WDM, Smith EB, Smith RA. Physicochemical approaches to the mode of action of general anesthetics. Anesthesiology 1972; 36: 339–51.[ISI][Medline]
18. Koblin DD, Fang Z, Eger EI, et al. Minimum alveolar concentrations of noble gases, nitrogen, and sulfur hexafluoride in rats: helium and neon as nonimmobilizers (nonanesthetics). Anesth Analg 1998; 87: 419–24.[Abstract/Free Full Text]
19. Cole DJ, Kalichman MW, Shapiro HM. The nonlinear contribution of nitrous oxide at sub-MAC concentrations to enflurane MAC in rats. Anesth Analg 1989; 68: 556–62.[Abstract/Free Full Text]
20. Drummond JC. MAC for halothane, enflurane, and isoflurane in the New Zealand white rabbit: and a test for the validity of MAC determinations. Anesthesiology 1985; 62: 336–8.[ISI][Medline]
21. Davson H. Physiology of the cerebrospinal fluid. Boston: Little Brown Co, 1967: 33–54.
22. Wahl M, Deetjen P, Thurau K, et al. Micropuncture evaluation of the importance of perivascular pH for the arteriolar diameter on the brain surface. Pflugers Arch 1970; 316: 152–63.[ISI][Medline]
23. Hartmann A, Wassman H, Czernicki Z, et al. Effect of stable xenon in room air on regional cerebral blood flow and electroencephalogram in normal baboons. Stroke 1987; 18: 643–8.[Abstract/Free Full Text]
24. Strebel S, Kaufmann M, Anselmi L, Schaefer HG. Nitrous oxide is a potent cerebrovasodilator in humans when added to isoflurane: a transcranial doppler study. Acta Anaesthesiol Scand 1995; 39: 653–8.[ISI][Medline]

This article has been cited by other articles:

				S. Rex, P. T. Meyer, J.-H. Baumert, R. Rossaint, M. Fries, U. Bull, and W. M. Schaefer Positron emission tomography study of regional cerebral blood flow and flow-metabolism coupling during general anaesthesia with xenon in humans Br. J. Anaesth., May 1, 2008; 100(5): 667 - 675. [Abstract] [Full Text] [PDF]

				Y. Yamamoto, M. Kawaguchi, M. Kakimoto, S. Inoue, and H. Furuya The Effects of Dexmedetomidine on Myogenic Motor Evoked Potentials in Rabbits Anesth. Analg., June 1, 2007; 104(6): 1488 - 1492. [Abstract] [Full Text] [PDF]

				Y. Yamamoto, M. Kawaguchi, M. Kakimoto, M. Takahashi, S. Inoue, T. Goto, and H. Furuya The effects of xenon on myogenic motor evoked potentials in rabbits: a comparison with propofol and isoflurane. Anesth. Analg., June 1, 2006; 102(6): 1715 - 1721. [Abstract] [Full Text] [PDF]

				R. D. Sanders, D. Ma, and M. Maze Xenon: elemental anaesthesia in clinical practice Br. Med. Bull., February 22, 2005; 71(1): 115 - 135. [Abstract] [Full Text] [PDF]

				B. Preckel and W. Schlack Editorial III: Xenon--cardiovascularly inert? Br. J. Anaesth., June 1, 2004; 92(6): 786 - 789. [Full Text] [PDF]

				R. D. Sanders, N. P. Franks, and M. Maze Xenon: no stranger to anaesthesia Br. J. Anaesth., November 1, 2003; 91(5): 709 - 717. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (9) Citing Articles via Google Scholar Google Scholar Articles by Fukuda, T. Articles by Toyooka, H. Search for Related Content PubMed PubMed Citation Articles by Fukuda, T. Articles by Toyooka, H. Related Collections Neuroanesthesia Pharmacology

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