Xenon Group Research Articles

Positron Emission Tomography Study of Regional Cerebral Metabolism during General Anesthesia with Xenon in Humans

The precise mechanism by which the gaseous anesthetic xenon exerts its effects in the human brain remains unknown. Xenon has only negligible effects on inhibitory gamma-aminobutyric acid receptors, one of the putative molecular targets for most general anesthetics. Instead, xenon has been suggested to induce anesthesia by inhibiting excitatory glutamatergic signaling. Therefore, the authors hypothesized that xenon, similar to ketamine and nitrous oxide, increases global and regional cerebral metabolism in humans. The regional cerebral metabolic rate of glucose (rcMRGlu) was sequentially assessed in two groups of six volunteers each, using F-fluorodeoxyglucose as tracer. In the xenon group, rcMRGlu was determined at baseline and during general anesthesia induced with propofol and maintained with 1 minimum alveolar concentration xenon. In the control group, rcMRGlu was measured using the identical study protocol but without administration of xenon. rcMRGlu was assessed after the plasma concentration of propofol had decreased to subanesthetic levels (< 1.0 microg/ml). rcMRGlu was quantified in 10 cerebral volumes of interest. In addition, voxel-wise changes in rcMRGlu were analyzed using statistical parametric mapping. Xenon reduced whole-brain metabolic rate of glucose by 26 +/- 7% (from 43 +/- 5 micromol x 100 g x min to 31 +/- 3 micromol x 100 g x min; P < 0.005) and significantly decreased rcMRGlu in all volumes of interest compared with the control group receiving propofol only. Voxel-based analysis revealed metabolic depression within the orbitofrontal, frontomesial, temporomesial, occipital, dorsolateral frontal, and lateral temporal cortices and thalami. No increases in rcMRGlu were detected during xenon anesthesia. Xenon induces metabolic depression in the human brain, suggesting that the inhibition of the glutamatergic system is likely to be of minor significance for the anesthetic action of xenon in vivo.

The Effects of Xenon on Myogenic Motor Evoked Potentials in Rabbits: A Comparison with Propofol and Isoflurane

We compared the effects of xenon on myogenic motor evoked potentials (MEPs) with those of propofol and isoflurane in rabbits under ketamine/fentanyl anesthesia. Thirty animals were randomly allocated to one of 3 groups (n = 10 in each group). In the propofol group, propofol was administered at a rate of 0.4 mg x kg(-1) x min(-1) (small) and 0.8 mg x kg(-1) x min(-1) (large). In the isoflurane group, isoflurane was administered at 0.8% (small) and 1.6% (large). In the xenon group, xenon was administered at 35% (small) and 70% (large). Myogenic MEPs in response to stimulation with single pulse and a train of 5 pulses were recorded from the soleus muscle before, during (at small and large doses), and after the administration of each anesthetic. With single-pulse stimulation, MEPs were recorded in 90% and 50% of animals at small and large doses of xenon, respectively, and MEP amplitudes in the xenon and isoflurane groups were significantly lower compared with those in the propofol group. With train pulse stimulation, MEPs were recorded in 100% and 90% of animals at small and large doses of xenon, respectively, and a reduction in MEP amplitudes by xenon was more prominent than by propofol but less than isoflurane at large doses. These results suggest that MEP recording may be feasible under xenon anesthesia if multipulse stimulation is used, although xenon has suppressive effects on myogenic MEPs.

This Month in Anesthesiology

This Month in Anesthesiology

Xenon Provides Short-Term Neuroprotection in Neonatal Rats When Administered After Hypoxia-Ischemia

