Usefulness of an anesthetic conserving device (AnaConDa™) in sevoflurane anesthesia.

BACKGROUND: The anesthetic conserving device (AnaConDaTM) is a disposable vaporizer that can save consumption of inhalational anesthetic used in low sevoflurane concentration. This study was performed to investigate whether AnaConDa when used at high sevoflurane concentration (1.5% to 2.0%) could save sevoflurane consumption and hasten emergence from anesthesia without any adverse effects. METHODS: Thirty patients for ear surgery were equally divided into AnaConDa and control groups. Anesthesia was induced with intravenous anesthetics. After intubation sevoflurane inhalation started by infusion at 25 mL/h in the AnaConDa group and by inhalation of 2.0% (conventional vaporizer setting) in the control group. During anesthesia, end-tidal sevoflurane concentration was kept between 1.5 and 2.0% in both groups. The time to first detection of end-tidal sevoflurane, the time to sevoflurane concentration reached 1.5%, sevoflurane consumption, and emergence time were compared between the two groups. Adverse effects were checked. RESULTS: Sevoflurane consumption was smaller, time to first detection of end-tidal sevoflurane was longer, time to sevoflurane concentration reached 1.5% was longer, emergence time was shorter, and decrease of end-tidal sevoflurane concentration after stop of administration was faster in the AnaConDa group significantly. Clear Water accumulation with no smell in the filter was observed in 12 of 15 patients in the AnaConDa group. CONCLUSION: In general anesthesia with sevoflurane 1.5% to 2.0%, AnaConDa could save sevoflurane consumption and fasten emergence from anesthesia compared to conventional vaporizer, while water accumulation in the filter should be cautioned.

Hedgehog signal activation in oesophageal cancer patients undergoing neoadjuvant chemoradiotherapy.

The zinc finger protein glioma-associated oncogene homologue 1 (Gli-1) is a critical component of the Hedgehog (Hh) signalling pathway, which is essential for morphogenesis and stem-cell renewal, and is dysregulated in many cancer types. As data were not available on the role of Gli-1 expression in oesophageal cancer progression, we analysed whether it could be used to predict disease progression and prognosis in oesophageal cancer patients undergoing neoadjuvant chemoradiotherapy (CRT). Among 69 patients with histologically confirmed oesophageal squamous cell carcinomas (ESCCs), 25 showed a pathological complete response after preoperative CRT. Overall survival (OS) was significantly associated with lymph-node metastasis, distant metastasis, and CRT, and was further correlated with the absence of both Gli-1 nuclear expression and residual tumour. All patients with Gli-1 nuclear expression (10.1%) had distant or lymph-node metastasis, and six out of seven died within 13 months. Furthermore, patients with Gli-1 nuclear-positive cancers showed significantly poorer prognoses than those without (disease-free survival: mean DFS time 250 vs 1738 months, 2-year DFS 0 vs 54.9%, P=0.009; OS: mean OS time 386 vs 1742 months, 2-year OS 16.7 vs 54.9%, P=0.001). Our study provides the first evidence that Gli-1 nuclear expression is a strong and independent predictor of early relapse and poor prognosis in ESCC after CRT. These findings suggest that Hh signal activation might promote cancer regrowth and progression after CRT.

Overproduction of the follistatin-related gene protein in the placenta and maternal serum of women with pre-eclampsia.

OBJECTIVE: To characterise the follistatin-related gene (FLRG) in pre-eclampsia, one of the differentially expressed genes in pre-eclamptic placenta. DESIGN AND METHODS: We examined and compared the messenger RNA (mRNA) and protein levels of FLRG in placentas and maternal sera from women with uncomplicated pregnancy, and those with pre-eclampsia using real-time reverse transcription polymerase chain reaction, Western blot, immunohistochemistry, and enzyme-linked immunosorbent assay. SETTING: Antenatal clinics in a teaching hospital. POPULATION: Women with uncomplicated pregnancy (n = 21) and those with pre-eclampsia (n = 21). RESULTS: FLRG mRNA is overexpressed in pre-eclamptic placental tissues (P < 0.01). Upregulated FLRG protein consists of both an immature 28-kDa cellular product and a mature 33-kDa secretory form, which are differentially glycosylated. FLRG is normally produced at its highest levels in endothelial cells and at moderate amounts in syncytiotrophoblast cells, but in pre-eclampsia, the syncytiotrophoblast FLRG levels are dramatically increased. We also determined the maternal serum concentrations of FLRG in our uncomplicated pregnancy subjects and in our pre-eclamptic groups, and found that they are significantly elevated in pre-eclampsia in a similar manner to activin A and inhibin A. However, the increase in FLRG in these cases is independent of activin A or inhibin A, and is associated with low-birthweight outcomes. CONCLUSION: Our current data show the placental and secretory changes of FLRG protein in pre-eclampsia, and also indicate the potential usefulness of FLRG as an additional diagnostic marker for pre-eclampsia.

