bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nonlinear Changes in Brain Dynamics during Emergence from Sevoflurane Anesthesia
Authors: Walling Peter T. , Hicks Kenneth N. 
Published: October 2006

Background
New software was used during a pilot study of nonlinear changes in the electroencephalogram during emergence from sevoflurane anesthesia.

Methods
Digitized electroencephalographic signals were recorded from bipolar forehead electrodes between 1.2 and 40 k s/sec. Trajectories derived from underlying attractors were displayed continuously, and attractor dimensions were estimated. Observations are reported from 13 patients emerging from sevoflurane anesthesia.

Results
Qualitative observations and quantitative analysis of the data demonstrated four dynamical stages during emergence from deep anesthesia to consciousness.

Conclusions
The dynamical stages of emergence from sevoflurane anesthesia into consciousness demonstrate a classic route toward chaos, but the presence of chaos in the conscious state remains unproven. These stages are apparent both pictorially and analytically. Pre-emergent attractor patterns are usually distinctive; their real-time display could be a useful adjunct to depth of anesthesia monitors because they may provide warning of an imminent return to consciousness.
Positron Emission Tomography Study of Regional Cerebral Metabolism during General Anesthesia with Xenon in Humans
Authors: Rex Steffen , Schaefer Wolfgang , Meyer Philipp H. , Rossaint Rolf , Boy Christian , Setani Keyvan , Büll Ulrich , Baumert Jan H. 
Published: October 2006

Background
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.

Methods
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.

Results
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.

Conclusions
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.
Performance Characteristics of Five New Anesthesia Ventilators and Four Intensive Care Ventilators in Pressure-support Mode
Authors: Jaber Samir , Tassaux Didier , Sebbane Mustapha , Pouzeratte Yvan , Battisti Anne , Capdevila Xavier , Eledjam Jean-Jacques , Jolliet Philippe 
Published: October 2006

Background
During the past few years, many manufacturers have introduced new modes of ventilation in anesthesia ventilators, especially partial-pressure modalities. The current bench test study was designed to compare triggering and pressurization of five new anesthesia ventilators with four intensive care unit ventilators.

Methods
Ventilators were connected to a two-compartment lung model. One compartment was driven by an intensive care unit ventilator to mimic "patient" inspiratory effort, whereas the other was connected to the tested ventilator. The settings of ventilators were positive end-expiratory pressures of 0 and 5 cm H2O, and pressure-support ventilation levels of 10, 15, and 20 cm H2O with normal and high "patient" inspiratory effort. For the anesthesia ventilators, all the measurements were obtained for a low (1 l/min) and a high (10 l/min) fresh gas flow. Triggering delay, triggering workload, and pressurization at 300 and 500 ms were analyzed.

Results
For the five tested anesthesia ventilators, the pressure-support ventilation modality functioned correctly. For inspiratory triggering, the three most recent anesthesia machines (Fabius, Drägerwerk AG, Lübeck, Germany; Primus, Drägerwerk AG; and Avance, GE-Datex-Ohemda, Munchen, Germany) had a triggering delay of less than 100 ms, which is considered clinically satisfactory and is comparable to intensive care unit machines. The use of positive end-expiratory pressure modified the quality of delivered pressure support for two anesthesia ventilators (Kion, Siemens AG, Munich, Germany; and Felix, Taema, Antony, France). Three of the five anesthesia ventilators exhibited pressure-support ventilation performance characteristics comparable to those of the intensive care unit machines. Increasing fresh gas flow (1 to 10 l/min) in the internal circuit did not influence the pressure-support ventilation performance of the anesthesia ventilators.

Conclusion
Regarding trigger sensitivity and the system's ability to meet inspiratory flow during pressure-supported breaths, the most recent anesthesia ventilators have comparable performances of recent-generation intensive care unit ventilators.
Epinephrine Increases the Extracellular Lidocaine Concentration in the Brain
Authors: Takahashi Ryota , Oda Yutaka , Tanaka Katsuaki , Morishima Hisayo O. , Inoue Koki , Asada Akira 
Published: October 2006

Background
Local anesthetics exert central nervous system (CNS) toxicity by inhibiting intracerebral neuronal activity, while epinephrine augments the CNS toxicity of intravenously administered local anesthetics. Viewed together, increases of extracellular concentrations of local anesthetics in the brain may be directly associated with increased CNS toxicity. The authors examined the hypothesis that epinephrine enhances the CNS toxicity of lidocaine by increasing the extracellular concentration in the brain.

