Biomedical subjects

N Adachi

Publications and source records attributed to N Adachi.

At least 91 records · Page 5Linked to original sources

PubMed1998

Characterization of the 3' untranslated region of mouse DNA topoisomerase IIalpha mRNA.

Expression of DNA topoisomerase IIalpha protein varies through the cell cycle with its peak in G2/M. This cell-cycle-dependent expression depends on changes in topoisomerase IIalpha mRNA stability as well as promoter activity. We isolated the 3' genomic region of the mouse topoisomerase IIalpha gene and investigated whether or not the 3' untranslated region (UTR) of the topoisomerase IIalpha mRNA participates in the cell-cycle-dependent mRNA stability. Interestingly, genomic- and RT-PCR analyses revealed that the topoisomerase IIalpha 3' UTR is formed via splicing in mouse, but not in human and hamster. Comparison of the mouse 3' region with the human and hamster regions suggests that this mouse-specific splicing has resulted from an accidental acquisition of the consensus 5' splice site. The minority of the non-spliced topoisomerase IIalpha 3' UTR in mouse was confirmed by Northern blot analysis. We performed transient expression assays using luciferase constructs with the mouse topoisomerase IIalpha 3' genomic region, or the major spliced form of the 3' UTR. However, neither construct affected the cell-cycle-dependent expression of the reporter gene driven by the topoisomerase IIalpha promoter. Our results strongly suggest that the mouse topoisomerase IIalpha 3' UTR by itself is not involved in the cell-cycle-dependent mRNA stability.

3T3 Cells↗

PubMed1998

Ex vivo malignant glioma cells are sensitive to Fas (CD95/APO-1) ligand-mediated apoptosis.

Fas (also known as CD95/APO-1) is a cell surface receptor and member of the tumor necrosis factor receptor superfamily which mediates apoptosis in sensitive cells upon oligomerization by specific antibodies or by its ligand (FasL). Recently, human glioma cell lines were found to be susceptible to Fas-mediated apoptosis triggered by alpha-Fas antibodies. However, whether the Fas system can also be targeted in ex vivo high grade gliomas is at present unknown. In the present investigation, alpha-Fas antibodies and FasL were tested in short-term monolayer cultures or in colony forming assays established from freshly resected tumors of patients with anaplastic astrocytomas (WHO grade III) and glioblastoma multiforme (WHO grade IV). Anti-Fas antibodies induced only moderate apoptosis in four of the 19 tested glioma cell cultures. This contrasts FasL which induced apoptosis in all of the 19 tumor cell cultures analyzed. Mean cytotoxicity of glioma cell cultures treated for 48 h with alpha-Fas antibodies or FasL was 9.6% and 44.3%, respectively. Irrespective of whether alpha-Fas antibodies or FasL were used, pretreatment with recombinant hu (rhu) IFN-gamma and rhuTNF-alpha for 48 h did not sensitize glioma cells to Fas-mediated cytotoxicity. The long-term effect by FasL on tumor colony formation was more striking. FasL treatment resulted in more than 90% inhibition of clonal tumor cell growth of all the eight high grade gliomas analyzed. These results suggest that Fas targeting by FasL but not by alpha-Fas antibodies may provide a promising approach for locoregional glioma treatment.

Antibodies↗

PubMed1998

Improvement of ischemic damage in gerbil hippocampal neurons by procaine.