Brain injury after hypoxic-ischemic insults evolves via an apoptotic/necrotic cascade. Glutamate over release and N-methyl-d-aspartate (NMDA) receptor over activation (excitotoxicity) are believed to trigger this process. Xenon is a nontoxic anesthetic gas that reduces neurotransmitter release and functionally antagonizes NMDA receptors. Administering xenon to hypoxic-ischemic newborns might be clinically effective if the neurotoxic processes continue evolving after delivery. We sought to determine whether xenon administration after the initial hypoxic-ischemic insult was neuroprotective. Fifty 7-day-old rats received a 90-minute hypoxic insult after unilateral carotid ligation. They were then randomized to breathe 1 of 2 gas mixtures for 3 hours: 50% Xe/30% O2/20% N2 or 30% O2/70% N2. One week after hypoxic-ischemic survival, significant global protection was seen in the xenon group (80% less injury); cortex/white matter (88% versus 25%), hippocampus (62% versus 0%), basal ganglia (81% versus 25%), and thalamus (50% versus 0%; percentage of global damage score in nonxenon versus xenon groups, respectively). Three hours of xenon administration commenced after hypoxia-ischemia in neonatal rats provides short-term neuroprotection. This finding suggests that treatment with xenon after perinatal asphyxia would also be neuroprotective. Because xenon does not cause other neurotoxic effects and has demonstrated minimal side effects in extensive anesthesia studies, it would make an ideal candidate for the treatment after human perinatal hypoxia-ischemia.

Xenon does not modify mivacurium induced neuromuscular block

The interaction between mivacurium and inhaled anesthetics is known, with the exception of xenon. We compared the pharmacodynamics of mivacurium during xenon anesthesia vs total iv anesthesia with propofol.This randomized controlled trial was carried out in the Aachen University Hospital. Forty-two adult patients ASA I or II, aged 18 to 60 yr, were randomized to receive either xenon or propofol anesthesia. Anesthesia was induced with propofol and remifentanil in both groups (each n = 21). The xenon group received xenon via face mask until an end-expiratory concentration of 60% was reached for one minute. Meanwhile, the acceleromyograph was calibrated and a train-of-four stimulation of the adductor pollicis muscle was started. After stabilization of the signal for five minutes, a single bolus of 0.16 mg.kg-1 mivacurium was injected. Anesthesia was maintained with xenon and remifentanil or with propofol and remifentanil.There were no significant differences between groups with respect to onset time (xenon 180 +/- 64 vs propofol 195 +/- 77 sec; P = 0.39), duration (xenon 16.18 +/- 4.97 vs propofol 15.68 +/- 6.17 min; P = 0.73), recovery index (xenon 5.63 +/- 2.48 vs propofol 5.73 +/- 2.12 min; P = 0.42) and clinical recovery (xenon 8.75 +/- 2.57 vs propofol 9.28 +/- 2.28 min; P = 0.22).We conclude that the neuromuscular blocking effects of mivacurium are similar when given during propofol vs xenon anesthesia.

Haemodynamic effects of haemorrhage during xenon anaesthesia in pigs

It was hypothesized that xenon would stabilize mean arterial pressure (MAP) in haemorrhagic shock, recovery, and volume resuscitation, because a higher MAP has been observed with xenon, when compared with isoflurane anaesthesia. The responses to haemorrhage and subsequent volume replacement were therefore compared between xenon and isoflurane anaesthesia, in pigs. Pigs were randomized to anaesthesia with xenon 0.55 MAC (group Xe, n=9) or isoflurane 0.55 MAC (group Iso, n=9), each with remifentanil 0.5 microg kg(-1) min(-1). MAP, heart rate, cardiac output (CO), and left ventricular fractional area change (FAC) were collected at control (1), after haemorrhage (20 ml kg(-1)) (2), after 10 min of recovery (3), after volume replacement (4), and 30 min later (5). Data were analysed by two-way repeated measures anova. Blood loss decreased MAP (Xe: 103 [21] to 53 [24] mm Hg; Iso: 92 [18] to 55 [14] mm Hg) and CO (Xe: 4.1 [0.8] to 2.6 [0.5] litre min(-1); Iso: 5.1 [1.1] to 3.8 [1.2] litre min(-1)), in spite of significant tachycardia. MAP and CO recovered to about 75% of control, and subsequent volume replacement completely reversed symptoms in both groups, but increased FAC only with xenon. Haemodynamic response to acute haemorrhage appeared faster with xenon/remifentanil than with isoflurane/remifentanil anaesthesia. In particular MAP decrease and short-term recovery were more marked with xenon (P<0.02). In the xenon group, volume replacement increased FAC compared with control and isoflurane (P<0.02).

