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PubMed2000

Transforming growth factor-beta 1-induced activation of the ERK pathway/activator protein-1 in human lung fibroblasts requires the autocrine induction of basic fibroblast growth factor.

Transforming growth factor-beta (TGF-beta) is involved in multiple processes including cell growth and differentiation. In particular, TGF-beta has been implicated in the pathogenesis of fibrotic lung diseases. In this study, we examined regulation of the mitogen-activated protein kinase pathway by TGF-beta1 in primary human lung fibroblasts. TGF-beta1 treatment resulted in extracellular signal-regulated kinase (ERK) pathway activation in a delayed manner, with maximal activity at 16 h. ERK activation occurred concomitantly with the induction of activator protein-1 (AP-1) binding, a nuclear factor required for activation of multiple genes involved in fibrosis. AP-1 binding was dependent on ERK activation, since the MEK-1 (mitogen-activated protein kinase kinase) inhibitor PD98059 inhibited TGF-beta1-induced binding. Induction of the receptor tyrosine kinase-linked growth factor, basic fibroblast growth factor (bFGF) protein expression temporally paralleled the activation of ERK/AP-1. Induction of AP-1 by TGF-beta1-conditioned medium was observed at 2 h, similar to AP-1 induction in response to exogenous bFGF. Dependence of ERK/AP-1 activation on bFGF induction was demonstrated by inhibition of TGF-beta1-induced ERK/AP-1 activation when conditioned medium from TGF-beta1-treated cells was incubated with bFGF-neutralizing antibody. Together, these results demonstrate that TGF-beta1 regulates the autocrine induction of bFGF, resulting in activation of the ERK mitogen-activated protein kinase pathway and induction of AP-1 binding.

Cell Line↗

PubMed2003

Induction of nonmuscle myosin heavy chain II-C by butyrate in RAW 264.7 mouse macrophages.

RAW 264.7 macrophages express nonmuscle myosin heavy chain II-A as the only significant nonmuscle myosin heavy chain isoform, with expression of nonmuscle myosin heavy chain II-B and II-C low or absent. Treatment of the cells with sodium butyrate, an inhibitor of histone deacetylase, led to the dose-dependent induction of nonmuscle myosin heavy chain II-C. Trichostatin A, another inhibitor of histone deacetylase, also induced nonmuscle myosin heavy chain II-C. Induction of nonmuscle myosin heavy chain II-C in response to these histone deacetylase inhibitors was attenuated by mithramycin, an inhibitor of Sp1 binding to GC-rich DNA sequences. Bacterial lipopolysaccharide alone had no effect on basal nonmuscle myosin heavy chain II-C expression, but attenuated butyrate-mediated induction of nonmuscle myosin heavy chain II-C. The effects of lipopolysaccharide were mimicked by the nitric oxide donors sodium nitroprusside and spermine NONOate, suggesting a role for nitric oxide in the lipopolysaccharide-mediated down-regulation of nonmuscle myosin heavy chain II-C induction. This was supported by experiments with the inducible nitric-oxide synthase inhibitor 1400W, which partially blocked the lipopolysaccharide-mediated attenuation of nonmuscle myosin heavy chain induction. 8-Bromo-cGMP had no effect on nonmuscle myosin heavy chain induction, consistent with a cGMP-independent mechanism for nitric oxide-mediated inhibition of nonmuscle myosin heavy chain II-C induction.

Acetyltransferases↗

PubMed2003

Connective tissue growth factor gene regulation. Requirements for its induction by transforming growth factor-beta 2 in fibroblasts.

