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PubMed1995

[Comparison of airway complications on tracheal extubation in deeply sevoflurane anesthetized versus awake children].

We investigated the incidence of respiratory complications and oxygen saturation level during emergence from sevoflurane anesthesia in children whose tracheas were extubated while they were anesthetized or after they became awake. Thirty children, aged 1-10 years, were studied. Anesthesia was induced with sevoflurane or thiopental and maintained with nitrous oxide, oxygen and sevoflurane. After nitrous oxide was discontinued at the end of surgery, the patients were randomly assigned to two groups: deeply anesthetized extubation group (anesthetized group) and awake extubation group (awake group). In anesthetized group, the patients were extubated while they were administered 1.5% or higher sevoflurane in 100% oxygen. In awake group, extubation was performed while the patients were awake. The incidence of respiratory complications such as apnea, laryngospasm, bronchospasm and arrythmias was not significantly different between the two groups. There was a significantly higher incidence of the airway obstruction but less incidence of cough and breath-holding in anesthetized group. Oxygen saturation level before and after tracheal extubation was not different between the two groups. In conclusion, with proper attention to airway obstruction, it may be possible to extubate while children are deeply anesthetized with sevoflurane.

Anesthesia, Inhalation↗

PubMed1996

Evaluation of five common induction protocols by comparison of hemodynamic responses to surgical manipulation in halothane-anesthetized horses.

OBJECTIVE: To determine whether hemodynamic responses of halothane-anesthetized horses undergoing surgical procedures depended on anesthetic induction protocols used, and to determine whether hemodynamic responses to surgical manipulation could be detected. DESIGN: Prospective experimental study without controls. ANIMALS: 36 clinically normal horses. PROCEDURE: Horses were allotted to 5 groups according to anesthetic induction protocol: acepromazine/guaifenesin/thiamylal, acepromazine/guaifenesin/ketamine, xylazine/guaifenesin/thiamylal, xylazine/guaifenesin/ketamine, and xylazine/diazepam/ketamine. Anesthesia was maintained with halothane. Hemodynamic measurements and blood gas values were obtained prior to the start of surgery, during surgery, and after surgery. RESULTS: Few differences in hemodynamic measurements existed between horses in which anesthesia was induced by 5 anesthetic induction protocols, whether prior to the start of surgery or for pooled values for all 3 measurement periods. Hemodynamic responses to surgical manipulation were marked and included increased mean arterial pressure and systemic vascular resistance, and decreased cardiac index and oxygen delivery. CLINICAL IMPLICATIONS: Choice of anesthetic induction protocol has little impact on hemodynamic function during surgery in halothane-anesthetized horses. Surgical stimulation may increase blood pressure, but does not improve cardiac index or oxygen delivery.

Acepromazine↗

PubMed1996

Effects of inhalation anesthetic agents on response of horses to three hours of hypoxemia.

OBJECTIVE: To study the effects of inhalation anesthetic agents on the response of horses to 3 hours of hypoxemia. DESIGN: Controlled crossover study. ANIMALS: Five healthy adult horses. PROCEDURE: Horses were anesthetized twice: once with halothane, and once with isoflurane in O2. Anesthetized horses were positioned in left lateral recumbency. Constant conditions for the study began at 2 hours of anesthesia. A constant agent dose of 1.2 minimum alveolar concentration, PaO2 of 50 +/- 5 mm of Hg, and PaCO2 of 45 +/- 5 mm of Hg were maintained for 3 hours. Circulatory measurements were made at 0.5, 1, 2, and 3 hours of hypoxemia (anesthesia hours 2.5, 3, 4, and 5). Blood was collected from horses for biochemical analyses before anesthesia, within a few minutes after standing, and at 1, 2, 4, and 7 days after anesthesia. RESULTS: Cardiac index was greater (P = 0.018) during isoflurane than halothane anesthesia. Cardiac index remained constant during the 3 hours of hypoxemia during halothane anesthesia, whereas it decreased from the baseline during isoflurane anesthesia. Marginally nonsignificant P values for an agent difference were detected for arterial O2 content (P = 0.051), and oxygen delivery (P = 0.057). Serum activities of aspartate transaminase (P = 0.050) and sorbitol dehydrogenase (P = 0.017) were higher in halothane-anesthetized horses than in isoflurane-anesthetized horses. Circulatory function was better in hypoxemic horses anesthetized with isoflurane than with halothane. Isoflurane resulted in less muscular injury in hypoxemia horses than did halothane anesthesia. Halothane anesthesia and hypoxemia were associated with hepatic insult. CONCLUSION: Isoflurane is better than halothane for hypoxemic horses.