Methods
An awake, spontaneously breathing rat model was used. Twenty male Sprague-Dawley rats received an intravenous infusion of lidocaine (3 mg x kg x min; group C) or lidocaine with epinephrine (3 mg x kg x min and 2 microg x kg x min, respectively; group E) for 10 min (n = 10 in each group). Effects of epinephrine on the convulsive dose and concentrations of total (protein-bound and unbound) and unbound lidocaine in plasma were examined. Concentrations of extracellular lidocaine in the cerebral nucleus accumbens were quantitatively determined by a microdialysis method.

Results
The convulsive dose of lidocaine was significantly lower in group E than in group C (22.4 +/- 5.5 vs. 27.9 +/- 3.1 mg/kg, respectively; P < 0.05). Overall concentrations and area under the plasma concentration-versus-time curve of unbound lidocaine in group E were significantly higher than those in group C. Concentrations of extracellular lidocaine in the nucleus accumbens in group E were comparable to those of unbound fraction in plasma and were also significantly higher than those in group C.

Conclusions
Concomitant administration of epinephrine significantly enhanced the CNS toxicity of intravenously administered lidocaine. Increased extracellular concentration in the brain would be related to this mechanism.
Sevoflurane Protects Rat Mixed Cerebrocortical Neuronal–Glial Cell Cultures against Transient Oxygen–Glucose Deprivation
Authors: Canas Paula T. , Velly Lionel J. , Labrande Christelle N. , Guillet Benjamin A. , Sautou-Miranda Valérie , Masmejean Frédérique M. , Nieoullon André L. , Gouin François M. , Bruder Nicolas J. , Pisano Pascale S. 
Published: October 2006

Background
The purpose of this study was to clarify the role of glutamate and reactive oxygen species in sevoflurane-mediated neuroprotection on an in vitro model of ischemia-reoxygenation.

Methods
Mature mixed cerebrocortical neuronal-glial cell cultures, treated or not with increasing concentrations of sevoflurane, were exposed to 90 min combined oxygen-glucose deprivation (OGD) in an anaerobic chamber followed by reoxygenation. Cell death was quantified by lactate dehydrogenase release into the media and cell viability by reduction of 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium by mitochondrial succinate dehydrogenase. Extracellular concentrations of glutamate and glutamate uptake were assessed at the end of the ischemic injury by high-performance liquid chromatography and incorporation of L-[H]glutamate into cells, respectively. Free radical generation in cells was assessed 6 h after OGD during the reoxygenation period using 2',7'-dichlorofluorescin diacetate, which reacts with intracellular radicals to be converted to its fluorescent product, 2',7'-dichlorofluorescin, in cell cytosol.

Results
Twenty-four hours after OGD, sevoflurane, in a concentration-dependent manner, significantly reduced lactate dehydrogenase release and increased cell viability. At the end of OGD, sevoflurane was able to reduce the OGD-induced decrease in glutamate uptake. This effect was impaired in the presence of threo-3-methyl glutamate, a specific inhibitor of the glial transporter GLT1. Sevoflurane counteracted the increase in extracellular level of glutamate during OGD and the generation of reactive oxygen species during reoxygenation.