In skin, the profibrotic protein connective tissue growth factor (CTGF) is not normally expressed. However, when skin cells are exposed to transforming growth factor-beta (TGF-beta), CTGF is induced in fibroblasts but not in epithelial cells. We have begun to investigate the requirements for the fibroblast-selective induction of CTGF by TGF-beta. Previously we found that this response was Smad-dependent. Now we show that protein kinase C and Ras/MEK/ERK are necessary for the TGF-beta induction of the CTGF promoter but not of a generic Smad-responsive promoter (SBE-lux). Induction of the CTGF promoter is antagonized by c-Jun or by MEKK1, suggesting that a proper balance between the Ras/MEK/ERK and JNK MAPK cascades is necessary for TGF-beta induction of CTGF. We identify the minimal CTGF promoter element necessary and sufficient to confer TGF-beta responsiveness to a heterologous promoter and show that a tandem repeat of a consensus transcription enhancer factor binding element, 5'-GAGGAATGG-3', is necessary for this induction. This element has not been previously shown to play a role in TGF-beta induction of gene expression in fibroblasts. Gel shift analysis shows that this sequence binds nuclear factors that are greatly enriched in fibroblasts relative to epithelial cells. Thus Smads, Ras/MEK/ERK, protein kinase C, and fibroblast-enriched factors that bind GAGGAATGG act together to drive the TGF-beta-mediated induction of CTGF in fibroblasts.

3T3 Cells↗

PubMed2004

The induction of cytochrome P450 3A5 (CYP3A5) in the human liver and intestine is mediated by the xenobiotic sensors pregnane X receptor (PXR) and constitutively activated receptor (CAR).

Induction of cytochrome P450 3A (CYP3A) by xenobiotics may lead to clinically relevant drug interactions. In contrast with other CYP3A family members, studies on the inducibility of CYP3A5 indicate conflicting results. We report the induction of CYP3A5 mRNA in 13 of 16 hepatocyte preparations exposed to rifampin. Furthermore, induction of CYP3A5 mRNA was observed in intestinal biopsies in three of eight probands following exposure to the antibiotic. The highest absolute levels of CYP3A5 transcripts were found following rifampin treatment in hepatocytes and intestines from carriers of CYP3A5*1 alleles. Elucidation of the mechanism involved in CYP3A5 induction revealed that constitutively activated receptor (CAR) and pregnane X receptor (PXR) transactivated the CYP3A5 promoter (-688 to +49) and that the transactivation was dependent on an everted repeat separated by 6 bp (ER6-dependent). Treatment with the prototypical PXR ligand rifampin led to a 2-fold induction of the CYP3A5 promoter activity. In agreement with these observations, PXR and CAR bound specifically to the ER6 motif. Hepatic expression of PXR correlated with that of CYP3A5 mRNA levels in a bank of liver samples. Taken together, studies here revealed the presence of a functional ER6 motif in the CYP3A5 promoter located -100 bp upstream from the transcription start site, suggesting that CYP3A5 is inducible by mechanisms similar to those involved in CYP3A4 induction. Enhanced expression of CYP3A5 caused by exposure to inducers may phenocopy the effects of the high expression allele CYP3A5*1. In this manner, induction of CYP3A5 may contribute to the overall importance of this P450 in drug metabolism and drug interactions.

Alleles↗

PubMed2005

Selective induction of the tumor marker glutathione S-transferase P1 by proteasome inhibitors.

Exposure of cells to a wide variety of chemoprotective compounds confers resistance to a broad set of carcinogens. For a subset of the chemoprotective compounds, protection is generated by an increase in the abundance of phase 2 detoxification enzymes such as glutathione S-transferases (GSTs). Transcription factor Nrf2, which is sequestered in the cytoplasm by Keap1 (Kelch-like ECH-associated protein-1) under unstimulated conditions, regulates the induction of phase 2 enzymes. In this study, to explore the role of the proteasome in the detoxification response, we tested the effect of proteasome inhibitors such as MG132, clasto-lactacystin beta-lactone, and lactacystin on the induction of GST isozymes and found that these inhibitors selectively induced the class Pi GST isozyme (GST P1). Down-regulation of the proteasome by antisense oligonucleotides or RNA interference indeed resulted in significant up-regulation of GST P1, suggesting that a decline in the proteasome activity could be directly or indirectly linked to the induction of GST P1. From the functional analysis of various deletion constructs of the upstream regulatory region of the GST P1 promoter, GST P1 enhancer I was identified as the response element for proteasome inhibition. Overexpression of the wild-type and dominant-negative forms of Nrf2 and Keap1 had little effect on the induction of GST P1 not only by the proteasome inhibitor, but also by phase 2-inducing isothiocyanate, suggesting that there may be a process of GST P1 induction distinct from other phase 2 gene induction mechanisms. Because GST P1 is highly and specifically induced during early hepatocarcinogenesis as well as in hepatocellular carcinoma cells, these data may provide a potential critical role for the proteasome in the induction of a cellular defense program associated with carcinogenesis.

