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Minimum Alveolar Concentration (minimum + alveolar_concentration)
Selected AbstractsRegional cerebral glucose metabolism during sevoflurane anaesthesia in healthy subjects studied with positron emission tomographyACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2010L. SCHLÜNZEN Background: The precise mechanism by which sevoflurane exerts its effects in the human brain remains unknown. In the present study, we quantified the effects of sevoflurane on regional cerebral glucose metabolism (rGMR) in the human brain measured with positron emission tomography. Methods: Eight volunteers underwent two dynamic 18F-fluorodeoxyglucose positron emission tomography (PET) scans. One scan assessed conscious-baseline metabolism and the other scan assessed metabolism during 1 minimum alveolar concentration (MAC) sevoflurane anaesthesia. Cardiovascular and respiratory parameters were monitored and bispectral index responses were registered. Statistical parametric maps and conventional regions of interest analysis were used to determine rGMR differences. Results: All subjects were unconsciousness at 1.0 MAC sevoflurane. Cardiovascular and respiratory parameters were constant over time. In the awake state, rGMR ranged from 0.24 to 0.35 ,mol/g/min in the selected regions. Compared with the conscious state, total GMR decreased 56% in sevoflurane anaesthesia. In white and grey matter, GMR was averaged 42% and 58% of normal, respectively. Sevoflurane reduced the absolute rGMR in all selected areas by 48,71% of the baseline (P,0.01), with the most significant reductions in the lingual gyrus (71%), occipital lobe in general (68%) and thalamus (63%). No increases in rGMR were observed. Conclusions: Sevoflurane caused a global whole-brain metabolic reduction of GMR in all regions of the human brain, with the most marked metabolic suppression in the lingual gyrus, thalamus and occipital lobe. [source] Sevoflurane-induced post-conditioning has no beneficial effects on neuroprotection after incomplete cerebral ischemia in ratsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2010H.-M. LEE Background: The aim of this study was to investigate whether sevoflurane-induced post-conditioning has a neuroprotective effect against incomplete cerebral ischemia in rats. Methods: After cerebral ischemia by right common carotid artery occlusion in combination with hemorrhagic hypotension (35 mmHg) for 30 min, 1.0 minimum alveolar concentration of sevoflurane was administered for 15 min (Post-C 15, n=8), 30 min (Post-C 30, n=8), or 60 min (Post-C 60, n=8) in rats. Sevoflurane was not administered in control (n=8) and sham control rats (n=8). Neurologic evaluations were performed at 24, 48, and 72 h after ischemia. Degrees of neuronal damage in ischemic hippocampal CA1 and the cortex were assessed by counting eosinophilic neurons, and detection of DNA fragmentation was performed by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Results: Neurologic deficit scores in the Post-C 60 group were higher than in the control group at 48 and 72 h post-ischemia (P<0.05). No differences were observed in the percentages of eosinophilic neurons among the control (CA1: 37.3 ± 25.4, cortex: 26.0 ± 8.9), Post-C 15 (CA1: 54.0 ± 21.4, cortex: 30.8 ± 19.9), or Post-C 30 (CA1: 68.4 ± 17.5, cortex: 38.0 ± 11.0) groups in ischemic CA1 and cortices. However, in the Post-C 60 group, the percentages of eosinophilic neurons were higher than in the control group in CA1 and cortices (P<0.05). The percentages of TUNEL-positive cell were similar in the control group and the post-conditioned groups. Conclusion: These findings show that sevoflurane administration after ischemia does not provide neuroprotection in rats subjected to incomplete cerebral ischemia. [source] Sevoflurane and propofol depolarize mitochondria in rat and human cerebrocortical synaptosomes by different mechanismsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009R. BAINS Background and objectives: The mitochondrial membrane potential drives the main functions of the mitochondria. Sevoflurane depolarizes neural mitochondria. There is still, however, limited information concerning the effect of anaesthetics on neural mitochondria in humans. The effect of sevoflurane and propofol on the intracellular Ca2+ concentration [Ca2+]i and the mitochondrial membrane potential (,,m) was therefore compared in rat and human synaptosomes, and the changes were related to interventions in the electron transport chain. Methods: Synaptosomes from rat and human cerebral cortex were loaded with the fluorescent probes fura-2 ([Ca2+]i) and JC-1 (,,m) before exposure to sevoflurane 1 and 2 minimum alveolar concentration (MAC), and propofol 30 and 100 ,M. The effect on the electron transport chain was investigated by blocking