Microarray analysis of differentially expressed fetal genes in placental tissue derived from early and late onset severe pre-eclampsia.

Although it has been well documented that pre-eclampsia is caused by a combination of maternal and fetal susceptibility genes, little is known about the precise etiology of this complicated disorder. To investigate how the expression of fetal genes contributes to the mechanisms underlying the progression of this disease, we have analyzed differentially expressed genes using placentas from 13 normal pregnancies and 14 pregnancies with severe pre-eclampsia. We performed genome-wide expression profiling using high-density oligonucleotide microarrays, followed by validation using real-time PCR. Among the 47,000 genes that were screened in the microarray, 137 genes were found to be differentially expressed between normal and pre-eclamptic tissues. Among these candidates, 70 were up-regulated and 67 were down-regulated. The up-regulated genes included leptin and inhibin A, which are well-known biological markers for pre-eclampsia, as well as FLT1, which was recently proved to be tightly linked with the etiology of this disease. Gene ontology analysis further revealed several biological processes that could be associated with the development of pre-eclampsia, including response to stress, host-pathogen interactions, lipid metabolism, and carbohydrate metabolism. Analyses of biological mechanisms highlighted some important pathways that may be involved in this disorder, such as the TGF-beta and CEBPA-related pathways. Furthermore, when our present subjects were classified as either severe cases of early onset or late onset pre-eclampsia, the expression of 11 genes could be correlated with the severity of this disorder. These genes may therefore prove to be novel biological markers by which the severity of this condition could be predicted. Our data are likely to be a useful future resource in the elucidation of the disease-process and in the identification of novel markers for pre-eclampsia.

Analysis of mRNAs that are enriched in the post-synaptic domain of the neuromuscular junction.

The identity of synaptically-enriched genes was investigated by comparing the abundance of various mRNAs in the synaptic and extra-synaptic regions of the same muscle fibers. The mRNAs for several known synaptic proteins were significantly elevated in the synaptic region when measured by real-time PCR. The synaptic mRNAs were then further analyzed using microarrays and real-time PCR to identify putative regulators of the neuromuscular junction (NMJ). MRF4 was the only member of the MyoD family that was concentrated at the mature NMJ, suggesting that it may have a unique role in the maintenance of post-synaptic specialization. Three potential regulators of the NMJ were identified and confirmed by real-time PCR: glia maturation factor gamma was concentrated at the NMJ whereas Unr protein and protein tyrosine phosphatase were repressed synaptically. The identification of synaptically-repressed genes may indicate that synaptic specialization is created by a combination of positive and negative signals.

Fibroblast growth factor-5 is expressed in Schwann cells and is not essential for motoneurone survival.

Fibroblast growth factor-5 (FGF-5) is a putative target-derived survival factor for motoneurones as it is concentrated in the synaptic portions of skeletal muscles and because it promotes the survival of embryonic motoneurones in vitro. A variety of experimental approaches have been used to examine this possibility. The expression of FGF-5 in the neuromuscular system was analysed using the reverse transcription-polymerase chain reaction (RT-PCR). Both splice variants of FGF-5 were detected in adult rat skeletal muscle, sciatic nerve, and spinal cord. The expression of FGF-5 in skeletal muscle was up-regulated after denervation. At first sight this appears to be consistent with FGF-5 being a target-derived factor. However, FGF-5 protein was detected in Schwann cells, macrophages, vascular smooth muscle and endothelial cells, but not in muscle fibres. The absence of FGF-5 in muscle fibres was confirmed by RT-PCR examination of isolated muscle fibres. Furthermore, FGF-5 protein was also not detected in denervated fibres, as would be expected for a neuronal survival factor. Denervation did however lead to up-regulation of FGF-5 in the Schwann cells of the distal nerve trunk. This may indicate that FGF-5 is either an autocrine regulator of Schwann cells or a Schwann cell-derived neurotrophic factor. The latter appears not to be the case for two reasons. First, the double-ligation technique was used to show that endogenous FGF-5 is not transported in motor axons. Second, stereological estimates of the number of motoneurones in an FGF-5 null mutant (Angora) mouse failed to reveal any loss of motoneurones. Collectively these experiments suggest that FGF-5 is not a physiological regulator of motoneurones, and therefore raise the possibility that it is an autocrine regulator of Schwann cells.