Acute cerebral ischemia induces membrane depolarization in the neuron, thereby incurring the simultaneous influx of various ions such as Na+ and Ca2+. Since procaine possesses the ability to inhibit the release of Ca2+ from intracellular Ca2+ stores to the cytosol as well as the ability to block Na+ channels, the effects of procaine on ischemia were investigated in the present study in gerbils both in vivo and in vitro. The histologic outcome was evaluated 7 days after 3 min of transient forebrain ischemia by assessing delayed neuronal death in hippocampal CA1 pyramidal cells in animals administered procaine (0.2, 0.4, or 2 micromol) intracerebroventricularly 10 min before ischemia and in animals given saline. The changes in the direct-current potential shift in the hippocampal CA1 area were measured using an identical animal model. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effects of procaine (10, 50, and 100 micromol/l) on the Ca2+ accumulation were examined. Additionally, the effect of procaine (100 micromol/l) in a Ca2+-free condition was investigated. The histologic outcome was improved and the onset of the ischemia-induced membrane depolarization was prolonged by the preischemic administration of procaine. The increase in the intracellular concentration of Ca2+ induced by the in vitro hypoxia was suppressed by the perfusion of procaine-containing mediums (50 and 100 micromol/l), regarding both the initiation and the extent of the increase. A hypoxia-induced intracellular Ca2+ elevation in the Ca2+-free condition was observed, and the perfusion with procaine (100 micromol/l) inhibited this elevation. Procaine helps protect neurons from ischemia by suppressing the direct-current potential shift and by inhibiting the release of Ca2+ from the intracellular Ca2+ stores, as well as by inhibiting the influx of Ca2+ from the extracellular space.

Anesthetics, Local↗

PubMed1998

Dexamethasone augments ischemia-induced extracellular accumulation of glutamate in gerbil hippocampus.

Glucocorticoids exacerbate neuronal damage due to hypoxia, ischemia, seizure and hypoglycemia. Because the release of glutamate is closely involved in neuronal damage, the effects of dexamethasone on the ischemia-induced accumulation of extracellular amino acids (aspartate, glutamate, and glycine) were investigated in the gerbil hippocampal CA1 region by a microdialysis-high-performance liquid chromatography procedure in vivo. There were no differences in the extracellular concentrations of amino acids before ischemia between the control group and the dexamethasone (3m microg, i.c.v.)-injected group. The concentration of glutamate reached 246% of that before ischemia within 2.5 min of transient forebrain ischemia. Dexamethasone augmented the increase in glutamate to 508% of that before ischemia. This finding suggests that glucocorticoids aggravate ischemic neuronal damage by causing glutamate to accumulate in the extracellular space.

Animals↗

PubMed1998

A new guide system for posteromedial portal in arthroscopic knee surgery.

A view through the posteromedial portal is necessary to observe the posterior portion of the knee joint such as the tibial attachment of the posterior cruciate ligament (PCL) or the posterior horn of the medial meniscus, which is barely, visible through anterior portals. Especially in arthroscopic PCL reconstruction, the arthroscopic view through the posteromedial portal is indispensable for boring a tibial bone tunnel that is correctly sited. However, it is difficult to create this portal safely without cartilaginous or meniscal damage. We have produced new guidelines to facilitate the process of creating the posteromedial portal even by inexperienced hands. With a cannulated K-wire and a cannulated rod with sharp teeth, the joint capsule of the posteromedial corner can be penetrated safely with or without viewing the posteromedial corner through the anterolateral portal. Based on our experience of using this guide system, we believe it will be a great help to many orthopaedic surgeons in performing various types of arthroscopic surgery, not only for PCL reconstruction but also for arthroscopic synovectomy.

Arthroscopes↗

PubMed1998

The polymorphic 43Thr bcl-2 protein confers relative resistance to autoimmunity: an analytical evaluation.

We have found a novel polymorphic (Ala43Thr; ACC-->GCC) bcl-2 allele in a Japanese population. An in vitro expression study with a mouse IL-7-dependent pre-B cell line has revealed that inhibition of the programmed cell death function of 43Thr bcl-2 protein is suppressed compared with that of normal 43Ala bcl-2 protein. Since bcl-2 expression in B-lymphoid cells elicits autoimmune disease in mice, we have investigated the possibility of whether a bcl-2 polymorphism has a different susceptibility to autoimmune disease. To evaluate the clinical impact of this polymorphism, the frequency of bcl-2 polymorphism was investigated in 221 children with insulin-dependent diabetes mellitus (IDDM), 237 adults with autoimmune disease (105 with rheumatoid arthritis, 57 with systemic lupus erythematosus, 55 with Sjögren's syndrome, and 20 others), and 290 healthy Japanese children and adults. The frequency of the 43Thr bcl-2 allele, either homozygous or heterozygous, was 14.5% in normal controls, 6.8% (P<0.01) in children with IDDM, and 8.0% (P<0.025) in adults with autoimmune disease. These results suggest that the 43Thr allele of bcl-2 confers resistance to autoimmune disease. The different anti-apoptotic function resulting from the different expression of bcl-2 protein in lymphocytes seems to be associated with the development of autoimmune disease, indicating that the bcl-2 gene affects human autoimmune disease.