Acetylcysteine↗

PubMed2006

Effects of polycyclic aromatic hydrocarbons (PAHs) on vascular endothelial growth factor induction through phosphatidylinositol 3-kinase/AP-1-dependent, HIF-1alpha-independent pathway.

Previous studies have demonstrated that exposure to polycyclic aromatic hydrocarbons (PAHs) and its derivatives is associated with an increased risk of skin cancers, and the carcinogenic effect of PAHs is thought to involve both tumor initiation and promotion. Whereas PAH tumor initiation is well characterized, the mechanisms involved in the tumor promotion of PAHs remain elusive. In the present study, we investigated the effects of PAHs on vascular endothelial growth factor (VEGF) expression by comparison of its induction between the active metabolite and its parent compound (B[a]PDE versus B[a]P) or between active compound and its relatively inactive analog (5-MCDE versus CDE). We found that exposure of cells to (+/-)-anti-benzo-[a]pyrene-7,8-diol-9,10-epoxide (B[a]PDE) or (+/-)-anti-5-methylchrysene-1,2-diol-3,4-epoxide (5-MCDE) led to marked induction of VEGF in Cl41 cells, whereas benzo[a]pyrene (B[a]P) or chrysene-1,2-diol-3,4-epoxide (CDE) did not exhibit significant inductive effects. Exposure of cells to B[a]PDE and 5-MCDE did not induce HIF-1alpha activation, whereas AP-1 was significantly activated. Moreover, overexpression of TAM67 (a dominant-negative mutant c-Jun) dramatically blocked that VEGF induction. Electrophoretic mobility shift assay showed that AP-1 was only able to specifically recognize and bind to its AP-1 potential binding site within -1136 and -1115 of the VEGF promoter region. Site-directed mutation of this AP-1 binding site eliminated the VEGF transcriptional activity induced by B[a]PDE, suggesting that the AP-1 binding site between -1136 and -1115 in the VEGF promoter region is critical for VEGF induction by B[a]PDE. In addition, overexpression of Deltap85 (a dominant-negative mutant PI-3K) impaired B[a]PDE- and 5-MCDE-induced VEGF induction. Considering our previous findings that PI-3K is an upstream mediator for c-Jun/AP-1 activation, we conclude that the VEGF induction by B[a]PDE and 5-MCDE is through PI-3K/AP-1-dependent and HIF-1alpha-independent pathways. These findings may help us to understand the mechanisms involved in PAH carcinogenic effects.

Animals↗

PubMed1994

A comparison of cognitive and behavioral inductions of negative mood.

Sixty undergraduate subjects were exposed to one of three depressive mood inductions: cognitive, behavioral, or control. Subjects in the cognitive induction group read negative self-statements consistent with Beck's (1974) cognitive theory of depression. Subjects in the behavioral induction group were exposed to insoluble discrimination problems consistent with Lewinsohn's (1974) behavioral theory that lack of reinforcement produces depression. The control group read a neutral passage. Following the mood induction, subjects rated their current moods using the Multiple Affect Adjective Checklist (MAACL; Zuckerman & Lubin, 1965). The cognitive and behavioral inductions produced significantly higher MAACL total and subscale scores than did the control condition; however, the cognitive and behavioral inductions did not differ from one another. Because the cognitive and behavioral mood inductions appear equally powerful, they may be used by researchers who are attempting to identify variables that are related to subjects' differing responses to behavioral and cognitive influences on depression.

Cognition↗

PubMed2006

Evaluation of the necessity of induction for lactose-[15N, 15N]-ureide to study the colonic ammonia metabolism.