Analysis of Variance↗

PubMed1996

Anesthetics produce subunit-selective actions on glutamate receptors.

We assessed the involvement of specific glutamate receptors in the action of anesthetics. In addition to the clinical anesthetics enflurane, isoflurane and halothane, we tested novel halogenated compounds, which are anesthetic or nonanesthetic in vivo, on glutamate receptor (GluR) subunits. these volatile compounds as well as pentobarbital and phenobarbital were tested on kainate-induced currents in Xenopus oocytes expressing GluR1, GluR3, GluR2+3 or GluR6 subunits. The anesthetic 1-chloro-1,2,2-triflurocyclobutane (F3) weakly inhibited kainate responses in oocytes expressing GluR3 receptors but not oocytes expressing GluR1 or GluR2+3 receptors. Surprisingly, F3 potentiated kainate responses in oocytes expressing the kainate-selective receptor GluR6. The nonanesthetics 2,3-chlorooctafluorobutane (F8) and 1,2-dichlorohexafluorocyclobutane (F6) did not affect GluR3 or GluR6 kainate responses. Isoflurane weakly inhibited although enflurane and halothane modestly inhibited kainate responses in oocytes expressing GluR1, GluR3 or GluR2+3 receptors. As with F3, isoflurane, enflurane and halothane potentiated kainate-induced currents of GluR6 receptors. The respective inhibitory and potentiating effects of halothane on GluR3 and GluR6 receptors were enhanced by increasing duration of halothane exposure. In contrast to the opposing action of volatile anesthetics, pentobarbital and phenobarbital inhibited GluR3 and GluR6 kainate responses and had a much greater effect on GluR6 receptors. These results provide novel evidence that anesthetics produce selective actions on glutamate receptors, suggesting that subunit composition may determine the role of glutamate receptors in anesthesia.

Anesthetics↗

PubMed1998

Cocaine and lidocaine with phenylephrine as topical anesthetics: antimicrobial activity against common nasal pathogens.

Topical anesthetics are commonly used in the evaluation of nasal pathology. The anesthetics routinely used, 4% lidocaine with phenylephrine, or 4% cocaine, have been demonstrated to have varying inhibitory effects on bacterial cultures. The present study examined the antimicrobial activity of these topical anesthetics used in nasal procedures. The pathogens used were Branhamella catarrhalis, Enterobacter sp., Haemophilus influenzae, Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus and Streptococcus pneumoniae. Organisms were against two-fold serial dilutions of stock preparations of 4% lidocaine with 0.25% phenylephrine, 0.25% phenylephrine, 0.1% methylparaben, 250 mg/ml ampicillin, and 4% cocaine. The minimum inhibitory concentration and minimum bactericidal concentration for each of the solutions were obtained. The bacteria studied varied gently in their susceptibility to lidocaine with phenylephrine versus cocaine: Cocaine consistently exhibited greater antimicrobial activity than lidocaine. Phenylephrine and methylparaben showed slight antimicrobial activity. These topical anesthetics have slight bactericidal activity against nasal pathogens, which can sometimes lead to false-negative results. Otolaryngologists should recognize the possible antimicrobial effects of topical anesthetics when culturing specimens. This is especially important when the specimen will be used for guidance of antimicrobial therapy, as in the case of the critically ill patient who requires aspiration for organism-specific therapy. Further studies, specifically in vivo experiments, are needed to determine if use of the drugs produces a significant change in the ability to culture organisms from these sites. This type of study would, however, be difficult to perform, since most patients requiring aspiration are already on high-dose antibiotics that would inhibit the growth of most microorganisms. A modified aspiration technique using a less concentrated topical anesthetic will likely be required to increase the chances of obtaining positive cultures.