complex V. Results: Sevoflurane and propofol decreased ,,m in rat synaptosomes in a dose-dependent manner, and to the same extent by equipotent doses. Inhibition of complex V enhanced the depolarizing effect of sevoflurane 2 MAC, but not of propofol 100 ,M. Neither sevoflurane nor propofol affected [Ca2+]i significantly. Sevoflurane and propofol decreased ,,m in human synaptosomes to the same extent as in the rat experiments. Conclusions: Sevoflurane and propofol at equipotent doses depolarize the mitochondria in rat and human nerve terminals to the same extent. The depolarizing effect of propofol on ,m was more rapid in onset than that of sevoflurane. Whereas sevoflurane inhibits the respiratory chain sufficiently to cause ATP synthase reversal, the depolarizing effect of propofol seems to be related to inhibition of the respiratory chain from complex I to V. [source] Isoflurane enhances spontaneous Ca2+ oscillations in developing rat hippocampal neurons in vitroACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2009Q. XIANG Background: During the nervous system development, spontaneous synchronized Ca2+ oscillations are thought to possess integrative properties because their amplitude and frequency can influence the patterning of neuronal connection, neuronal differentiation, axon outgrowth, and long-distance wiring. Accumulating studies have confirmed that some drugs such as volatile anesthetic isoflurane produced histopathologic changes in the central nervous system in juvenile animal models. Because the hippocampus plays an important role in learning and memory, the present work was designed to characterize the Ca2+ oscillations regulated by volatile anesthetic isoflurane in primary cultures of developing hippocampal neurons (5-day-cultured). Methods: Primary cultures of rat hippocampal neurons (5-day-cultured) were loaded with the Ca2+ indicator Fluo-4AM (4 ,M) and were studied with a confocal laser microscope. Results: Approximately 22% of 5-day-cultured hippocampal neurons exhibited typical Ca2+ oscillations. These oscillations were dose-dependently enhanced by isoflurane (EC50 0.5 MAC, minimum alveolar concentration) and this effect could be reverted by bicuculline (50 ,M), a specific ,-aminobutyric acid (GABAA) receptor antagonist. Conclusion: Unlike its depressant effect on the Ca2+ oscillations in adult neurons in previous researches, isoflurane dose-dependently enhanced calcium oscillations in developing hippocampal neurons by activating GABAA receptors, a major excitatory receptor in synergy with N -methyl- d -aspartate receptors at the early stages of development. It may be involved in the mechanism of an isoflurane-induced neurotoxic effect in the developing rodent brain. [source] Isoflurane-induced depolarization of neural mitochondria increases with ageACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2009RAVI BAINS Background and objectives: The mitochondrial membrane potential (,,m) drives the three fundamental functions of mitochondria, namely adenosine triphosphate (ATP) generation, Ca2+ uptake/storage, and generation/detoxification of ROS. Isoflurane depolarizes neural mitochondria. The sensitivity for general anesthetics increases with age, but the mechanism for this age-related sensitivity is still unknown. We compared the effect of isoflurane on [Ca2+]i and ,,m in isolated pre-synaptic terminals (synaptosomes) from neonatal, adolescent, and adult rats and the influence of interventions in the respiratory chain was assessed. Methods: Synaptosomes were loaded with the fluorescent probes fura-2 ([Ca2+]i) and JC-1 (,,m) and exposed to isoflurane 1 and 2 minimum alveolar concentration (MAC). The effect on the electron transport chain was investigated by blocking complexes I and V. Results: In neonatal rats isoflurane had no significant effect on ,,m. In adolescent and adult synaptosomes, however, isoflurane 1 and 2 MAC decreased ,,m. Isoflurane 2 MAC increased [Ca2+]i in neonatal and adolescent rats, but not in adult synaptosomes. In Ca2+ -depleted medium, isoflurane still decreased ,,m, while [Ca2+]i remained unaltered. By blocking complex V of the respiratory chain, the isoflurane-induced mitochondrial depolarization was enhanced in all age groups. Blocking complex I depolarized the mitochondria to the same extent as isoflurane 2 MAC, but without any additive effect. Conclusions: The depolarizing effect of isoflurane on neural mitochondria is more pronounced in the adolescent and adult than in neonatal synaptosomes. The increased mitochondrial sensitivity with age seems to be related to the reversed function of the ATP synthase of the electron transport chain. [source] Effect of anesthetic structure on inhalation anesthesia: Implications for the mechanismJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 6 2008Michael H. Abraham Abstract