Conclusion
Sevoflurane had a neuroprotective effect in this in vitro model of ischemia-reoxygenation. This beneficial effect may be explained, at least in part, by sevoflurane-induced antiexcitotoxic properties during OGD, probably depending on GLT1, and by sevoflurane-induced decrease of reactive oxygen species generation during reoxygenation.
Ambulatory Continuous Interscalene Nerve Blocks Decrease the Time to Discharge Readiness after Total Shoulder Arthroplasty
Authors: Ilfeld Brian M. , Vandenborne Krista , Duncan Pamela W. , Sessler Daniel I. , Enneking F Kayser , Shuster Jonathan J. , Theriaque Douglas W. , Chmielewski Terese L. , Spadoni Eugene H. , Wright Thomas W. 
Published: October 2006

Background
A continuous interscalene nerve block (CISB) may be used to provide analgesia after shoulder arthroplasty. Therefore, inpatient stays may be shortened if CISB (1) provides adequate analgesia without intravenous opioids and (2) improves shoulder mobilization. This study investigated the relationship between ambulatory CISB and the time to reach three discharge criteria after shoulder arthroplasty.

Methods
Preoperatively, patients received a CISB. All patients received a perineural 0.2% ropivacaine infusion from surgery until 06:00 the following morning, at which time they were randomly assigned either to continue perineural ropivacaine or to switch to normal saline. The primary endpoint was the time from the end of surgery until three discharge criteria were attained (adequate analgesia, independence from intravenous analgesics, and tolerance to 50% of shoulder motion targets). Patients were discharged home as early as the afternoon after surgery with their CISB using a portable infusion pump.

Results
Patients receiving perineural ropivacaine (n = 16) attained all three discharge criteria in a median (10th-90th percentiles) of 21 (16-41) h, compared with 51 (37-90) h for those receiving perineural normal saline (n = 13, P < 0.001). Unlike patients receiving perineural ropivacaine, patients receiving perineural normal saline often required intravenous morphine, but still experienced a higher degree of pain and tolerated less external rotation.

Conclusions
An ambulatory CISB considerably decreases the time until readiness for discharge after shoulder arthroplasty, primarily by providing potent analgesia that permits greater passive shoulder movement and the avoidance of intravenous opioids. Additional research is required to define the appropriate subset of patients and assess the incidence of complications associated with earlier discharge.
Modulation of Remifentanil-induced Analgesia and Postinfusion Hyperalgesia by Parecoxib in Humans
Authors: Tröster Andreas , Sittl Ruth , Singler Boris , Schmelz Martin , Schüttler Jürgen , Koppert Wolfgang 
Published: October 2006

Background
Numerous experimental and clinical studies suggest that brief opioid exposure can enhance pain sensitivity. It is suggested that spinal cyclooxygenase activity may contribute to the development and expression of opioid tolerance. The aim of the investigation was to determine analgesic and antihyperalgesic properties of the cyclooxygenase-2 inhibitor parecoxib on remifentanil-induced hypersensitivity in humans.

Methods
Fifteen healthy male volunteers were enrolled in this randomized, double-blind, placebo-controlled study in a crossover design. Transcutaneous electrical stimulation at high current densities was used to induce spontaneous acute pain (numeric rating scale 6 of 10) and stable areas of pinprick hyperalgesia. Pain intensities and areas of hyperalgesia were assessed before, during, and after a 30-min intravenous infusion of remifentanil (0.1 microg x kg x min) or placebo (saline). Parecoxib (40 mg) was administered intravenously either with onset of electrical stimulation (preventive) or in parallel to the remifentanil infusion.

Results
Remifentanil reduced pain and mechanical hyperalgesia during the infusion, but upon withdrawal, pain and hyperalgesia increased significantly above control level. Preventive administration of parecoxib led to an amplification of remifentanil-induced antinociceptive effects during the infusion (71.3 +/- 7 vs. 46.4 +/- 17% of control) and significantly diminished the hyperalgesic response after withdrawal. In contrast, parallel administration of parecoxib did not show any modulatory effects on remifentanil-induced hyperalgesia.