Administration, Topical↗

PubMed1998

E. Coli bacteremia-induced changes in the skeletal muscle microcirculation vary with anesthetics.

AIM: To test if anesthetic procedures change the hemodynamic pattern in animals with experimental septic shock. METHODS: The effect of two anesthetics on systemic hemodynamic and skeletal muscle microcirculatory responses in high cardiac output live E. coli bacteremia was studied in rats and compared to the effect of two other anesthetic procedures in previously published studies. RESULTS: Baseline blood pressures and cardiac outputs were similar in rats with decerebrate, ketamine/xylazine, pentobarbital or urethane/chloralose anesthesia. There was a relative baseline tachycardia in decerebrate rats. Ketamine/xylazine anesthetized rats had reduced blood pressure, cardiac output, and heart rate. In decerebrate, pentobarbital, and urethane/chloralose anesthesia, cardiac output increased initially during bacteremia but did not remain elevated in pentobarbital anesthesia. Blood pressure and heart rate remained constant in pentobarbital, decerebrate, and urethane/chloralose anesth esia. During bacteremia, cardiac output, blood pressure, and vascular resistance did not change with ketamine/xylazine, but the heart rate increased. Baseline diameters of cremaster muscle large (A1) arterioles were higher in decerebrate anesthesia. A1 arterioles constricted during high cardiac output bacteremia in decerebrate rats, and pentobarbital or urethane/chloralose-anesthetized rats. A4 arterioles in bacteremia dilated in decerebrate and pentobarbital anesthesia, but did not change under urethane/chloralose and ketamine/xylazine anesthesia. CONCLUSION: Anesthetics influence baseline systemic variables and the response of systemic hemodynamics of rats to E. coli bacteremia. During bacteremia, anesthetics primarily affect the reactivity of skeletal muscle small arterioles. Ketamine/xylazine anesthesia has the most pronounced effect on systemic and microcirculatory variables and seems to be an inappropriate choice in sepsis experiments in rats.

Anesthetics↗

PubMed1997

Anesthetic regimen effects on a pediatric porcine model of asphyxial arrest.

The effects of three anesthetic regimens on an established model of pediatric porcine hypoxic-hypercarbic arrest were examined. Twenty-four preadolescent miniature piglets were paralyzed, mechanically ventilated and anesthetized with one of three regimens: IM + IV pentobarbital (n = 8); IM + IV ketamine (n = 8); or IM ketamine+inhaled isoflurane (n = 8). Asphyxial cardiopulmonary arrest was induced and, after and 8 min cardiac arrest nonintervention interval, a standardized protocol of manual CPR with mechanical ventilation was performed. Outcome variables included incidence of ventricular fibrillation, time to cardiac arrest, endogenous plasma epinephrine levels and arteriovenous epinephrine gradients. IV Ketamine anesthesia produced the highest incidence of ventricular fibrillation (P < 0.01 vs. pentobarbital and isoflurane). Time to asphyxia induced cardiac arrest was greatest for the pentobarbital group (P < 0.05 vs. ketamine and isoflurane). During induction of asphyxial cardiac arrest (low cardiac flow), endogenous venous epinephrine accumulation was highest in the pentobarbital anesthetized group (P < 0.05). After 8 min of untreated cardiac arrest and 1 min of CPR (low flow), arterial epinephrine levels were highest in the ketamine group (P < 0.05). Endogenous epinephrine gradients were venous > arterial in all groups at the end of the 8 min cardiac arrest non-intervention interval (no flow). After 1 min of CPR, the gradients had either equalized or reversed to arterial > venous in all groups except for pentobarbital. As designed and expected, return of spontaneous circulation did not occur in any animal. We conclude that, in developing models of porcine asphyxial cardiopulmonary arrest and resuscitation to simulate pediatric human arrest, variations in anesthetic regimen produce significant differences in parameters that are important to consider: time to asphyxia induced cardiac arrest, fibrillation threshold, plasma epinephrine level and arteriovenous epinephrine gradient. Anesthetic effects need to be carefully considered and clearly explained to facilitate the interpretation of studies of interventions in cardiopulmonary arrest and resuscitation.

Adjuvants, Anesthesia↗

PubMed2002

Anesthetics and the brain.

