記述言語：英語  

Background: The Laryngeal Tube Suction II (LTSII; VBM, Medizintechnik, Sulz, Germany) is a recent revision of the Laryngeal Tube Suction. This study compared insertion and ventilation profiles of the LTSII and the ProSeal™ Laryngeal Mask Airway (PLMA™; Laryngeal Mask Company, Henley-on-Thames, United Kingdom) in anesthetized and paralyzed patients. Methods: One hundred adult male patients were randomly allocated to an LTSII or PLMA™ group. The rate of successful insertion, insertion time, airway leak pressure at a cuff pressure of 60 cm H2O, tidal volume during pressure-controlled ventilation, incidence of gas leakage with cuff pressure reduced and with the shaft inclined, position of LTSII under fluoroscopic observation, and postoperative airway morbidity were determined. Results: Insertion was successful in 37 and 48 of 50 patients with LTSII and PLMA™, respectively (P = 0.002), with similar insertion times. Tidal volume was lower with LTSII than with PLMA™. Median airway leak pressures of LTSII and PLMA™ were 16 and 21 cm H2O, respectively (P = 0.006). Gas leakage around the cuff was observed more frequently with LTSII than with PLMA™ when the cuff pressure was reduced or the shaft of the device inclined. The position of LTSII varied significantly and did not statistically correlate with patient height. Postoperative airway-related morbidity was not significantly different. Finally, tracheal misplacement of LTSII occurred in 5 of 50 patients (10%), but ventilation was possible in 4 of them, and misplacement was identified only after fluoroscopic examination was performed. Conclusion: Airway management with LTSII is inferior to that with PLMA™. Copyright © 2008 The American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc.

DOI： 10.1097/ALN.0b013e318178819b

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記述言語：英語   出版者・発行元：BLACKWELL PUBLISHING  

Background and aim: The Airway Scope (AWS) is a new video laryngoscope. The purpose of this study was to compare the AWS and Macintosh laryngoscopes with regard to their usefulness for beginners in tracheal intubation.
Methods: Thirty-one nurses with no previous experience of tracheal intubation used each device 10 times to intubate the trachea of a manikin (Laerdal Airway Managemant Trainer, Laerdal, Stavanger, Norway). Intubation correctly completed within 30 s was regarded as successful. The intubation time, success rate, number of esophageal intubations and dental clicks, and subjective evaluation of difficulty of intubation [rated from 1 (extremely easy) to 5 (extremely difficult)] were recorded.
Results: The average intubation time was significantly shorter for AWS than for the Macintosh laryngoscope (16.7 +/- 11.0 s vs. 23.2 +/- 24.9 s; mean +/- standard deviation; P = 0.0297), and the success rate with AWS was significantly greater (91.3% vs. 79.4%; P < 0.001). In the total of 310 intubation attempts for each device, the number of esophageal intubations (0/310 with AWS vs. 20/310 with the Macintosh laryngoscope) and dental clicks (0/310 with AWS vs. 40/310 with the Macintosh laryngoscope) differed significantly (P < 0.001). AWS was rated as easier to use than the Macintosh laryngoscope (P < 0.001).
Conclusion: AWS is more useful for beginners as it provides quicker and easier tracheal intubation.

DOI： 10.1111/j.1399-6576.2007.01450.x

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記述言語：英語  

We compared the Airway Scope® with a gum elastic bougie and fibreoptic bronchoscope in a manikin with a simulated Cormack and Lehane Grade 3 laryngoscopic view. Twenty-seven anaesthetists intubated the trachea of the manikin with these devices and the time required for intubation was measured. They were then asked to rate the subjective difficulty of intubation (1 = very easy; 5 = very difficult). Mean (SD) intubation times were 16.6 (11.2) s with the Airway Scope, 29.4 (10.9) s with the gum elastic bougie (p < 0.0001), and 30.6 (20.0) s with the fibreoptic bronchoscope (p < 0.0001). The median (range) difficulty was 2 (1-4) with the Airway Scope, 3 (2-4) with the gum elastic bougie (p < 0.001), and 2 (1-5) with the fibreoptic bronchoscope (p = 0.014). In Cormack and Lehane grade 3 laryngoscopic views, the Airway Scope may enable faster and easier tracheal intubation than does a Macintosh laryngoscope with a gum elastic bougie or a fibreoptic bronchoscope. © 2007 The Authors Journal compilation 2007 The Association of Anaesthetists of Great Britain and Ireland.