Conclusion
The results confirm clinically relevant interaction of mu opioids and prostaglandins in humans. Adequate timing seems to be of particular importance for the antihyperalgesic effect of cyclooxygenase-2 inhibitors.
Neurotoxicity of Lidocaine Involves Specific Activation of the p38 Mitogen-activated Protein Kinase, but Not Extracellular Signal–regulated or c-jun N-Terminal Kinases, and Is Mediated by Arachidonic Acid Metabolites
Authors: Haller Ingrid , Hausott Barbara , Tomaselli Bettina , Keller Christian , Klimaschewski Lars , Gerner Peter , Lirk Philipp 
Published: October 2006

Background
Pharmacologic inhibition of the p38 mitogen-activated protein kinase (MAPK) leads to a reduction in lidocaine neurotoxicity in vitro and in vivo. The current study investigated in vitro the hypotheses that lidocaine neurotoxicity is specific for dorsal root ganglion cells of different size or phenotype, involves time-dependent and specific activation of the p38 MAPK, that p38 MAPK inhibitors are only effective if applied with local anesthetic, and that p38 MAPK activation triggers activation of lipoxygenase pathways.

Methods
The authors used primary sensory neuron cultures and pheochromocytoma cell line cultures to detect time-dependent activation of the p38 MAPK or related pathways such as extracellular signal-regulated kinases and c-jun N-terminal kinases. Cells were divided by size or by immunoreactivity for calcitonin gene-related peptide or isolectin B4, indicative of nociceptive phenotype. The authors also investigated whether arachidonic acid pathways represent a downstream effector of the p38 MAPK in local anesthetic-induced neurotoxicity.

Results
All types of dorsal root ganglion cells were subject to neurotoxic effects of lidocaine, which were mediated by specific activation of the p38 MAPK but not extracellular signal-regulated kinases or c-jun N-terminal kinases. Neuroprotective efficacy of p38 MAPK inhibitors declined significantly when administered more than 1 h after lidocaine exposure. Activation of p38 MAPK preceded activation of arachidonic acid pathways. Neurotoxicity of lidocaine, specific activation of p38 MAPK, and neuroprotective effects of a p38 MAPK inhibitor were further confirmed in pheochromocytoma cell line cultures.

Conclusions
Specific and time-dependent activation of the p38 MAPK is involved in lidocaine-induced neurotoxicity, most likely followed by activation of lipoxygenase pathways.
Peptide signaling paths related to intoxication, memory and addiction
Authors: Lands William E. M. 
Published: October 2006

AbstractMany peptides bind to G protein‐coupled receptors and activate intracellular signaling paths for adaptive cellular responses. The components of these paths can be affected by signals from other neurotransmitters to produce overall integrated results not easily predicted from customary a priori considerations. This intracellular cross‐talk among signaling paths provides a “filter” through which long‐term tonic signals affect short‐term phasic signals as they progress toward the nucleus and induce long‐term adaptation of gene expression which provide enduring attributes of acquired memories and addictions. Peptides of the PACAP family provide intracellular signaling that involves kinases, scaffolding interactions, Ca2 + mobilization, and gene expression to facilitate development of tolerance to alcohol and development of associative memories. The peptide‐induced enhancement of NMDA receptor responses to extracellular glutamate also may increase behavioral sensitization to the low doses of alcohol that occur at the onset of each bout of drinking. Because many gene products participate in each signaling path, each behavioral response to alcohol is a polygenic process of many steps with no single gene product sufficient to interpret fully the adaptive response to alcohol. Different susceptibility of individuals to alcohol addiction may be a cumulative result of small differences among the many signaling components. Understanding this network of signals may help interpret future “magic bullets” proposed to treat addiction.
Susceptibility for alcoholism: DRD4 exon III polymorphism: a case–control and a family‐based association approach
Authors: Franke Petra , Wang Tao , Möthen Markus M. , Knapp Michael , Neith Helge , Lichtermann Dirk , Capellen Kathrin Meyer Zur , Sander Thomas , Propping Peter , Maier Wolfgang 
Published: October 2006