The action of anesthetics on the nervous system can be understood by considering their possible interactions with neuronal function. Anesthesia may be produced by a change in the balance of inhibitory synapses (notable via GABAa receptors) and excitatory synapses (notably glutamate receptors). Our knowledge of the specific mechanisms of anesthetic drugs and the structures in the CNS remains inadequate to explain the anesthetic state by one mechanism. The action of anesthetics can also be considered based on the action of the drugs on cerebral physiology, notably CMR, CBF, metabolic coupling, and autoregulation. Some specific anesthetic recommendations can be made for certain neurosurgical procedures and pathology based on the effects on physiology.

Anesthetics↗

PubMed2002

Influence of non-volatile anesthetics on the migration behavior of the human breast cancer cell line MDA-MB-468.

BACKGROUND: Anesthetic agents are known to influence functions of the immune system. Anesthetic drugs also support cancer progression by suppressing the activity of immune cells. In breast carcinoma an increase in expression of peripheral-type benzodiazepine receptors (PBR) and the gamma aminobutyl acid (GABA) level has been discovered. Therefore, an investigation of a direct influence of GABA-A agonist propofol, GABA-A and PBR-agonist etomidate, and the local anesthetic drug lidocaine, which can also bind to the GABA-A receptor and PBR, on migration of breast carcinoma cells was performed. METHODS: MDA-MB-468 cells were incubated with anesthetic agents using clinically relevant concentrations (propofol 3, 6, 9 mg/l, etomidate 2, 3, 4 mg/l, and lidocaine 1.25, 2.5, 5 mg/l). Locomotion was investigated in a three-dimensional collagen matrix using time-lapse video microscopy and computer-assisted cell-tracking. RESULTS: The percentage of migrating cells (57.4+/-1.9) as well as the velocity (0.22+/-0.09 microm/min) and distance migrated (89.4+/-66.8 microm/10 h) increased in the presence of propofol in a dose-dependent manner (up to 74.4+/-7.5, 0.30+/-0.09, 143.8+/-89.1, respectively) compared with the long chain triglyceride (LCT) control. In contrast, no influence of etomidate on the number of migrating cells could be observed. The velocity and distance migrated at 3 and 4 mg/l were found to be statistically significantly enhanced. Treatment with lidocaine caused an increase in the percentage of migrating cells (up to 75.0+/-5.6) in velocity dose dependently (up to 0.33+/-0.06) and in distance migrated (up to 151.5+/-92.9). CONCLUSION: These results show that different anesthetic drugs are able to modulate the migratory machinery of human breast carcinoma cells in vitro.

Adenocarcinoma↗

PubMed2006

Anesthetic technique (sufentanil versus ketamine plus midazolam) and quantitative electroencephalographic changes after cardiac surgery.

OBJECTIVES: Cardiac surgery involving cardiopulmonary bypass is associated with neurologic deterioration. Several interventions, including anesthetic techniques, have been designed to limit ischemic brain damage and have been evaluated in animals. Markers of neurologic injury may facilitate the assessment of these interventions in humans. DESIGN: A blinded randomized prospective study comparing 2 anesthetic techniques (one sufentanil-based, the other ketamine and midazolam-based) in patients undergoing cardiac surgery. Quantitative electroencephalography was used to detect postoperative neurologic injury. SETTING: Major teaching hospital. PARTICIPANTS: Forty-two patients aged 18 to 70 years undergoing cardiac surgery. INTERVENTIONS: Patients were anesthetized with either a sufentanil-based or a ketamine and midazolam-based technique for cardiac surgery with cardiopulmonary bypass. Quantitative electroencephalography was performed preoperatively as well as 5 to 6 days postoperatively. MEASUREMENTS AND MAIN RESULTS: Quantitative electroencephalography outcome did not differ (p > 0.05) between the 2 groups. It showed significant deterioration between preoperative and postoperative assessments with a decrease in faster and an increase in slower frequencies. In addition, the alpha attenuation index decreased. This may reflect a decrease in alertness. Both the intergroup comparisons and the assessment of individual changes failed to reveal significant differences between the anesthetic techniques. The adjuvant use of isoflurane correlated with less deterioration of quantitative electroencephalographic variables. CONCLUSIONS: The use of either sufentanil-based or ketamine and midazolam-based anesthetic techniques for cardiac surgery with cardiopulmonary bypass had no effects on a marker of postoperative neurologic injury (ie, quantitative electroencephalography).