DOI： 10.1111/j.1365-2044.2007.05152.x

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記述言語：英語   掲載種別：速報，短報，研究ノート等（学術雑誌）   出版者・発行元：ELSEVIER SCIENCE INC  

DOI： 10.1016/j.jclinane.2007.01.001

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記述言語：英語   出版者・発行元：OXFORD UNIV PRESS  

Background. The aim of this study was to examine ethanol-consumption-related changes in the effects of propofol on rat hippocampal acetylcholine (ACh) release.
Methods. Male Sprague-Dawley rats received a solution of ethanol (20% v/v) for 24 weeks while controls received tap water. The effects of propofol were examined by in vivo microdialysis, with ACh release from the hippocampal regions determined by high-performance liquid chromatography with electrochemical detection (HPLC-ECD).
Results. Propofol 50 mg kg(-1) i.p. significantly decreased basal hippocampal ACh release in ethanol-treated and control rats by 50.4 (sem 4.7)% and 38.3 (11.1)%, respectively. Propofol 100 mg kg(-1) i.p. significantly decreased basal hippocampal ACh release in ethanol-treated and control rats by 67.5 (3.7)% and 55.9 (7.4)%, respectively. The reduction in hippocampal ACh release induced by 50 or 100 mg kg(-1) i.p. propofol was not significantly different between ethanol-treated and control rats. There was no significant difference in the duration of sleep between the two groups.
Conclusions. These results demonstrate that chronic ethanol consumption does not augment the inhibitory actions of propofol on rat hippocampal ACh release. These findings appear to be inconsistent with the notion that chronic ethanol intake enhances the propofol-induced inhibition of the hippocampal cholinergic system and related mental dysfunction.

DOI： 10.1093/bja/aeh263

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記述言語：英語   出版者・発行元：OXFORD UNIV PRESS  

Background. It has been shown that the R(-) isomer of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) induces loss of the righting reflex (LRR), while S(+)-MPPB causes pure excitatory effects, including convulsions, in vivo.
Methods. We studied the effects of the depressant and convulsant MPPB stereoisomers on rat hippocampal acetylcholine (ACh) release in vivo, using a brain microdialysis technique in freely moving animals.
Results. R(-)-MPPB 60 and 90 mg kg(-1) i.p. decreased ACh release from the rat hippocampus by 44.1 (8.2)% and 60.8 (8.2)%, respectively. In the hippocampus, the local application of bicuculline, a gamma-aminobutyric acid (GABA)(A) receptor antagonist, 1 mumol litre(-1) antagonized the inhibitory effects of R(-)-MPPB 90 mg kg(-1) i.p. In contrast, R(-)-MPPB, S(+)-MPPB 60 and 90 mg kg(-1) i.p. increased ACh release to 151.8 (6.8)% and 169.6 (11.1)% of the basal release, respectively.
Conclusions. Our results demonstrated that R(-)-MPPB decreased, while S(+)-MPPB increased, rat hippocampal ACh release and that the inhibitory effects of R(-)-MPPB may involve the GABA(A) receptor in vivo. These data imply that changes in hippocampal ACh due to these agents may be related to their central inhibitory and stimulatory actions in vivo.