OBJECTIVE: Stable isotope labelled glycosyl ureides have been described as non-invasive markers for measurement of gastrointestinal processes. Lactose-[13C]-ureide is used for the evaluation of orocaecal transit time (OCTT), whereas lactose-[15N, 15N]-ureide is used to study the fate of the NH3 metabolism in the colon. Induction with unlabelled lactose ureide is necessary for the determination of the OCTT. In the present study, the effect of a preceding induction on the fate of 15NH3 in the colon was evaluated. MATERIAL AND METHODS: Ten healthy volunteers performed two tests: the first test without induction, the second test one week later with induction, i.e. administration of 1 g lactose ureide the evening before the test. Each test consisted of a fractionated 24-h urine collection after the subjects had received a pancake test meal labelled with 75 mg lactose-[15N, 15N]-ureide. All samples were analysed for [15N]-content by combustion IRMS (isotope ratio mass spectrometry) and results were expressed as a percentage of the administered dose. RESULTS: No significant differences were found in the percentage dose 15N excreted in the different urine fractions between the test without and with preceding induction. The cumulative excretion rates of the 15N-isotope after 24 h were 44.35% without induction and 44.27% with induction. CONCLUSIONS: The results in this study show that predosing with unlabelled lactose ureide is unnecessary for the evaluation of the ammonia metabolism in the colon by means of lactose-[15N, 15N]-ureide.

Adult↗

PubMed2002

Permissive and suppressive effects of dexamethasone on enzyme induction in hepatocyte co-cultures.

1. Steroids are known to act as permissive factors in hepatocytes. This study shows that dexamethasone (DEX) is a permissive factor for induction of CYP2B1/2, CYP3A1, CYP2A1 and probably also CYP2C11 in cultures with primary rat hepatocytes. 2. The induction factor of phenobarbital (PB)-induced formation of 16beta-hydroxytestosterone (OHT), a testosterone biotransformation product predominantly formed by CYP2B1, is increased 18-fold by the addition of 32 nM DEX to the culture medium. Interestingly, higher concentrations of DEX up to 1000 nM led to a concentration-dependent maximally 5-fold decrease (p = 0.002) of phenobarbital-induced 16beta-OHT formation compared with the effect observed with 32 nM DEX. Thus, DEX shows permissive and suppressive effects on enzyme induction depending on the concentration of the glucocorticoid. 3. Qualitatively similar but smaller permissive and suppressive effects of DEX were observed for PB-induced CYP3A1 activity as evidenced by formation of 2beta-, 6beta- and 15beta-OHT. 4. DEX is a permissive factor for induction of CYP2A1 activity by 3-methylcholanthrene (3MC), as evidenced by the formation of 7alpha-OHT. Without addition of DEX, 3MC did not induce formation of 7alpha-OHT, whereas an almost 3-fold induction occurred in the presence of DEX. In contrast to CYP2B and CYP3A, concentrations up to 1000 nM DEX were not suppressive for the induction of CYP2A1. 5. We described recently a technique that allows preparation of cultures from cryopreserved hepatocytes. An almost identical influence of dexamethasone on enzyme induction was observed here in cultures from cryopreserved compared with freshly isolated hepatocytes. 6. Cultures with primary hepatocyte cultures represent a well-established technique for the study of drug-drug interactions. However, a large interlaboratory variation is known. Our study provides evidence that differences in glucocorticoid concentration in the culture medium contribute to this variation.

Animals↗

PubMed1999

A reporter gene assay to assess the molecular mechanisms of xenobiotic-dependent induction of the human CYP3A4 gene in vitro.