The influence of xenon, nitrous oxide and nitrogen on gas bubble expansion during cardiopulmonary bypass

Xenon may have favourable applications in the setting of cardiac surgery. Its advantages include a desirable haemodynamic profile as well as potential cardiac and neuroprotective properties. However, its low solubility may lead to enhanced diffusion into enclosed gas spaces. The purpose of this study was to compare the effects of xenon (Xe), nitrous oxide (N2O) and nitrogen (N2) on gas bubble size during cardiopulmonary bypass (CPB). Rats were randomized to receive 70% Xe, 26% oxygen (O2), 4% carbon dioxide (CO2) (xenon group); 70% N2O, 26% O2, 4% CO2 (nitrous oxide group) or 70% N2, 26% O2, 4% CO2 (nitrogen group) during 90 min of normothermic CPB. Small gas bubbles (300-500 microL; n = 12 per group) were injected into a bubble chamber on the venous side of the bypass circuit. After 10 min of equilibration, they were removed for volumetric analysis. The increase in bubble size was 2 +/- 2% with nitrogen, 17 +/- 6% with xenon (P = 0.0192 vs. nitrogen) and 63 +/- 23% with nitrous oxide (P = 0.0001 vs. nitrogen). The nitrous oxide group had significantly increased bubble size compared to the xenon group (P = 0.0001). During CPB, xenon anaesthesia produced a small increase in gas bubble size compared to nitrogen. Nitrous oxide resulted in significantly larger bubbles compared to both nitrogen and xenon.

Xenon Attenuates Cerebral Damage after Ischemia in Pigs

Cerebral blood flow may be compromised in a variety of anesthetic procedures, and ischemic cerebral complications represent the leading cause of morbidity after cardiac operations. With the growing importance of neuroprotective strategies, the current study was designed to determine whether xenon would attenuate cardiac arrest-induced brain injury in pigs. Twenty-four pigs (aged 12-16 weeks) were investigated in a randomized design. General hemodynamics, intracranial pressure, brain tissue oxygenation, and cerebral microdialysis parameters were investigated. The animals were assigned to two groups to receive anesthesia with either xenon (75%) in oxygen (25%) or total intravenous anesthesia combined with air in oxygen (25%) ventilation 15 min before cardiac arrest. After induction (t0) of cardiac arrest of 4 min, cardiopulmonary resuscitation was performed for 1 min, and the induced ventricular fibrillation was terminated by electrical defibrillation. The investigation time was 240 min. Approximately 60 s after cardiac arrest, brain tissue oxygenation decreased to a critical level of less than 5 mmHg, paralleled by a decrease in electroencephalographic activity. Glycerol as a damage marker increased significantly (> 200 m; P < 0.05), with a peak 90 min after cardiac arrest in both groups. Glycerol concentrations during reperfusion were significantly lower and normalized faster in the xenon group as compared with the total intravenous anesthesia group. Although the primary ischemic lesion in this model was similar in both groups, the cerebral microdialysis data show that xenon induces a differential neurochemical benefit in cerebral cell damage and metabolism as compared with total intravenous anesthesia in vivo during cerebral reperfusion after cardiac arrest in a pig model.

Xenon anaesthesia may preserve cardiovascular function in patients with heart failure