Adjuvants, Anesthesia↗

PubMed2005

Anesthetic-induced burst suppression EEG activity requires glutamate-mediated excitatory synaptic transmission.

Many anesthetics evoke electroencephalogram (EEG) burst suppression activity in humans and animals during anesthesia, and the mechanisms underlying this activity remain unclear. The present study used a rat neocortical brain slice EEG preparation to investigate excitatory synaptic mechanisms underlying anesthetic-induced burst suppression activity. Excitatory synaptic mechanisms associated with burst suppression activity were probed using glutamate receptor antagonists (CNQX and APV), GABA receptor antagonists, and simultaneous whole cell patch clamp and microelectrode EEG recordings. Clinically relevant concentrations of thiopental (50--70 microM), propofol (5--10 microM) or isoflurane (0.7--2.1 vol%, 0.5--1.5 rat minimum aveolar concentration (MAC), 200--700 microM) evoked delta slow wave activity and burst suppression EEG patterns similar to in vivo responses. These effects on EEG signals were blocked by glutamate receptor antagonists CNQX (8.6 microM) or APV (50 microM). Depolarizing intracellular bursts (amplitude=34.7+/-4.5 mV; half width=132+/-60 ms) always accompanied EEG bursts, and hyperpolarization increased intracellular burst amplitudes. Barrages of glutamate-mediated excitatory events initiated EEG bursting activity. Glutamate-mediated excitatory postsynaptic currents were significantly depressed by higher anesthetic concentrations that depressed burst suppression EEG activity. A GABA(A) agonist produced a similar EEG effect to the anesthetics. It appears that anesthetic effects at both glutamate and GABA synapses contribute to EEG patterns seen during anesthesia.

Anesthetics↗

PubMed2002

The effects of intravenous anesthetics and lidocaine on proliferation of cultured type II pneumocytes and lung fibroblasts.

UNLABELLED: Type II pneumocytes synthesize surfactant and differentiate into type I pneumocytes to maintain the epithelium (1). Alveolar type II cell proliferation is required for reepithelization after acute lung injury (ALI) and is thought to minimize the subsequent fibrotic response (1). Keratinocyte growth factor (KGF) and hepatocyte growth factor (HGF) are among the most potent mitogen for type II epithelial cells, but not for fibroblasts in the lung (1). These growth factors attenuate several experimental ALI models by promoting epithelial repair (2,3). Thus, KGF and HGF may be a promising therapeutic approach to ALI. Critically ill patients with ALI often receive IV anesthetics or sedatives to facilitate mechanical ventilation. Furthermore, these patients sometimes undergo bronchoscopy under local anesthesia to obtain bronchoalveolar lavage fluid or to remove respiratory secretions. Several IV and local anesthetics inhibit proliferation of various cells including epithelium (4,5). If these anesthetics impede proliferation of type II pneumocytes, this suppressive effect may be a disadvantage for alveolar reepithelization in the course of recovery from ALI. In this study, we examined the effects of midazolam, propofol, ketamine, thiopental, and lidocaine on proliferation of type II alveolar epithelial cells using in vitro culture system. Because fibroblast proliferation is a key event in late phase of ALI, inhibition of this fibroproliferation is probably beneficial. Thus, we further determined whether these anesthetics could regulate proliferation of lung fibroblasts. In the current study, rolipram was used as a positive control. In our previous preliminary experiment, we found that rolipram, a phosphodiesterase inhibitor type IV, augments spontaneous or KGF-/HGF-promoted type II cell proliferation (6). IMPLICATIONS: Midazolam, ketamine, thiopental, propofol, or lidocaine did not inhibit proliferation of cultured rat type II pneumocytes. Our findings suggest that these anesthetics do not impede alveolar reepithelization after acute lung injury.

Anesthetics, Dissociative↗

PubMed1997

Increase of glutamate uptake in astrocytes: a possible mechanism of action of volatile anesthetics.