1. A plasmid containing 1 kb of the CYP3A4 regulatory (promoter) region coupled to a reporter gene for secretary placental alkaline phosphatase (SPAP) was transfected into HepG2 cells. Transfected cells were dosed with several known inducers of CYP3A4 and the levels of SPAP were measured. The effect of co-transfecting a plasmid encoding the human glucocorticoid receptor on reporter gene activity was also examined. 2. Dexamethasone induced CYP3A4-dependent reporter gene expression in a concentration-dependent manner and induction was approximately doubled in the presence of the glucocorticoid receptor. Dexamethasone-dependent induction was blocked by RU-486 (a glucocorticoid receptor antagonist), in the presence of the co-transfected glucocorticoid receptor. 3. Induction of CYP3A4-dependent reporter gene expression and enhancement of the induction by the glucocorticoid receptor was also observed with pregnenolone-16alpha-carbonitrile (PCN), rifampicin, phenytoin, carbamazepine, phenylbutazone and phenobarbitone, all known in vivo inducers of CYP3A4 in man. 4. Metyrapone and sulfinpyrazone induced CYP3A4-dependent reporter gene expression, but induction was not enhanced by the glucocorticoid receptor. 5. Clotrimazole, erythromycin and triacetyloleandomycin (TAO) did not induce CYP3A4-dependent reporter gene expression, consistent with the observation that these inducers act through post-transcriptional mechanisms. 6. These results highlight differences in the molecular mechanisms of induction of CYP3A4 by the xenobiotics studied and indicate that the glucocorticoid receptor is involved in the induction of the CYP3A4 gene by some, but not all, CYP3A4 inducers. 7. We propose that the approach described here provides a useful in vitro approach for the identification of transcriptional regulators of the CYP3A4 gene.

Alkaline Phosphatase↗

PubMed2005

Randomised trial of intravaginal misoprostol and intracervical Foley catheter for cervical ripening and induction of labour.

Induction of labour may be indicated despite an unripe cervix. The purpose of this study was to compare the safety and efficacy of intravaginal misoprostol and an intracervical Foley's balloon catheter for preinduction cervical ripening and labour induction. A total of 120 patients requiring indicated induction of labour with an unfavourable cervix (Bishop's score < or =4) were randomised prospectively to receive either 50 mug intravaginal misoprostol every 6 h for a maximum of two doses, or an intracervical Foley balloon catheter for 12 h followed by an intravenous oxytocin infusion. The two arms of the study were comparable with respect to maternal age, parity, gestational age, indication for induction, and initial Bishop's scores. There were significant change in the Bishop's score in the two groups (5.9 +/- 0.2 and 4.0 +/- 0.2, respectively, p < 0.001) but no inter group differences. Oxytocin induction or augmentation of labour occurred more in the catheter group (95%) than in the misoprostol group (43.3%) (p < 0.0001). Induction to delivery interval was significantly shorter in the misoprostol group than in the catheter group (8.7 +/- 2.4 vs 11.9 +/- 2.7 h p < 0.0001). There was no significant difference noted in the caesarean or other operative delivery rates among patients in the two treatment groups. There was a higher incidence of tachysystole and hyperstimulation in the misoprostol group than in the catheter group (p < 0.03). No differences were observed between groups for meconium passage, 1- or 5-min Apgar scores < 7 and admission into the neonatal intensive care unit. In conclusion, the maternal and perinatal outcomes in this study have shown no difference confirming the efficacy and safety of both methods, however we observe a decrease in the induction-to-delivery interval when misoprostol is used for this purpose.

Administration, Intravaginal↗

PubMed2006

Induction when rats lick for 1% liquid-sucrose reinforcement.

Previous research reported that rats responding for 1% liquid-sucrose reinforcement when 32% sucrose reinforcement is upcoming will decrease their response rate (contrast) if licking is the dependent measure and increase their response rate (induction) if pressing a lever is the dependent measure. The present study investigated whether induction could be observed when licking served as the dependent measure and whether induction in lever pressing and contrast in licking behaviour could be concurrently observed. Experiment 1 found induction when rats licked to earn the rewards but consumed them at a location separate from the spout licked to earn them. Experiment 2 also found induction when rats earned (and consumed) rewards by licking the same spout throughout the session. Experiment 3 separately measured instrumental lever pressing for sucrose rewards and licking the sucrose during the reward period. We found that both measures increased for 1% sucrose when 32% sucrose reinforcement was upcoming. The present results indicate that the type of response is not the sole determinant of whether contrast or induction is observed. Rather, they suggest that other procedural details, such as the location of reinforcer delivery, influence which effect is observed. The results also indicate that associative processes underlie the appearance of induction in responding for 1% sucrose.