Animals↗

PubMed1998

Ischemic preconditioning suppresses the noradrenaline turnover in the rat heart.

OBJECTIVE: The mechanism by which ischemic preconditioning protects the heart is presumed to be related to the reduction of energy consumption during a subsequent myocardial infarction. Since the sympathetic nervous system enhances cardiac function and energy consumption, we investigated the relation between ischemic preconditioning and the turnover rate of noradrenaline (NA) in the rat heart. METHODS: The effect of 3 cycles of 5-min occlusions of the rat left coronary artery on changes in arterial blood pressure and heart rate provoked by a subsequent 30 min of ischemia were examined until 60 min after reperfusion. The effect of 3 cycles of occlusions on the infarct size was also evaluated 60 min after reperfusion by comparing the infarcted area with the area at risk in these animals (6 per preconditioned and sham-operated group). The tissue concentration of NA during sustained ischemia was determined in the left ventricle, the intraventricular septum, and the right ventricle in the preconditioned and sham-operated groups. Changes in the turnover rate of NA after 3 cycles of occlusions were also evaluated by assessing the alpha-methyl-p-tyrosine-induced depletion of NA (n = 7 per group). RESULTS: A series of transient occlusions reduced the infarct size 60 min after a sustained ischemia for 30 min. Arterial pressure and heart rate were not affected. The concentration of NA was decreased in the left ventricle 60 min after the onset of sustained ischemia in both the preconditioned and sham-operated groups. The treatment with alpha-methyl-p-tyrosine decreased the NA concentration in all regions of the heart in the sham-operated group after 60 min. However, the treatment with alpha-methyl-p-tyrosine did not deplete the NA concentration in both the occluded and nonoccluded regions in the preconditioned group. CONCLUSIONS: Transient ischemia ameliorated the heart injury induced by a subsequent sustained ischemia, as assessed histologically. The activity of the sympathetic nervous system in all regions of the heart was reduced by transient ischemia in the left coronary vascular bed. These findings suggest that the inhibition of the sympathetic nervous system by the treatment of ischemic preconditioning takes part in the cardiac protection.

Animals↗

PubMed1998

Effects of basic fibroblast growth factor on proliferation and phenotype expression of chondrocytes embedded in collagen gel.

1. Whether basic fibroblast growth factor (bFGF) can stimulate proliferation and synthesis of chondroitin sulfate of chondrocytes in gel culture while maintaining the phenotype was studied. 2. At 3 weeks in culture, the cell number in 1.0 ng/ml (18.5+/-2.1 x 10(5)) and 10.0 ng/ml of the bFGF group (15.3+/-1.9 x 10(5)) was significantly larger than that in 0 ng/ml (12.3+/-2.1 x 10(5)), 0.1 ng/ ml (11.7+/-2.2 x 10(5)) and 100.0 ng/ml of the bFGF group (9.8+/-2.3 x 10(5)). 3. All doses of bFGF used in this study suppressed synthesis of chondroitin 6-sulfate. 4. Chondrocyte phenotype in gel culture was maintained for 4 weeks even with stimulation of bFGF.

Animals↗

PubMed1998

The effects of 17beta-estradiol on ischemia-induced neuronal damage in the gerbil hippocampus.