BACKGROUND: Glutamate is the most ubiquitous excitatory neurotransmitter in the vertebrate central nervous system. Astrocytes play an important role in terminating glutamatergic neurotransmission by removing released glutamate from the synaptic cleft. The authors examined the effects of several anesthetics on the glutamate uptake activity of astrocytes. METHODS: Cultured astrocytes from hippocampi of rat embryos were incubated with solution containing [3H]glutamate, which was pre-equilibrated with 0-4% halothane at 37 degrees C. The uptake activity was evaluated as the amount of radioactivity per cell of protein. RESULTS: When the reaction solution was equilibrated with 4% halothane, glutamate uptake increased to about 165% of the control. The effect of halothane was dose-dependent, and a significant augmentation (30-50%) of glutamate uptake was observed at a range in clinical use concentrations (1-2%). On the other hand, the uptake of gamma-aminobutyric acid, an inhibitory transmitter, was hardly affected by 1-4% halothane. The effect of halothane on glutamate uptake was also examined in neuron-rich culture, and similar augmentation was observed, although the extent was less than that in astrocyte culture. Biochemical subcellular fractions (i.e., glial plasmalemmal vesicles and synaptosomes) were also examined, however, only slight (not significant) increase was detected in the glutamate uptake activity. Other volatile anesthetics, such as enflurane, isoflurane, and sevoflurane, also enhanced glutamate uptake, whereas the intravenous anesthetics ketamine and pentobarbital showed no effect on glutamate uptake. CONCLUSIONS: The increase of glutamate uptake by astrocytes in the presence of volatile anesthetics potentially attenuates excitatory synaptic transmission in the entire central nervous system, a finding that may explain in part the action of volatile anesthetics.

Adjuvants, Anesthesia↗

PubMed2006

Effects of anesthetics on mutant N-methyl-D-aspartate receptors expressed in Xenopus oocytes.

Alcohols, inhaled anesthetics, and some injectable anesthetics inhibit the function of N-methyl-d-aspartate (NMDA) receptors, but the mechanisms responsible for this inhibition are not fully understood. Recently, it was shown that ethanol inhibition of NMDA receptors was reduced by mutation of residues in the transmembrane (TM) segment 3 of the NR1 subunit (F639A) or in TM4 of the NR2A subunit (A825W), suggesting putative ethanol binding sites. We hypothesized that the actions of other anesthetics might also require these amino acids and evaluated the effects of anesthetics on the NMDA receptors expressed in Xenopus oocytes with two-electrode voltage-clamp recording. Effects of hexanol, octanol, isoflurane, halothane, chloroform, cyclopropane, 1-chloro-1,2,2-trifluorocyclobutane, and xenon were reduced or eliminated in the mutant NMDA receptors, whereas the inhibitory effects of nitrous oxide, ketamine, and benzene were not affected by these mutations. Rapid applications of glutamate and glycine by a T-tube device provided activation time constants, which suggested different properties of ketamine and isoflurane inhibition. Thus, amino acids in TM3 and TM4 are important for the actions of many anesthetics, but nitrous oxide, benzene, and ketamine seem to have distinct mechanisms for inhibition of the NMDA receptors.

Amino Acid Substitution↗

PubMed1989

Anesthetic techniques for the management of cancer pain.

This review focuses on available anesthetic techniques for cancer patients, the indications, and appropriate agents for these potent tools in a stepwise approach to cancer pain. Anesthetic procedures are desirable when they will not compromise bodily functions important to the patient, and when tumor-directed therapy and noninvasive or less-invasive, low-risk approaches (primarily pharmacologic tailoring of analgesic drugs) fail to control pain. Nondestructive techniques include the epidural/intrathecal use of opioids via an implanted catheter, and local anesthetic blocks of nerves and sympathetic ganglia. Chronic intrathecal or epidural opioid infusion seems ideal if the life expectancy is 2 to 3 months. Local anesthetic blocks can help prognosticate results of subsequent neurolytic blocks, including undesirable effects. Destructive anesthetic procedures comprise injections of neurolytic agents (most commonly phenol or alcohol), and insertion of freezing probes, into nerves and ganglia. The types of nerve blocks performed, their complications, and success rates, and limitations of commonly used neurolytic agents as well as their proper applications, are described. The importance of proper patient selection and knowledge of the pathophysiology of the pain being treated is stressed, as is the appropriate timing of anesthetic procedures in the course of the disease.

Analgesics, Opioid↗

PubMed1993

Effects of four intravenous anesthetic agents on motor evoked potentials elicited by magnetic transcranial stimulation.