The hypothesis that xenon anaesthesia provided haemodynamic stability was tested in patients with heart failure in a prospective, randomized, single-blind design. Twenty-six patients scheduled for implantation of a cardioverter-defibrillator (ICD) received xenon 60-65% in oxygen (xenon group, n = 12) or propofol 3 mg/kg/h (propofol group, n = 14), both combined with remifentanil 0.2 microg/kg/min. After induction of anaesthesia with etomidate and remifentanil, heart rate (HR), mean arterial pressure (MAP) and left ventricular ejection fraction (LVEF) were recorded. After 60 min of propofol or xenon anaesthesia, the same parameters were recorded. While HR decreased in both groups, MAP was unchanged with xenon (73 vs. 76 mmHg) and decreased with propofol (from 78 to 64 mmHg, P < 0.02). LVEF was stable in both groups [32% vs. 37%, xenon (NS), and 30% vs. 34%, propofol (NS)]. Preload, as measured by end-diastolic volume (EDV), did not change (66 vs. 63 ml with xenon; 79 vs. 81 ml with propofol, both NS). Afterload, as determined by end-systolic pressure-volume product (ESPV), decreased with propofol (6760 vs. 4920 ml mmHg) but not with xenon (4060 vs. 3780 ml mmHg, P < 0.01 between groups). With propofol, MAP is reduced and LVEF is not increased in spite of reduced afterload. In contrast, MAP and LVEF are maintained with xenon.

Randomized controlled trial of the haemodynamic and recovery effects of xenon or propofol anaesthesia

There is limited clinical experience with xenon in a large number of patients. We present intra- and postoperative haemodynamic and recovery data comparing xenon and total intravenous anaesthesia with propofol. A total of 160 patients aged 18-60 years (ASA I and II) undergoing elective surgery took part in this prospective non-blinded randomized controlled trial. After local ethics committee approval and written informed consent, patients were allocated randomly to either the xenon or the propofol group. Anaesthesia was induced with propofol and remifentanil and was maintained with xenon at 60% (minimal alveolar concentration 0.95) or with propofol 0.1-0.12 mg kg(-1) min(-1). Remifentanil was titrated to clinical need in both groups. The two study groups were comparable with respect to age, weight, height, gender and ASA classification. Baseline in heart rate and systolic arterial pressure (SAP) were comparable in both groups. Following induction, SAP initially decreased but returned to baseline values over 15 min in the xenon group and differed significantly from the propofol group. Heart rate decreased significantly only in the xenon group and remained at stable values. Occurrence and duration of hypertension, hypotension and bradycardia showed no significant difference between groups. Patient recovery time in the post-anaesthetic care unit and recovery from anaesthesia was similar in the two groups. After induction the xenon/opioid regimen maintains systolic blood pressure at baseline levels and a low heart rate. No differences between groups were found in haemodynamic stability during anaesthesia. Recovery from xenon anaesthesia was similar to that observed in the propofol group.

Effects of xenon anaesthesia on intestinal oxygenation in acutely instrumented pigs

Xenon is a narcotic gas that might be able to replace volatile anaesthetics or nitrous oxide due to its favourable pharmacological properties, such as providing haemodynamic stability. Intestinal oxygenation is affected by most volatile anaesthetics as a result of cardiodepressive effects. Reducing oxygenation of the gut might be a factor leading to perioperative organ dysfunction. This animal study was designed to assess the effects of xenon on intestinal oxygenation. After ethical approval, 24 anaesthetized, acutely instrumented pigs were randomly assigned to three groups: nine animals received xenon anaesthesia with inspiratory concentrations of 0, 20, 50 and 65% in addition to their basic i.v. anaesthesia, nine animals served as a study control group, and five animals were used to assess model stability. Measurement of systemic and regional haemodynamic and oxygenation parameters was made 30 min after changing the xenon concentration. Xenon elicited dose-dependent systemic haemodynamic changes: heart rate and cardiac output decreased by 30%, while mean arterial pressure was stable. Superior mesenteric artery blood flow was lower in the xenon group. Vascular resistance of the superior mesenteric artery increased. The small intestinal oxygen supply decreased with increasing xenon concentration; the mucosal tissue oxygen partial pressure decreased but did not reach hypoxic (<5 mm Hg) values. Serosal tissue oxygen partial pressure was maintained. Xenon, in addition to basic i.v. anaesthesia, elicited a decrease in cardiac output and maintained mean arterial pressure. Intestinal oxygenation was maintained, although regional macrohaemodynamic perfusion decreased. Xenon does not impair intestinal oxygenation under physiological conditions.