The effects of 17beta-estradiol, a potent estrogen, on ischemia-induced neuronal damage, membrane depolarization and changes in intracellular Ca2+ concentration were studied in gerbil hippocampi. The histological outcome evaluated seven days after 3 min of transient forebrain ischemia in hippocampal CA1 pyramidal cells was improved by high doses of 17beta-estradiol (30 microg, i.c.v. and 4 mg/kg, i.p.), whereas low doses of 17beta-estradiol (3 and 10 microg, i.c.v.) showed no protective effect. Administration of 17beta-estradiol did not affect the changes in the direct current potential shift in ischemia in the hippocampal CA1 area at any dosage. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices. Pretreatment of 17beta-estradiol (4 mg/kg, injected i.p. 1 h before decapitation) suppressed the increase in the intracellular concentration of Ca2+ due to the in vitro hypoxia, affecting both the onset of the increase and the extent. The in vitro hypoxia in the Ca2+-free condition induced an elevation of the intracellular concentration of Ca2+, although the increase was gradual. Pretreatment of 17beta-estradiol (4 mg/kg, i.p.) also inhibited this elevation. These findings imply that high doses of 17beta-estradiol protect the neurons from ischemia by inhibiting the release of Ca2+ from the intracellular Ca2+ stores, as well as by inhibiting the influx of Ca2+ from the extracellular space.

Action Potentials↗

PubMed1998

Measurement of the extracellular H2O2 in the brain by microdialysis.

This paper reports on the protocol for the determination of H2O2 in the brain using in vivo microdialysis coupled with fluorometry of dichlorofluorescin oxidation. We applied this protocol to monitor changes in the concentration of H2O2 in the brain, in vivo, during ischemia and reperfusion. Using this method, changes in the level of H2O2 in the brain during ischemia and reperfusion were effectively determined. The present protocol provides a novel tool to study the production of reactive oxygen species in the brain.

Animals↗

PubMed1998

Improvement in nerve regeneration by monoclonal antibodies to ICAM-1 and LFA-1 in allogeneic mice.

We examined whether giving monoclonal antibodies (MoAb) to intercellular adhesion molecule 1 (ICAM-1) and leucocyte function associated antigen (LFA-1), which have important roles in the initial stage of rejection after allografts, can improve nerve regeneration in allogeneic mice. Fresh sciatic nerves were grafted using BALB/c mice as donors and C3H/He mice as recipients. Nerve regeneration at six weeks was significantly better in the mice given MoAbs at one and five days than in those given none (n = 5 in each group), although nerve regeneration even in the five-day group was significantly inferior to that in the syngeneic nerve graft group (n = 5). The survival time of the nerve donor skin graft at 12 weeks was not prolonged by treatment with MoAbs, indicating a failure to induce immunological tolerance. However, at 10 months after nerve grafting there were fewer Mac-1, Lyt-1, and Thy-1 positive cells in the five-day group and they showed less immunoreactivity than the untreated group. We conclude that giving MoAbs could effectively improve nerve regeneration in grafted allogeneic nerve segments, although it did not induce immunological tolerance.

Animals↗

PubMed1998

Changes in the brain monoamine metabolism in acute liver failure produced by ischemia-reperfusion injury in rats.

OBJECTIVE: To investigate the relationship between behavioral alterations and changes in monoaminergic systems provoked by ischemia-reperfusion liver injury in rats. DESIGN: Prospective, randomized, controlled animal study. SETTING: University animal laboratory. SUBJECTS: Male Wistar rats. INTERVENTIONS: Acute liver failure was induced by occlusion of the left portal vein and the hepatic artery for 90 mins. Twenty animals were subjected to the behavioral examination. The brain water content was measured in 12 animals. Forty-two animals were used for the evaluation of brain monoamine turnover. Half of animals in each experiment were subjected to the ischemic operation. MEASUREMENTS AND MAIN RESULTS: A step-through passive avoidance test was used for the behavioral evaluation 48 hrs after the ischemic operation. Then, plasma concentrations of amino acids were determined. The brain water content was measured with the dry weight method. The brain monoamine turnover was evaluated by the depletion of norepinephrine and dopamine induced by alpha-methyl-p-tyrosine, or the accumulation of 5-hydroxyindoleacetic acid induced by probenecid. In the plasma analysis performed 48 hrs after the operation, marked damage was found in animals subjected to liver ischemia. Injured rats demonstrated impairment in the passive avoidance test. The plasma concentrations of branch-chain amino acids were decreased, and the plasma concentrations of aromatic amino acids were increased. However, the brain water content was not changed by liver ischemia. The turnover of both norepinephrine in the cerebral cortex and dopamine in the striatum was decreased. The turnover of 5-hydroxytryptamine in the cerebral cortex was increased markedly. CONCLUSION: In liver injury caused by liver ischemia, the excitatory neurotransmission by norepinephrine and dopamine is depressed and the inhibitory neurotransmission mediated by 5-hydroxytryptamine is facilitated, especially in the telencephalon.