Many previous attempts (e.g., the Meyer,Overton hypothesis) to provide a single set of physical or chemical characteristics that accurately predict anesthetic potency have failed. A finding of a general predictive correlation would support the notion of a unitary theory of narcosis. Using the Abraham solvation parameter model, the minimum alveolar concentration, MAC, of 148 varied anesthetic agents can be fitted to a linear equation in log (1/MAC) with R2,=,0.985 and a standard deviation, SD,=,0.192 log units. Division of the 148 compounds into a training set and a test set shows that log (1/MAC) values can be predicted with no bias and with SD,=,0.20 log units. The two main factors that determine MAC values are compound size and compound hydrogen bond acidity, both of which increase anesthetic activity. Shape has little or no effect on anesthetic activity. Our observations support a unitary theory of narcosis by inhalation anesthetics. A two-stage mechanism for inhalation anesthesia accounts for the observed structural effects of anesthetics. In this mechanism, the first main step is transfer of the anesthetic to the site of action, and the second step is interaction of the anesthetic with a receptor(s). © 2007 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 97:2373,2384, 2008 [source] Volatile anaesthetics depolarize neural mitochondria by inhibiton of the electron transport chainACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2006R. Bains Background:, The mitochondrial membrane potential (,,m) controls the generation of adenosine triphosphate (ATP) and reactive oxygen species, and sequesteration of intracellular Ca2+[Ca2+]i. Clinical concentrations of sevoflurane affect the ,,m in neural mitochondria, but the mechanisms remain elusive. The aim of the present study was to compare the effect of isoflurane and sevoflurane on ,,m in rat pre-synaptic terminals (synaptosomes), and to investigate whether these agents affect ,,m by inhibiting the respiratory chain. Methods:, Synaptosomes were loaded with the fluorescent probes JC-1 (,,m) and Fura-2 ([Ca2+]i) and exposed to isoflurane or sevoflurane. The effect of the anaesthetics on the electron transport chain was investigated by blocking complex I and complex V. Results:, Isoflurane 1 and 2 minimum alveolar concentration (MAC) decreased the normalized JC-1 ratio from 0.92 ± 0.03 in control to 0.86 ± 0.02 and 0.81 ± 0.01, respectively, reflecting a depolarization of the mitochondrial membrane (n = 9). Isoflurane 2 MAC increased [Ca2+]i. In Ca2+ -depleted medium, isoflurane still decreased ,,m while [Ca2+]i remained unaltered. The effect of isoflurane was more pronounced than for sevoflurane. Blocking complex V of the respiratory chain enhanced the isoflurane- and sevoflurane-induced mitochondrial depolarization, whereas blocking complex I and V decreased ,,m to the same extent in control, isoflurane and sevoflurane experiments. Conclusions:, Isoflurane and sevoflurane may act as metabolic inhibitors by depolarizing pre-synaptic mitochondria through inhibition of the electron transport chain, although isoflurane seems to inhibit mitochondrial function more significantly than sevoflurane. Both agents inhibit the respiratory chain sufficiently to cause ATP synthase reversal. [source] Effect of acepromazine and butorphanol on isoflurane minimum alveolar concentration in goatsJOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2002T. J. DOHERTY No abstract is available for this article. [source] Inhibitory effects of desflurane and sevoflurane on oxytocin-induced contractions of isolated pregnant human myometriumACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 9 2005K. Yildiz Background:, In this study, we investigated the inhibitory effects of desflurane and sevoflurane on oxytocin-induced contractions of isolated human myometrium. Methods:, Following delivery of the infant and placenta, a small segment of myometrium was excised from the upper incisional surface of the lower uterine segment and 20 strips, randomly assigned into two groups (n = 10), were obtained from 20 non-laboring term parturients. The study protocol consisted of a 60-min period of spontaneous contractions, control recording with oxytocin 2 × 109 m (10-min period), washout interval of 10 min, volatile administration (three times per 15-min period) of 0.5, 1 and 2 minimum alveolar concentration (MAC), response to oxytocin (10-min period), a further washout interval (10-min period) and subsequent control recording with oxytocin without anesthetics. Results:, After oxytocin administration, the frequency and amplitude of contractions increased (P < 0.05) and the duration decreased (P < 0.05). The frequency and amplitude of contractions induced with oxytocin decreased significantly at 0.5, 1 and 2 MAC of desflurane and sevoflurane (P < 