DOI： 10.1093/bja/aeh070

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記述言語：英語   出版者・発行元：PROF SCI PUBL  

Using microdialysis, we have examined the effects of ketamine on concentrations of total nitric oxide oxidation products (NOx-) in the rat hippocampus and striatum in vivo to investigate the relationship between anaesthesia and NOx- production in the brain. Ketamine 25, 50 and 100 mg kg(-1) i.p. increased NOx- concentrations to mean 125 (SD 13)%, 165 (11)% and 193 (13)% of basal, respectively, in the hippocampus and to 122 (12)%, 147 (7)% and 177 (14)% of basal in the striatum. Local perfusion with ketamine 50 and 100 mu mol litre(-1) into the hippocampus or striatum increased NOx- concentrations to 212 (32)% and 291 (17)% of basal, respectively, in the hippocampus and to 148 (20)% and 201 (18)% of basal in the striatum. Ketamine 50 and 100 mg kg(-1) i.p. caused dose-dependent prolongation of loss of the righting reflex (LRR) and 100 mg kg(-1) i.p. also caused loss of the corneal reflex (LCR). Local perfusion of ketamine did not provoke LRR or LCR. Inhibition of NOS by L-NAME 100 mg kg(-1) i.p. decreased hippocampal NOx- concentrations to 58 (7)% of basal and did not provoke LRR or LCR. Although the effect of ketamine-induced increases in hippocampal NOx- concentrations was significantly depressed by L-NAME, LRR was not affected. These data imply that NOx-concentrations in the hippocampus or striatum have no direct relationship to the anaesthetic efficacy of ketamine, although this requires further investigation.

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記述言語：英語   出版者・発行元：MUNKSGAARD INT PUBL LTD  

Background: We sometimes encounter impairment of learning and memory after general anesthesia in elderly patients. The aim of this study was to examine age-related modifications of the effects of ketamine and propofol on rat hippocampal acetylcholine (ACh) release because hippocampal cholinergic neurons are supposed to be involved in learning and memory.
Methods: The experiments were performed on male Wistar young rats (2 months old) and old rats (18 months old), using in vivo brain microdialysis technique under freely moving condition. After initial sampling of three collections, test drugs were administered. The ACh release was determined by the HPLC-ECD method.
Results: In old rats, the hippocampal basal ACh release was significantly lower than in young rats. Ketamine (25 and 50 mg kg(-1) i.p.) increased and propofol (25 and 50 mg kg(-1) i.p.) decreased the hippocampal ACh release in both young and old rats. Furthermore, ketamine 50 mg kg(-1) i,p. (anesthetic dose) produced facilitatory effects on the hippocampal ACh release in young rats (193% of the basal release), while in old rats the same dose of ketamine i.p. produced more pronounced facilitatory effects on the hippocampal ACh release (317% of the basal release). On the other hand, propofol 50 mg kg(-1) i.p. (anesthetic dose) produced inhibitory effects on the hippocampal ACh release in young rats (56% of control) and in old rats (77% of control). Although the maximal inhibitory peak effects of propofol 50 mg kg(-1) i.p. did not differ significantly between young rats and old rats, decrease of the hippocampal ACh release in old rats persisted longer than in young rats.
Conclusion: Ketamine produced more pronounced facilitatory effects on the hippocampal ACh release in old rats, as compared with young rats. On the other hand, propofol has inhibitory effects on the hippocampal ACh release in young and old rats. The aging process may suppress the ability to recover from the inhibitory anesthetic state induced by propofol.

DOI： 10.1034/j.1399-6576.2000.440120.x

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記述言語：英語   出版者・発行元：American Lung Association  

Aspiration of gastric contents is one of leading causes of the acute respiratory distress syndrome (ARDS). The pathogenesis of acid aspiration-induced acute lung injury is well understood. Less clear is why patients who have suffered acid aspiration are susceptible to ARDS. We studied the effects of acid instillation on the inflammatory response to subsequent lipopolysaccharide (LPS) challenge in rats. Instillation of acid into the right lung worsened the pathology induced by LPS that was administered 24 h after acid instillation. This included worsened oxygenation, increased pulmonary edema, increased production of tumor necrosis factor-alpha (TNF-α) and cytokine-induced neutrophil chemoattractant, neutrophil accumulation and mobilization to the alveolar spaces, and nitric oxide (NO) production. Of interest, neutrophil mobilization, NO production, and protein permeability were also magnified in the left lung. These effects were attenuated by administration of the protein tyrosine kinase (PTK) inhibitors genistein and tyrphostin AG556. These data suggest that acid instillation primes the rat to enhance the inflammatory response to subsequent endotoxin challenge and that at least part of the augmented inflammatory response depends on PTK.