Analysis of Variance↗

PubMed2000

Induction by carbon-ion irradiation of the expression of vascular endothelial growth factor in lung carcinoma cells.

PURPOSE: To investigate the induction by carbon- ion irradiation of vascular endothelial growth factor (VEGF) mRNA and protein. MATERIALS AND METHODS: RERF-LC-AI lung squamous carcinoma cells were irradiated with carbon ions of either 13.3, 50 or 90keV/microm. Colony formation was used to determine cell survival. VEGF mRNA and protein of the irradiated cells were quantified by Northern blot analysis and ELISA assay, respectively. Genistein, Src tyrosine kinase inhibitor and H7, protein kinase C inhibitor, were used to inhibit VEGF mRNA expression. RESULTS: The relative biological effectiveness (RBE) of carbon ions (13.3, 50 and 90keV/microm) was 1.10, 1.97 and 2.30, respectively, in terms of D10 values. Single doses of 15 Gy with either X-rays or carbon ions significantly induced VEGF mRNA expression at 16-24h after irradiation with a maximum induction of 2.81-fold. A significant increase was also observed in VEGF protein levels, detected in culture supernatant 24h after irradiation with 50 and 90keV/microm carbon ions. Neither mRNA nor protein induction showed a dependence on LET. The induction of VEGF mRNA by carbon-ion irradiation was completely inhibited by pretreating cells with genistein and H7, indicating that Src tyrosine kinase and protein kinase C on cell surface membranes is involved in the induction. CONCLUSION: Irradiation of lung carcinoma cells with carbon ions induced VEGF mRNA expression and increased protein levels. The induction was dose-dependent. Radiation-induced DNA damage and/or its repair may not be a prerequisite for the induction of VEGF mRNA.

Carbon↗

PubMed1990

Lambda-prophage induction in repair-deficient and wild type E. coli strains by gamma-rays and heavy ions.

Lambda-prophage induction in repair-deficient and wild-type E. coli strains by heavy ions and gamma-rays has been investigated. The dose dependence of the fraction of induced cells has been measured and its initial slope (lambda-induction potency) determined. The induction by gamma-rays was found to be more efficient in a polA-repair-deficient strain; the value of lambda-induction potency is zero in lexA- and recA- strains. The lambda-induction potency increased with LET for wild-type cells but remained constant in the case of polA- mutant cells. It is suggested that the DNA damage triggering the lambda-prophage induction in the case of ionizing radiation could be a type of DNA single-strand break with complex structure which cannot be repaired by fast repair processes, and which requires a substantial level of energy deposition for induction in a DNA molecule.

Bacteriophage lambda↗

PubMed1994

Design of an inductive plethysmograph for ventilation measurement.

We have designed an inductive plethysmograph to obtain a non-invasive measure of ventilation. Two elastic bands containing insulated wires encircle the chest and abdomen--the inductance of each band depends on the enclosed cross sectional area. Each inductive band forms an element in a tank circuit, which determines the resonant frequency of a Colpitts oscillatory. By measuring the oscillatory frequency, we indirectly measure the changes in cross sectional area that occur during breathing. Independent measures of chest and abdominal cross sectional area provide a way to detect both normal breathing and airway obstruction. Magnetic coupling due to the mutual inductance between chest and abdominal bands modulates the desired oscillation frequencies. When modulation is excessive, frequency locking occurs and we cannot make independent measures of chest and abdominal area. We have performed simulations that show that, as the chest and abdominal band oscillator frequencies are sufficiently separated, we decrease modulation and avoid frequency locking. We have compared simulataneous recordings of ventilation using our inductive plethysmography and a commercial impedance pneumograph and spirometer. Recordings of normal ventilation by all methods appear similar; however, our inductive device is less prone than the impedance pneumography to artifacts caused by applied pressure and body movements. In addition, during simulated airway obstruction, signals from the chest and abdominal bands are out of phase--suggesting that the inductive technique may be useful for detecting airway obstruction.