TGF-beta 2 attenuates the injury-induced death of mature motoneurons.

The distributions of transforming growth factor-betas (TGF-betas) and their receptors suggest that the TGF-betas regulate motoneuron survival. This hypothesis was tested by avulsing the hypoglossal nerve of adult rats and perfusing either TGF-beta 2 or vehicle adjacent to the hypoglossal nucleus. By 4 weeks, half of the avulsed motoneurons had died. Infusion of 6 ng of TGF-beta 2 adjacent to the avulsed motor nucleus caused a significant attenuation of this death. This dose of TGF-beta 2 is low compared to that used with GDNF or BDNF in previous studies of avulsed motoneurons, indicating that TGF-beta 2 may be one of the more potent survival factors for adult motoneurons. TGF-beta 2 was, however, unable to prevent or reduce the axotomy-induced down regulation of choline acetyltransferase. Other motoneuron survival factors also have a narrow-spectrum of actions, suggesting that the homeostasis of motoneurons is regulated by a cocktail of growth factors with distinct but partially overlapping actions.

The expression and structure of TGF-beta2 transcripts in rat muscles.

The transforming growth factor-beta2 (TGF-beta2) transcripts expressed in various tissues of rat were characterised by RT-PCR and the nucleotide sequence of the cDNAs determined. A transcript with an 84-nucleotide insert in the latency-associated peptide region, the long form, was found. The long form of TGF-beta2 was detected in the aorta, primary bronchus, uterus, heart, skeletal muscle, sciatic nerve and spinal cord but not in the intestine. The 3' untranslated region of TGF-beta2 contained several putative AU-rich elements and multiple polyadenylation sites, indicating post-transcriptional regulation of TGF-beta2 synthesis. The levels of TGF-beta2 transcripts were estimated using semi-quantitative RT-PCR. They were down-regulated during muscle development and up-regulated after denervation. The long form constituted approximately 6% of the total TGF-beta2 messages in skeletal muscle.

Anterograde axonal transport of glial cell line-derived neurotrophic factor and its receptors in rat hypoglossal nerve.

Glial cell line-derived neurotrophic factor is one of the most potent motoneuron survival factors yet identified. Although retrograde transport of trophic factors to the cell body is thought to be an important process in motoneuron survival, the transport pathways that lead to interaction of glial cell line-derived neurotrophic factor with its receptors is not known. We have used a double ligated hypoglossal nerve preparation to investigate transport of endogenous glial cell line-derived neurotrophic factor and its receptors, glial cell line-derived neurotrophic factor family receptor alpha1 and receptor re-arranged during transfection. Glial cell line-derived neurotrophic factor was found to accumulate at the distal ligature, indicating retrograde transport and consistent with its motoneuron survival effects. In addition, we observed accumulation of glial cell line-derived neurotrophic factor and its receptors at the proximal ligature, indicating anterograde transport. This finding is not predicted by neurotrophic theory. Staining for glial cell line-derived neurotrophic factor in the motor axons was punctate, suggesting involvement of transport vesicles. Results obtained using immunohistochemistry and reverse transcription-polymerase chain reaction provide evidence for the synthesis of glial cell line-derived neurotrophic factor and glial cell line-derived neurotrophic factor family receptor alpha1 in Schwann cells and glial cell line-derived neurotrophic factor family receptor alpha1 and receptor re-arranged during transfection in motoneuron cell bodies. When the motor axons were separated from the cell body by avulsion, glial cell line-derived neurotrophic factor remained in the vicinity of the Schwann cells and did not accumulate at the proximal ligature. Our results indicate anterograde transport of Schwann cell-derived glial cell line-derived neurotrophic factor, which is dependent on binding to its cell body-derived receptors. These findings suggest a mechanism for collection of glial cell line-derived neurotrophic factor from multiple Schwann cells which surround motor axons. We propose that in addition to its role in motoneuron survival, glial cell line-derived neurotrophic factor may also modulate local neuronal effects in distal regions of the nerve.