Xenon Does Not Prolong Neuromuscular Block of Rocuronium

With the exception of xenon, the interaction between muscle relaxants and inhaled anesthetics is known. We therefore compared the pharmacodynamics of rocuronium during xenon anesthesia versus a total IV anesthesia with propofol. Anesthesia was induced with propofol and remifentanil in both the xenon and propofol groups (each n = 20). The xenon group received xenon via face mask until an end-expiratory concentration of 60% was maintained for 1 min. Meanwhile, the acceleromyograph (TOF-Watch SX(R)) was calibrated and a frequent train-of-four stimulation of the musculus adductor pollicis was started. After stabilization of the signal for 5 min, a single bolus of 0.6 mg/kg rocuronium was injected. Anesthesia was maintained with xenon and remifentanil (xenon group) or with propofol and remifentanil (propofol group). There were no significant differences between the groups concerning the onset time (xenon group 125 +/- 33 and propofol group 144 +/- 43 s), duration (xenon group 33.2 +/- 10.8 and propofol group 32.6 +/- 8.4 min), recovery index (xenon group 9.4 +/- 6.6 and propofol group 8.4 +/- 5.3 min), and clinical recovery (xenon group 18.0 +/- 10.2 and propofol group 17.1 +/- 8.5 min). We conclude that the neuromuscular blocking effects of rocuronium are not different when given during propofol versus xenon anesthesia.

Xenon improves recovery from myocardial stunning in chronically instrumented dogs.

In this study we tested the hypothesis that inhalational administration of xenon improves recovery from myocardial stunning. Ten dogs were chronically instrumented for measurement of heart rate; left atrial, aortic, and left ventricular pressure; coronary blood-flow velocity; and myocardial wall-thickening fraction. Regional myocardial blood flow was determined with fluorescent microspheres. Catecholamine plasma levels were measured by high-performance liquid chromatography. An occluder around the left anterior descending artery (LAD) allowed the induction of a reversible LAD ischemia. Animals underwent 2 experimental conditions in a randomized crossover fashion on separate days: (a) 10 min of LAD occlusion under fentanyl (25 microg. kg(-1). h(-1)) and midazolam (0.6 mg. kg(-1). h(-1)) (control) and (b) a second ischemic episode under the same basal anesthesia with concomitant inhalational administration of 75 +/- 1 vol% xenon (intervention). Anesthesia was induced 35 min before LAD occlusion and was discontinued after 20 min of reperfusion. Dogs receiving xenon showed a significantly better recovery of wall-thickening fraction up to 12 h after ischemia. The increase in plasma epinephrine during emergence from anesthesia and in the early reperfusion period was significantly attenuated in the xenon group. There were no differences between groups concerning global hemodynamics, blood-flow velocity, or regional myocardial blood flow. In conclusion, inhalational administration of 75 vol% xenon improves recovery from myocardial stunning in chronically instrumented dogs under fentanyl/midazolam anesthesia.

Xenon modulates neutrophil adhesion molecule expression in vitro

Background and objective: Xenon reduces the infarct size after regional ischaemia in the rabbit heart in vivo, but the underlying mechanisms are unknown. Since adhesion molecules on neutrophils are closely involved in the pathophysiology of ischaemia/reperfusion injury and modulation of neutrophil function, we investigated the effect of xenon on neutrophil adhesion molecule expression in vitro. Methods: Freshly isolated neutrophils were incubated with 30% or 60% xenon for 60 min. In unstimulated and after stimulation with either N-formyl-methionyl-leucyl-phenylalanine or phorbol-12-myristate-13-acetate neutrophil surface expression of PSGL-1, L-selectin, CD11a and CD11b were measured by flow cytometry. Results: At both concentrations, xenon reduced the surface expression of PSGL-1 by 10% (P < 0.05), and of L-selectin by 15% (P < 0.05) in the 60% xenon group. Furthermore, N-formyl-methionyl-leucyl-phenylalanine activated neutrophils showed an increased removal of L-selectin from the neutrophil surface following incubation with xenon (30% compared to controls, P < 0.05). Neutrophil β2-integrin expression was not altered by xenon. Conclusions: Xenon increases the removal of the selectins PSGL-1 and L-selectin from the neutrophil surface in vitro. Since both selectins are involved in the initial contact between neutrophils and endothelial cells, xenon may affect neutrophil adhesion to endothelium during ischaemia/reperfusion injury. However, because the β2-integrin expression was unaffected by xenon, further investigations are required to clarify whether xenon may modulate neutrophil transmigration through endothelial cells in vivo.