Abdomen↗

PubMed1986

Benzo[a]pyrene metabolites: effects on viral interferon induction.

Benzo[a]pyrene (BaP) metabolites were assessed, with and without enzymatic activation by rat liver S9, for their inhibitory activities on influenza virus induction of interferon-alpha/beta (IFN-alpha/beta) in mammalian (LLC-MK2) cell cultures. Although BaP per se was inactive, metabolized BaP reduced viral IFN induction by approximately 80%. BaP metabolites (phenols, diols, 6-substituted derivatives) exhibited significant inhibitory activity (50% or greater) only when they were activated enzymatically. Although not significant, the diol metabolites without activation mildly reduced IFN induction on the average of 32%. The quinones did not adversely affect the IFN induction process, but three of the seven metabolites tested showed approximately 30% inhibitory activity in the presence of S9. BaP diol epoxides were direct inhibitors of viral IFN induction while derivatives of these epoxides, tetrols and triols, showed negligible inhibition even with S9. In general, the reported microbial mutagenicities of BaP metabolites could be correlated with their abilities to inhibit IFN induction. That activation-dependent hydrocarbons can be metabolized by S9 added to mammalian cell cultures resulting in the inhibition of viral IFN induction extends the capability and credibility for assessing suspect mutacarcinogens on this basis.

Animals↗

PubMed1997

Rapid inhalation induction in children: 8% sevoflurane compared with 5% halothane.

Sevoflurane has a lower blood-gas solubility and a less pungent odour than halothane; this may allow more rapid induction of anaesthesia. In a randomized, blinded study, we compared the induction characteristics of maximum initial inspired concentration of 8% sevoflurane and 5% halothane using conventional vaporizers in children aged 3 months to 3 years. There was no statistically significant difference in induction times between the two groups: mean times to loss of consciousness were 1 min 12 s (SD 18 s, range 40 s-1 min 44 s) for sevoflurane and 1 min 16 s (SD 17 s, range 50 s-1 min 52 s) for halothane, although these times were shorter than in previous studies using a gradual increase in vapour concentration. A small number of complications were noted in both groups, although none interfered with induction of anaesthesia. Struggling scores were lower in the sevoflurane group than in the halothane group (chi-square for trends = 6.34, P < 0.02). A significant number (11 of 15) of parents of children in the sevoflurane group who had previous experience of halothane induction preferred sevoflurane (chi-square for trends = 4.03, P < 0.05). We conclude that with this technique, induction was rapid with both sevoflurane and halothane. Our assessment of patient struggling and parents' perceptions suggests that induction with sevoflurane was more pleasant than with halothane.

Anesthesia, Inhalation↗

PubMed2001

Influence of nitrous oxide on induction of anaesthesia with sevoflurane.

Nitrous oxide is often used during inhalation induction of anaesthesia with sevoflurane. Although the value of using nitrous oxide during inhalation induction with other volatile anaesthetics has been studied, the popularity of sevoflurane induction and the different characteristics of this agent make a study of the combination of nitrous oxide with this agent of interest. We compared induction times, oxygenation, and excitatory events during inhalation induction of anaesthesia using sevoflurane, with and without nitrous oxide. We studied 64 female patients, randomly allocated to receive inhalation induction of anaesthesia using sevoflurane with or without 50% nitrous oxide in the fresh gas, using a co-axial breathing system (Mapleson D) and a fresh gas flow rate of 3-6 litre min(-1). Mean time to induction of anaesthesia (fall of an outstretched arm) was 102 s in both groups, but excitation (limb or head movement) was more frequent in those receiving nitrous oxide (10 patients) than in those receiving oxygen only (five patients) (P<0.05). Oxygenation was similar in both groups. We conclude that nitrous oxide confers no advantage when anaesthesia is induced with sevoflurane in this way.

Adolescent↗