Transforming growth factor-beta 2 is anterogradely and retrogradely transported in motoneurons and up-regulated after nerve injury.

The survival of motoneurons is dependent on them receiving continual trophic support from muscle fibres and various other cell types. Numerous putative survival factors have been identified and a set of criteria established by which these candidates can be assessed. These criteria include the need for the factor and its receptors to be in appropriate locations and for the factor or its second message to be retrogradely transported. In this paper, we demonstrate that a multifunctional cytokine, transforming growth factor-beta 2, appears to meet these criteria. The locations of the transforming growth factor-beta 2 and its receptors in the neuromuscular system were determined by reverse transcriptase-polymerase chain reaction and immunohistochemistry. Motoneurons were shown to synthesize the three proteins involved in transforming growth factor-beta 2 signalling (types I and II transforming growth factor-beta receptor and betaglycan) and to transport them anterogradely, where they were inserted into the axonal membrane and nerve terminal. Transforming growth factor-beta 2 was detected in the synaptic portions of muscle fibres, motoneurons and in injured nerves, indicating that motoneurons may be exposed to multiple and potentially redundant sources of transforming growth factor-beta 2. Double-ligation experiments were used to demonstrate that motoneurons transport transforming growth factor-beta 2 up and down their axons. The anterograde transport of both transforming growth factor-beta 2 and its receptors, coupled with the fact that most of a motoneuron's mitochondria are located in the axon, raises the issue of whether the repression of the initiation of apoptosis is restricted to the cell body or occurs along the entire length of a neuron.

Expression of MyoD and myogenin in dystrophic mice, mdx and dy, during regeneration.

Expression of two myogenic regulatory factors, MyoD and myogenin, was studied in regenerating muscles of dystrophic mice and compared to a chemically induced regeneration process. First, the distribution of the two proteins was determined immunohistochemically at various time points after single administrations of a local anaesthetic, bupivacaine hydrochloride, which causes myonecrosis followed by regeneration. Detectable levels of MyoD appeared at 18 h and the expression reached their maximum levels at 48 h after the injection, which coincide with the stage when satellite cells are activated and start to proliferate. Myogenin became detectable in 24 h and its expression reached its highest level at 72 h after injection when newly formed myotubes appeared. The two genes were also expressed in the dystrophic muscles from dy and mdx mice which exhibit dystrophic pathological features but are associated with different phenotypes. In mdx mice the two genes were expressed at reasonably high levels in parallel with the active regenerating process, whereas in dy mice MyoD and myogenin expressions decreased as fibrosis progressed. However, MyoD was relatively more strongly expressed in the larger mature myotubes of dy mice than in those of mdx mice, suggesting prolonged regenerative activity. In dy and mdx mice, MyoD and myogenin were expressed in different quantities, indicating that these animals have distinct regenerating activities. Our findings confirm that expression of both MyoD and myogenin genes is necessary in the regenerative process for the proliferation of satellite cells (myoblasts) and for the development of early regenerating fibers (myotubes) even in dystrophic muscles.

Development of skeletal muscles in transforming growth factor-beta 1 (TGF-beta1) null-mutant mice.

Fetal transforming growth factor-beta 1 (TGF-beta1) has been postulated to regulate the onset of myotube formation and/or pattern formation in developing skeletal muscles. In apparent contradiction of these hypotheses, the development of the extensor digitorum longus and soleus in TGF-beta1 null-mutant muscle was normal. The onset of secondary myotube formation, the numbers of myotubes formed, the proportion of fast and slow fibers, and the patterns of fiber types and connective tissues were essentially identical in TGF-beta1(+/+) and TGF-beta1(-/-) mice. A portion of the TGFbeta1 in skeletal muscles is derived from the mother, via the placenta. This maternal-derived TGF-beta1 was also not essential for the development of skeletal muscles, as the characteristics of pups born to a TGF-beta1(-/-) mother were normal TGF-beta1(-/-) mice die at weaning due to a generalized autoimmune attack. This postnatal death was circumvented by breeding the TGF-beta1 null mutation into nude mice (Whn(-/-)). Like many other strains of TGF-beta1(-/-) mice, extensive loss of Whn(-/-), TGF-beta1(-/-) embryos occurred in utero. However, a portion of the Whn(-/-), TGF-beta1(-/-) mice survived past weaning, remained healthy, and were fertile. The TGF-beta1(-/-) x Whn(-/-) mouse thus represents a valuable tool for the study of the function of TGF-beta1 in the adult, including its putative role as a pregnancy-related hormone.