Amino Acids↗

PubMed1998

Dexamethasone aggravates ischemia-induced neuronal damage by facilitating the onset of anoxic depolarization and the increase in the intracellular Ca2+ concentration in gerbil hippocampus.

The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 microg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 microg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

Animals↗

PubMed1998

Predictive value of interictal epileptiform discharges during non-REM sleep on scalp EEG recordings for the lateralization of epileptogenesis.

PURPOSE: EEG recording during sleep is widely used in the assessment of epilepsy, particularly in candidates for surgery, yet the diagnostic value of this procedure is not well established. We evaluated the predictive reliability of interictal epileptiform discharges (IEDs) for localization in presurgical patients with temporal lobe epilepsy (TLE) during non-REM sleep. METHODS: Preoperative scalp EEG recordings with waking and sleep states were assessed in 83 patients with TLE in whom localization of the epileptogenic zone was subsequently confirmed by successful surgical treatment (patient seizure-free >1 year). RESULTS: The accuracy of EEG recordings for prediction of lateralization significantly changed from 51.8% during waking to 78.3% during sleep. After exclusion of patients who showed no discharges, the predictive value changed from 74.1 to 86.7%. However, in patients in whom the waking scalp EEG lateralized incorrectly, no improvement in reliability was achieved by sleep recording. CONCLUSIONS: Our results suggest that IEDs occurring in non-REM sleep provide more accurate information for lateralization of epileptogenesis than do those occurring during waking. This gain of diagnostic information was obtained in patients who showed either bilateral or no discharges in waking records, because unilateral discharges arising de novo in sleep were always correctly lateralizing. On the other hand, in patients who showed unilateral discharges in the awake state, whether ipsilateral or contralateral to the epileptogenic zone, the findings were generally unchanged during sleep.

Adult↗

PubMed1998

Prevalence of human calicivirus infections in Kenya as determined by enzyme immunoassays for three genogroups of the virus.

An epidemiological survey on human calicivirus (HuCV) infections and associated gastroenteritis in infants was conducted to clarify the prevalence of HuCV infections in infants and adults in Kenya. Enzyme immunoassays (EIAs) for three genogroups of HuCVs, Norwalk virus (NV), Mexico virus (MXV), and Sapporo virus (SV), were used to detect antigen or antibody. We tested 1,431 stool samples obtained from children younger than 6 years old with acute gastroenteritis who visited outpatient clinics in three districts in Kenya from August 1991 to July 1994. Thirty-two (2.2%) of these stool samples were positive for SV antigen. Only one (0.1%) of 1,186 samples was positive for NV antigen and none of 246 samples was positive for MXV antigen. One hundred ninety-three serum samples were tested for antibodies to NV and MXV, and 64 of them were examined for antibody to SV. The pattern of the age-related prevalence of serum antibody to NV was different from that of antibodies to MXV and SV. The acquisition of serum antibodies to HuCVs in the three genogroups appeared in early childhood, at about 1 to 2 years of age. The prevalence of serum antibody to NV was low (about 60%) throughout adulthood compared with a high prevalence of antibody (approximately 80 to 90%) to MXV and SV. These data indicate that infections with viruses in the three genogroups of HuCVs are common in Kenya, and immunological responses to NV may be different from those to MXV and SV. The EIAs for the detection of NV and MXV antigens appear to be quite specific for prototype NV and MXV strains, respectively, so that they can detect only a few strains of HuCVs related to them. Alternatively, NV and MXV caused less severe infections that did not bring children to the outpatient clinics for gastroenteritis in Kenya.