0.05). The amplitude of contractions was significantly different at 1 MAC between the two groups (P < 0.05). The duration of contractions at 2 MAC decreased in both groups (P < 0.05). Conclusions:, Desflurane and sevoflurane at 0.5, 1 and 2 MAC inhibit the frequency and amplitude of myometrial contractions induced with oxytocin in a dose-dependent manner. However, desflurane inhibits the amplitude less than sevoflurane at 1 MAC. We suggest that 0.5 MAC of both agents and 1 MAC of desflurane may be safely used in the presence of oxytocin following delivery of the infant and placenta during Cesarean section without fear of uterine atony and hemorrhage. [source] Comparison of recovery after intermediate duration of anaesthesia with sevoflurane and isofluranePEDIATRIC ANESTHESIA, Issue 4 2001Pierre-Yves Le Berre MD Background:,The purpose of this study was to compare recovery from anaesthesia after sevoflurane and isoflurane were administered to children for more than 90 min. Methods:,After parental informed consent and ethical committee approval, children aged between 2 months and 6 years, ASA I or II, were randomly allocated to sevoflurane (n=20) or isoflurane (n=20) groups. Halogenated agents were discontinued following skin closure and patients were ventilated mechanically with 100% oxygen until minimum alveolar concentration (MAC) values awake were obtained (endtidal concentrations 0.6 MAC for sevoflurane and 0.4 MAC for isoflurane). Effective perioperative analgesia was provided by a caudal block. Results:,The mean (± SD) duration of anaesthesia was 132 ± 38 min and 139 ± 49 min for sevoflurane and isoflurane, respectively. Early recovery occurred sooner in the isoflurane group (time to extubation was 16 ± 7 min and 11 ± 5 min, P<0.01; Aldrete's score at 0 min was 5.5 ± 1.5 and 7.4 ± 1.8, P<0.001, respectively). But the time to be fit for discharge from recovery room was similar at 136 ± 18 min and 140 ± 20 min, respectively. Conclusions:,After intermediate duration of anaesthesia administered to children for up to 90 min, isoflurane and sevoflurane allow recovery after approximatively the same lapse of time. [source] Minimum local analgesic concentration of ropivacaine for intra-operative caudal analgesia in pre-school and school age childrenANAESTHESIA, Issue 10 2010X. M. Deng Summary We compared the minimum local analgesia concentration of ropivacaine for intra-operative caudal analgesia in pre-school and school age children. Fifty-one boys, undergoing hypospadius repair surgery, were stratified into pre-school or school age groups. After induction of anaesthesia, caudal block was performed with ropivacaine 1 ml.kg,1 of the desired concentration. The first child in each group received ropivacaine 0.125%, and subsequent concentrations were determined by the analgesic response of the previous patient using Dixon's up-and-down method. Under general anaesthesia with 0.7 minimum alveolar concentration of sevoflurane, the minimum local analgesia concentration of ropivacaine for intra-operative caudal block was 34% greater in school age than in pre-school age boys (0.143% (95% CI 0.132,0.157%) vs 0.107% (95% CI 0.089,0.122%), respectively; p < 0.001). This study indicates that a higher concentration of ropivacaine is needed for school age than pre-school age children to provide intra-operative caudal analgesia when combined with general anaesthesia. [source] Nociceptin system does not affect MAC of volatile anaestheticsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2005S. Himukashi Background:, Nociceptin is the endogenous agonist of the opioid receptor-like (ORL) 1 receptor (NOP), and both nociceptin and NOP are widely expressed in the brain and spinal cord, which are target organs of general anaesthetics. As nociceptin has been reported to be involved in modulating pain mechanisms and stress responses, it is possible that the activity of the nociceptin system affects the anaesthetic potency of general anaesthetics. To address this possibility, we investigated the minimum alveolar concentrations (MACs) of various volatile anaesthetics in nociceptin receptor knockout mice (NOP,/,) and wild-type mice (NOP+/+). Methods:, We used male NOP,/, mice and NOP+/+ mice. MACs for halothane, isoflurane and sevoflurane were determined by the tail-clamp method. Results:, MACs for halothane, isoflurane and sevoflurane in NOP,/, mice were 1.60 (SD 0.06), 1.68 (0.08) and 3.36 (0.07)%, respectively. In NOP+/+ mice, MACs for halothane, isoflurane and sevoflurane were 1.59 (SD 0.07), 1.72 (0.07) and 3.38 (0.09)%, respectively. Conclusion:, MACs in NOP,/, mice did not significantly differ from those in NOP+/+ mice for halothane, isoflurane and sevoflurane. This result suggests that the nociceptin system does not affect the anaesthetic potency of volatile anaesthetics. [source] | ||||||||||