DOI： 10.1164/ajrccm.162.4.9907060

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記述言語：英語   出版者・発行元：PROF SCI PUBL  

Using in vivo microdialysis, we have investigated the effects of propofol on acetylcholine (ACh) release from various regions of the rat brain. Propofol 25 and 50 mg kg(-1) i.p. decreased basal ACh release from the frontal cortex by 70% and 85%, respectively. Propofol 25 and 50 mg kg(-1) i.p. decreased basal ACh release from the hippocampus by 47% and 72%, respectively. However, in rat striatum, propofol 25 mg kg(-1) i.p. did not affect basal ACh release and 50 mg kg(-1) i.p. produced slight inhibition of basal ACh release (by 19%) only in the second sample after i.p. injection. In addition, we also examined the pharmacological mechanisms mediating the interaction between propofol and a gamma-aminobutyric acid A (GABA(A)) receptor complex. In the rat hippocampus, local application of bicuculline 1 mu mol litre(-1), a GABA(A) receptor antagonist, significantly antagonized the inhibitory effects of propofol 50 mg kg(-1) i.p. on basal ACh release. In the rat frontal cortex, local application of bicuculline 1 mu mol litre(-1) did not antagonize the inhibitory effects of propofol 50 mg kg(-1) i.p. on basal ACh release, while systemic application of bicuculline 1 mg kg(-1) i.p. significantly antagonized the inhibitory effects of propofol 50 mg kg(-1) i.p. These results suggest that propofol has powerful depressant effects on ACh release from the rat frontal cortex and hippocampus but not from the striatum, indicating that propofol has a "region-selective" anaesthetic action. Further, these results suggest that the inhibitory effects of propofol in the rat hippocampus may involve "intra" hippocampal GABA(A) receptors while the inhibitory effects in the rat frontal cortex may be mediated by GABA(A) receptors other than "intra" frontal cortex GABA(A) receptors.

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記述言語：英語   出版者・発行元：PROF SCI PUBL  

We have studied the effects of ketamine and pentobarbitone on acetylcholine (ACh) release from the rat frontal cortex using microdialysis. Ketamine 25, 50 and 100 mg kg(-1) increased ACh release from the frontal cortex to 286%, 253% and 381% of basal release, respectively. In contrast, pentobarbitone 10, 20 and 40 mg kg(-1) caused 73%, 78% and 96% inhibition of basal levels, respectively. The results suggest that ketamine and pentobarbitone have opposite effects on ACh release from the rat frontal cortex, as seen previously in the rat hippocampus.

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記述言語：英語   出版者・発行元：PROF SCI PUBL  

Using microdialysis, we examined the effects of ketamine and pentobarbitone on acetylcholine (ACh) release from the rat hippocampus and striatum. Ketamine 25 and 50 mg kg(-1) increased ACh release from the hippocampus to 295% and 353% of basal release, respectively, but not from the striatum. SCH 23390 1 mu mol litre(-1), a D1 antagonist, significantly inhibited the facilitatory effect of ketamine 50 mg kg(-1) on hippocampal ACh release (to 241% of basal level). In contrast, pentobarbitone 20 and 40 mu mg kg(-1) decreased basal ACh release from both the hippocampus by 41% and 69%, respectively, and the striatum by 37% and 58%, respectively. The results suggest that ketamine and pentobarbitone exert opposite effects on ACh release from the rat hippocampus and that the stimulating effect of ketamine may involve dopamine D1 receptors.

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