The influence of four intravenous anesthetic agents on motor evoked potentials (MEPs) elicited by transcranial magnetic stimulation (magnetic MEP) was examined in 77 subjects. The patients were anesthetized by a continuous intravenous infusion of one of the following anesthetic agents: propofol, etomidate, methohexital, or thiopental. Comparable anesthetic effects among the four agents were achieved by computing an infusion scheme for each drug. Infusion rates were increased slowly in a step-wise manner in order to reach minimal anesthetic blood concentrations within 15 minutes. During anesthesia induction, magnetic MEPs were recorded every 2 minutes from the abductor pollicis brevis muscle. The patient's level of consciousness was assessed and documented in the alternating minutes. A dose-related reduction of the MEP amplitudes was seen in all drug groups, while the latencies remained constant. Reduction of the amplitude was occasionally so prominent that the MEP was completely abolished before adequate anesthesia was achieved. MEPs were obtainable at the end of anesthesia induction in 14% of the propofol group (n = 22), 57% of the etomidate group (n = 21), 53% of the methohexital group (n = 19), and 20% of the thiopental group (n = 15). Propofol and thiopental showed significantly stronger suppression of MEP, when compared to etomidate (both P < 0.01) and to methohexital (P = 0.01 and 0.05, respectively). Etomidate was the least detrimental anesthetic agent for intraoperative monitoring of magnetic MEP. Nonetheless, the low incidence of 57% of preserved MEP in subjects without motor deficits indicated the inadequacy of this technique for intraoperative monitoring. More effective transcranial stimulation techniques are required for successful intraoperative MEP monitoring.

Adult↗

PubMed1991

Effect of inhalation anesthetics on swimming activity of artemia salina.

The swimming movement of artemia salina in the artificial sea water was measured by using the video camera system in the absence and presence of anesthetics, i.e. enflurane, halothane, and isoflurane. The movement of artemia looked random at a glance but the obtained distribution curve for the swimming speed was skewed toward the high speed side somewhat resembling a Maxwellian distribution curve seen in the statistics of ideal gases. When anesthetic were added, the distribution curve became sharpened and shifted to the low speed side, which is similar to a behavior of ideal gases when they are cooled down. The mean swimming-speed was decreased eventually leading to an irreversible death with increasing the anesthetic dose. The activity was analyzed by using the hydrodynamic equation. The ED(50), which is a dose that causes a 50% reduction in the activity, of all anesthetics used in this study was quite similar to the MAC values for human. It was also suggested that an interaction between anesthetics and artemia was highly cooperative since the larger Hill coefficients were obtained for all three anesthetics used.

Journal Article↗

PubMed1982

Interfacial adsorption of an inhalation anesthetic onto ionic surfactant micelles and its desorption by high pressure.

The effects of pressure and temperature on the critical micelle concentration (CMC) of sodium dodecylsulfate (SDS) wer measured in the presence of various concentrations of an inhalation anesthetic, methoxyflurane. The change in the partial molal volume of SDS on micellization delta Vm, increased with the increase in the concentration of methoxyflurane. The CMC-decreasing power, which is defined as the slope of the linear plot between In(CMC) vs. mole fraction of anesthetic, was determined as a function of pressure and temperature. Since the CMC-decreasing power is correlated to the micelle/water partition coefficient of anesthetic, the volume change of the transfer (delta Vop) of methoxyflurane from water to the micelle can be determined from the pressure dependence of the CMC-decreasing power. The value of delta Vop amounts 6.5 +/- 1.8 cm3.mol-1, which is in reasonable agreement with the volume change determined directly from the density data, 5.5+/-0.6 cm3.mol-1. Under the convention of thermodynamics, this indicates that the application of pressure squeezes out anesthetic molecules from the micelle. The transfer enthalpy of anesthetic from water to the micelle is slightly endothermic. The partial molal volume of methoxyflurane in the micelle (112.0 cm3.mol-1) is smaller than that in decane (120.5 cm3.mol-1) and is larger than that in water (108.0 cm3. mol-1. This indicates that the anesthetic molecules are incorporated into the micellar surfaces region, i.e., the palisade layer of the micelle in contact with water molecules, rather than into the micelle core.

Anesthesia, Inhalation↗