[Respiratory muscle weakness after prolonged use of hydrocortisone and pancuronium bromide].

A 30-year-old man was admitted because of status asthmaticus. He required 7 days of artificial ventilation and was treated with hydrocortisone 1.2 g.day-1 and bronchodilaters. Pancuronium bromide 0.08 mg.kg-1.hr-1 was given for 64 hours for the ease of artificial ventilation. On day 3, severely elevated airway pressure resulted in left pneumothorax and isoflurane 1% was given for the following 2 days. Respiratory muscle weakness was evident 24 hours after discontinuation of pancuronium infusion on day 5 while full 4 twitches of TOF on the adductor pollicis muscle were seen at the time. The respiratory muscle weakness continued for another 3 days and he was extubated on day 8. Serum creatine kinase concentration rose to 2178 U.l-1 on day 6 and returned to normal on day 11. Hematurea, hyperpyrexia and metabolic acidosis were never seen during the course. Acute corticosteroid myopathy was suspected to be the cause of the prolonged respiratory muscle weakness.

Transforming growth factor-beta2 is elevated in skeletal muscle disorders.

The transforming growth factor betas (TGF-betas) are multifunctional growth factors that act on both fibroblasts and myosatellite cells. In rodent models of muscle diseases, high levels of TGF-beta2 are expressed by myogenic cells. We have examined whether the expression of TGF-beta2 is also elevated in diseased human muscles. The disorders examined were Duchenne muscular dystrophy, myotonic dystrophy, myotubular myopathy, spinal muscular atrophy, and amyotrophic lateral sclerosis. The levels of TGF-beta2 immunoreactivity were elevated in atrophic, necrotic, and regenerating fibers and in fibers with central nuclei or cytoplasmic masses, irrespective of whether fibrosis was present. We therefore suggest that TGF-beta2 is important for muscle repair and that the presence of a TGF-beta within a muscle only leads to fibrosis if certain other factors are present.

[Changes in SpO2 during total intravenous anesthesia combined with propofol and SpO2 during one-lung anesthesia ventilation].

We retrospectively examined SpO2 during one-lung anesthesia (OLA). One hundred and fifty patients of ASA 1 or 2 for thoracoscopic surgery were anesthetized with propofol and fentanyl (n = 93) or pentazocine (n = 57) and mechanically ventilated with FIO2 = 0.6 in the lateral decubitus position. Twelve patients (8%) developed SpO2 < or = 95% in the first 20 minutes of OLA. It has been reported that hypoxemia during OLA occurs in 13-40% of patients under inhalation anesthesia with FIO2 = 1.0. Our results show the total intravenous anesthesia using propofol is useful to maintain SpO2 during OLA. SpO2 during OLA tended to fall in the patients for right side operation, with lower SpO2 during two-lung ventilation and higher body mass index (BMI). However BMI has never been reported as a predictor of hypoxemia during OLA. A gravity-dependent mechanism is considered to be more responsible for the dependent regional volume reduction during OLA in patients in the lateral decubitus position.

The non-synaptic expression of transforming growth factor-beta 2 is neurally regulated and varies between skeletal muscle fibre types.

In adult skeletal muscles, transforming growth factor-beta 2 is restricted to the postsynaptic domain of the neuromuscular junction. The various putative functions of this transforming growth factor-beta 2 predict different patterns of transforming growth factor-beta 2 expression in denervated muscles. We therefore denervated rat tibialis anterior, extensor digitorum longus and soleus muscles and examined the expression of transforming growth factor-beta 2 using semi-quantitative reverse-transcription polymerase chain reaction and immunohistochemistry. Denervation up-regulated transforming growth factor-beta 2 expression extrasynaptically with little or no effect on synaptic expression. The up-regulation was detectable by one day, had become significant by three days and remained elevated for at least two weeks. This proves that the transforming growth factor-beta 2 associated with the neuromuscular junction is not under neural control and is consistent with transforming growth factor-beta 2 being a trophic factor for motoneurons. This pattern of transforming growth factor-beta 2 expression is similar to that described for other proteins associated with the neuromuscular junction, notably the acetylcholine receptor subunit genes. However, in contrast to the acetylcholine receptor subunit genes, the extent of up-regulation of transforming growth factor-beta 2 varied between fibre types, with the glycolytic IIB fibres being less affected than other fibre types.