Xenon modulates neutrophil adhesion molecule expression in vitro.

Xenon reduces the infarct size after regional ischaemia in the rabbit heart in vivo, but the underlying mechanisms are unknown. Since adhesion molecules on neutrophils are closely involved in the pathophysiology of ischaemia/reperfusion injury and modulation of neutrophil function, we investigated the effect of xenon on neutrophil adhesion molecule expression in vitro. Freshly isolated neutrophils were incubated with 30% or 60% xenon for 60 min. In unstimulated and after stimulation with either N-formyl-methionyl-leucyl-phenylalanine or phorbol-12-myristate-13-acetate neutrophil surface expression of PSGL-1, L-selectin, CD11a and CD11b were measured by flow cytometry. At both concentrations, xenon reduced the surface expression of PSGL-1 by 10% (P < 0.05), and of L-selectin by 15% (P < 0.05) in the 60% xenon group. Furthermore, N-formyl-methionyl-leucyl-phenylalanine activated neutrophils showed an increased removal of L-selectin from the neutrophil surface following incubation with xenon (30% compared to controls, P < 0.05). Neutrophil beta2-integrin expression was not altered by xenon. Xenon increases the removal of the selectins PSGL-1 and L-selectin from the neutrophil surface in vitro. Since both selectins are involved in the initial contact between neutrophils and endothelial cells, xenon may affect neutrophil adhesion to endothelium during ischaemia/reperfusion injury. However, because the beta2-integrin expression was unaffected by xenon, further investigations are required to clarify whether xenon may modulate neutrophil transmigration through endothelial cells in vivo.

Xenon attenuates cardiopulmonary bypass-induced neurologic and neurocognitive dysfunction in the rat.

With clinical data suggesting a role for excitatory amino acid neurotransmission in the pathogenesis of cardiopulmonary bypass (CPB)-associated brain injury, the current study was designed to determine whether xenon, an N-methyl-D-aspartate receptor antagonist, would attenuate CPB-induced neurologic and neurocognitive dysfunction in the rat. Following surgical preparation, rats were randomly divided into four groups: (1) sham rats were cannulated but did not undergo CPB; (2) CPB rats were subjected to 60 min of CPB using a membrane oxygenator receiving a gas mixture of 30% O2, 65% N2, and 5% CO2; (3) CPB + MK801 rats received MK801 (0.15 mg/kg intravenous) 15 min prior to 60 min of CPB with the same gas mixture; and (4) CPB + xenon rats underwent 60 min of CPB using an oxygenator receiving 30% O2, 60% xenon, 5% N2, and 5% CO2. Following CPB, the rats recovered for 12 days, during which they underwent standardized neurologic and neurocognitive testing (Morris water maze). The sham and CPB + xenon groups had significantly better neurologic outcome compared to both the CPB and CPB + MK801 groups on postoperative days 1 and 3 (P < 0.05). Compared to the CPB group, the sham, CPB + MK801, and CPB + xenon groups had better neurocognitive outcome on postoperative days 3 and 4 (P < 0.001). By the 12th day, the neurocognitive outcome remained significantly better in the CPB + xenon group compared to the CPB group (P < 0.01). These data indicate that CPB-induced neurologic and neurocognitive dysfunction can be attenuated by the administration of xenon, potentially related to its neuroprotective effect via N-methyl-D-aspartate receptor antagonism.

Diffusion of xenon and nitrous oxide into the bowel.