Adolescent↗

PubMed1998

Stretch-activated channels in arterial smooth muscle of genetic hypertensive rats.

Electrical and contractile responses of small arteries to mechanical stress are reportedly enhanced in spontaneously hypertensive rats (SHR), compared with those in Wistar Kyoto rats (WKY). We have previously shown that stretch-activated cation channels exist in arterial smooth muscle membrane, of which opening causes Na+ and Ca2+ influx and membrane depolarization. We thus hypothesize that activation of stretch-activated channels is enhanced in arterial smooth muscle of SHR compared with WKY. To test this hypothesis, stretch-activated currents were recorded in single smooth muscle cells of resistance mesenteric arteries from SHR and WKY (16 to 24 weeks of age). In the whole-cell recording, membrane stretch was applied by inflating the cell with positive pressure to the recording pipette. Cell-inflation evoked Gd3+-sensitive cation currents. This current appeared with less stretch stimulation and its amplitude was larger in SHR cells compared with WKY cells. In the cell-attached recording, suction to the recording pipette evoked single stretch-activated channel currents (conductance of 32 pS with 150 mmol/L Na+), which were blocked by Gd3+. Channels were activated with less negative pressure and their availability was greater in SHR cells than in WKY cells. Results suggest that the activation of stretch-activated channels is enhanced in smooth muscle of resistance arteries from SHR compared with WKY, which may contribute to the enhanced vascular responses to mechanical stress in SHR.

Animals↗

PubMed1998

SPET study of verbal fluency in schizophrenia and epilepsy.

BACKGROUND: The association between temporal lobe epilepsy and schizophrenia suggests that the critical abnormality may be pathology within the temporal lobes. People with schizophrenia-like psychosis of epilepsy (SLPE) provide a useful group in which to examine the importance of temporal and frontal lobe dysfunction in schizophrenia. METHOD: A verbal fluency activation paradigm and a 99mTc HMPAO SPET were used to study frontotemporal function in people with SLPE (n = 12), schizophrenia (n = 11) and epilepsy (n = 16). RESULTS: People with SLPE differed from both other groups by showing lower blood flow in the left superior temporal gyrus during performance of a verbal fluency task compared with a word repetition task (F = 5.4, P = 0.01). During the verbal fluency task people with primary schizophrenia showed a greater increase in blood flow in anterior cingulate (F = 4.5, P = 0.02) than the other two groups. There were no between-group differences in frontal brain regions. CONCLUSION: Our findings support an association between left temporal lobe abnormality and SLPE. The different patterns of activation observed in people with primary schizophrenia and SLPE suggests that different pathophysiological mechanisms may operate in these two groups. In SLPE the pathophysiology may be relatively confined to the dominant temporal lobe.

Adult↗

PubMed1998

[Placement of self-expanding metallic stents in the stenotic trachea and bronchus under the support of gas exchange by extracorporeal lung assist (ECLA)].

Three self-expanding metallic stents (MS) were placed in a patient with severe dyspnea due to tracheo-bronchial stenosis caused by a large metastatic malignant tumor. To ensure adequate gas exchange, we used ECLA during surgery. After ECLA was started with V-V bypass (blood flow 1.3 l.min-1, 100% O2 flow 10 l.min-1), the patient was administered droperidol and fentanyl, and orotracheally intubated with an endotracheal tube (7.0 mm ID) using a bronchofiberscope. Anesthesia was maintained with midazolam, but no neuromuscular blocking agent was used. The pulmonary ventilation was withheld 3 times during each period of 5-10 min for MS placement through the endotracheal tube. The patient was ventilated for a few min between each procedure. Values of arterial blood gas were maintained within physiological ranges throughout the surgery. ECLA was a useful means of ensuring adequate gas exchange in perioperative patients with difficult airway.

Adolescent↗