Cell heterogeneity upon myogenic differentiation: down-regulation of MyoD and Myf-5 generates 'reserve cells'.

When a proliferating myoblast culture is induced to differentiate by deprivation of serum in the medium, a significant proportion of cells escape from terminal differentiation, while the rest of the cells differentiate. Using C2C12 mouse myoblast cells, this heterogeneity observed upon differentiation was investigated with an emphasis on the myogenic regulatory factors. The differentiating part of the cell population followed a series of well-described events, including expression of myogenin, p21(WAF1), and contractile proteins, permanent withdrawal from the cell cycle and cell fusion, whereas the rest of the cells did not initiate any of these events. Interestingly, the latter cells showed an undetectable or greatly reduced level of MyoD and Myf-5 expression, which had been originally expressed in the undifferentiated proliferating myoblasts. When these undifferentiated cells were isolated and returned to the growth conditions, they progressed through the cell cycle and regained MyoD expression. These cells demonstrated identical features with the original culture on the deprivation of serum. They produced both MyoD-positive differentiating and MyoD-negative undifferentiated populations once again. Thus the undifferentiated cells in the serum-deprived culture were designated 'reserve cells'. Upon serum deprivation, MyoD expression rapidly decreased as a result of down-regulation in approximately 50% of the cells. After this heterogenization, MyoD positive cells expressed myogenin, which is the earliest known event of terminal differentiation and marks irreversible commitment to this, while MyoD-negative cells did not differentiate and became the reserve cells. We also demonstrated that ectopic expression of MyoD converted the reserve cells to differentiating cells, indicating that down-regulation of MyoD is a causal event in the formation of reserve cells.

A murine specific splicing variant of the acetylcholine receptor epsilon-subunit gene transcript.

The acetylcholine receptor (AChR) is an ion channel involved in signal transmission from motorneuron to skeletal muscle. We describe here a murine-specific splicing variant of the epsilon subunit of the AChR (epsilon s), which lacks exon 5 epsilon s has a truncated extracellular domain which may affect the physiological characteristics of the resulting AChR channel.

Skeletal muscle fibre types: detection methods and embryonic determinants.

Muscle fibres used to be simply classified as either type I, IIa or IIb. Advances in molecular and histological techniques have, however, lead to the realisation that the phenotypes of muscles are more varied than this. An additional fibre type (IIX/IID) has been discovered, fibres with intermediate fibre types have been described and there is accumulating evidence that the fibres types described from the study of limb muscles are not necessarily applicable to other skeletal muscles, such as the jaw and extra-ocular muscles. Further to this has been the discovery that diversity occurs at all stages of muscle development. There are subpopulations of myoblasts and myotubes as well as various types of muscle fibres. The relationships between the different stages of development is still under study. However, it is clear that each stage of muscle development is influenced to a certain degree by prior events. Consequently, the characteristics of mature fibres reflect both their developmental origins and influences from the adult environment, such as their patterns of muscle activation.

[Hypercapnea during thoracoscopic surgery under regional anesthesia].

A 23-year-old woman was supposed to undergo thoracoscopic surgery for the 10th pneumothorax that accompanied histiocytosis X. The past history included Lylle's disease, asthma, myocarditis, drug-induced leucocytopenia and bronchitis obliterans. The preoperative arterial blood gas analysis under receiving O2 at rate of 2 l.min-1 via a nasal cannula revealed normal values. General anesthesia and intubation with a double-lumen endotracheal tube would have been preferable, but regional anesthesia was chosen because of her medical history and positive results of the skin tests for vecuronium, pancronium, diazepam and midazolam. During the first 10 min of thoracoscopic procedure, her respiration became rapid and shallow and she was restless and comatose. The operation was cancelled. Arterial blood gas analysis under receiving O2 at rate of 4 l.min-1 via a face mask revealed: pH 7.025, PaO2 113.8 mmHg, PaO2 244.8 mmHg, HCO3- 29.7 mEq.l-1, BE-5.6, and O2 saturation 99.1%. Manual artificial ventilation with a mask and bag was initiated. Her spontaneous respiration and consciousness recovered in next 30 min. The postoperative course was uneventful. Tachypnea, caused from anxiety, dyspnea and stimulation of irritant receptors in the airway, were considered to be responsible for the event. The duration of inspiration became shorter as tachypnea developed, that made the tidal volume to decrease and hypercapnea ensued.