Nitrous oxide diffuses easily from blood into air filled spaces. Xenon is also a relatively insoluble gas, like nitrous oxide. Therefore, the authors measured xenon diffusion into obstructed bowel segments during xenon anesthesia and compared this with nitrous oxide and nitrogen diffusion. Twenty-one pentobarbital-anesthetized pigs were randomly assigned to three groups to receive either xenon-oxygen, nitrous oxide-oxygen, or nitrogen-oxygen (75%-25%), respectively. In each animal four bowel segments of 15-cm length were isolated. A pressure-measuring catheter was inserted into the lumen, and 30 ml of room air was injected into the segments. Anesthesia with the selected gas mixture was performed for 4 h. Pressure in the segments was measured continuously. The volume of gaseous bowel content was measured on completion of the study. The median volume of bowel gas in animals breathing nitrous oxide was 88.0 ml as compared with 39.0 ml with xenon anesthesia and 21.5 ml in the nitrogen-oxygen group. After 4 h of anesthesia, the intraluminal pressures in the nitrous oxide group were found to be significantly greater than in the control group and in the xenon group. The amount of diffused gas was significantly lower during xenon anesthesia than with nitrous oxide anesthesia but greater than with controls. Blood solubility can therefore be regarded as an important factor influencing gas diffusion into air filled cavities.

A closed xenon anesthesia delivery system.

A closed xenon anesthesia delivery system.

Continuous arterial P(O2) and P(CO2) measurements in swine during nitrous oxide and xenon elimination: prevention of diffusion hypoxia.

During nitrous oxide (N2O) elimination, arterial oxygen tension (PaO2) decreases because of the phenomenon commonly called diffusive hypoxia. The authors questioned whether similar effects occur during xenon elimination. Nineteen anesthetized and paralyzed pigs were mechanically ventilated randomly for 30 min using inspiratory gas mixtures of 30% oxygen and either 70% N2O or xenon. The inspiratory gas was replaced by a mixture of 70% nitrogen and 30% oxygen. PaO2 and carbon dioxide tensions were recorded continuously using an indwelling arterial sensor. The PaO2 decreased from 119+/-10 mm Hg to 102+/-12 mm Hg (mean+/-SD) during N2O washout (P<0.01) and from 116+/-9 mm Hg to 110+/-8 mm Hg during xenon elimination (P<0.01), with a significant difference (P<0.01) between baseline and minimum PaO2 values (deltaPaO2, 17+/-6 mm Hg during N2O washout and 6+/-3 mm Hg during xenon washout). The PaCO2 value also decreased (from 39.3+/-6.3 mm Hg to 37.6+/-5.8 mm Hg) during N2O washout (P<0.01) and during xenon elimination (from 35.4+/-1.6 mm Hg to 34.9+/-1.6 mm Hg; P< 0.01). The deltaPaCO2 was 1.7+/-0.9 mm Hg in the N2O group and 0.5+/-0.3 mm Hg in the xenon group (P<0.01). Diffusive hypoxia is unlikely to occur during recovery from xenon anesthesia, probably because of the low blood solubility of this gas.

Vecuronium-induced neuromuscular block during xenon or sevoflurane anaesthesia in humans

Twitch response using accelerometry and plasma concentrations, of vecuronium and its metabolite were studied in 27 surgical patients during xenon or sevoflurance anaesthesia after administration of vecuronium 0.05 mg kg-1. Anaesthesia was maintained using oxygen-xenon (MAC = 71%) or oxygen-sevoflurane (MAC = 2%) at an end-tidal concentration equal to 0.8 MAC (i.e. 57% xenon and 1.6% sevoflurane). Mean time from administration of vecuronium to 25% recovery of the first twitch of the train-of-four response was significantly shorter in the xenon group than in the sevoflurane group (12.9 (SD 2.5) min vs 19.4 (6.0) min, respectively). Plasma concentrations of vecuronium at 25% recovery were significantly higher during xenon than during sevoflurane anaesthesia (187 (49) ng ml-1 vs 136 (40) ng ml-1, respectively), while those of 3-desacetylvecuronium were similar in both groups.