AbstractThe present investigation explored whether the 7‐repeat allele of the exon III polymorphism in the dopamine D4 receptor gene confers to susceptibility of alcoholism. Using a classical case‐control approach we first compared DRD4 exon III VNTR frequencies between alcoholics and ethnically matched controls (sample I). Secondly, we applied a family‐based association approach in an independent parent‐offspring sample of alcoholics (sample II). All patients underwent an inpatient treatment for alcohol detoxification: sample I comprised 218 alcoholics and 197 ethnically matched controls, sample II included 76 alcoholics plus their biological parents. A higher proportion of addicted individuals in sample I revealed the 7‐repeat allele compared to the control sample yielding an odds ratio (OR) of 1.43 (individuals homozygous for 7‐repeat allele) and an OR of 1.69 (homozygous and heterozygous 7‐repeat allele individuals together). However, we failed to detect preferential transmission from parents to offspring of either the 7‐repeat allele or the long alleles (5–7 repeats) of the DRD4 exon III VNTR in the family‐based association approach (sample II). The impact of the DRD4 exon III polymorphism on susceptibility to addictive behaviour putatively plays only a minor role in our sample of alcohol‐dependent patients, since we were not able to replicate our findings by the family‐based association approach. However, a larger sample size by the family‐based approach would be needed (approximately > 300 parent‐offspring trios) to definitely corroborate or reject the findings from our case‐control sample.
Possible association between loudness dependence of auditory evoked potentials and tryptophan hydroxylase‐alleles in alcoholics
Authors: Preuss U. W. , Bondy B. , Zill P. , Frodl T. , Soyka M. , Möller H. J. , Hegerl U. 
Published: October 2006

AbstractThe serotonergic neurotransmission was suggested to play an important role in the aetiology of alcoholism. This study explores the association between tryptophan hydroxylase (TPH)‐alleles and Loudness Dependence of Auditory Evoked N1/P2 Potentials (LDAEP). The TPH is the rate‐limiting biosynthetic enzyme in serotonergic pathway. The LDAEP is one of the best validated non‐invasive indicators for serotonergic neurotransmission. A sample of 54 alcoholics was recruited. N1/P2 potentials were evoked by five different sound intensities. A dipole source analysis using BESA (brain electric signal topography) was performed and intensity dependence was computed. The TPH intron 7 polymorphism was determined by using PCR in DNA samples. There was a weak but significant association between low LDAEP and the L‐TPH allele. No influence from an individual's history of alcohol dependence or a positive family history of alcohol dependence on LDAEP was found. The weak but significant relationship found between L‐TPH‐allele and high serotonergic neurotransmission may contribute to a more detailed neurobiological characterization of alcohol dependents using functional and genetic parameters.
Relevance of urinalysis monitoring of methadone maintenance patients: a clinical–biological agreement on 41 patients
Authors: Fellous J. , Lowenstein W. , Gourarier L. , Bonan B. , Manuel N. , Dauphin A. , Fermanian J. , Durand H. 
Published: October 2006

AbstractThis study evaluated the concordance of concomitant urinalysis and clinical assessments of drug abusers included in a methadone maintenance programme. The agreement between a clinical subjective score and an objective biological score, both measuring the evolution of illicit substance consumption over 12 months, was analysed. The clinical score, established by physicians and applied during patient interviews, was determined at entry into the programme and re‐evaluated after 6 and 12 months. Forty‐one patients were evaluated. The urinalysis score was based on regular screening of urine samples with the EMIT method. Agreement between the two scores was determined by using the kappa coefficient for each substance (opiates, benzodiazepines and cocaine) for each time‐point. The calculated kappa coefficients showed poor agreement between the two scores, but could indicate the complementarity of these clinical and biological appraisals. Indeed, the urinalysis objectively detected change in drug use before the clinician. Thus, urinalysis monitoring should be considered as an additional and complementary biological procedure for patient follow‐up by physicians.
Ofloxacin causes false‐positive immunoassay results for urine opiates
Authors: Backmund Markus , Meyer Kirsten , Von Zielonka Michael , Eichenlaub Dieter 
Published: October 2006

AbstractImmunoassay drug screening tests are usually used as a control during methadone maintenance programmes, to check cleanliness of drugs during detoxification treatment and abstinence programmes. False‐positive results can have catastrophic consequences for the patient, as shown in the case report. False‐positive results were reported for opioids following ofloxacin or rifampicin and for LSD following mucolytic. Since inpatient and outpatient units usually employ an urine quick test (immunoassay), positive results should be checked with gas chromatography/mass spectroscopy (GC‐MS) or high pressure liquid chromatography (HPLC) before conclusions from the positive urine screening results can be drawn.