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At least 19 recordsLinked to original sources
PubMed1998

Unifying characteristics of sites of anesthetic action revealed by combined use of anesthetics and non-anesthetics.

1. The usefulness of nonanesthetics in the study of mechanisms of general anesthesia lies in the possibility to identify the unifying characteristics of molecular sites that are shared by the anesthetics but not by the structurally similar nonanesthetics. 2. In model membranes, pairs of structurally similar anesthetics and nonanesthetics showed distinctly different submolecular distributions. 3. This difference may be the underlying cause for the different anesthetic and nonanesthetic interaction with gramicidin A, a model transmembrane cation channel. 4. Generalization of our findings suggests that the nature of the sites, whether in lipids or proteins, must be neither extremely hydrophilic nor extremely lipophilic, but amphiphilic.

Anesthetics↗
PubMed1997

Inhibition of nitric oxide synthase decreases anesthetic requirements of intravenous anesthetics in Xenopus laevis.

BACKGROUND: Acute inhibition of nitric oxide synthase (NOS) has been demonstrated to reduce the anesthetic requirements of volatile anesthetics. Recent data suggest that not only volatile but also intravenous anesthetic agents interact with nitric oxide (NO) metabolism. The aim of this study was to examine the effect of NOS inhibition by nitroG-L-arginine-methyl-ester (L-NAME) on the anesthetic action of the intravenous anesthetics thiopental, propofol, and ketamine. METHODS: The anesthetic potencies of thiopental, propofol, and ketamine were determined in Xenopus laevis tadpoles in the absence and presence of L-NAME. Anesthesia was defined as loss of righting reflex for 5 s. A nonlinear logistic regression curve was fitted to the data and half-maximal effective concentrations (EC50) were calculated. A second set of experiments was performed with different concentrations of L-NAME in the presence of the previously determined the EC50 of the intravenous anesthetics. RESULTS: The EC50s of the anesthetics thiopental, propofol, and ketamine were determined to be 25.5 +/- 2.0 microM, 1.9 +/- 0.1 microM, and 59.7 +/- 0.7 microM, respectively. The addition of L-NAME shifted the concentration-response curves to the left in a concentration-dependent manner. In the presence of 1 mM L-NAME, the EC50 of thiopental was reduced by 43%, the EC50 of propofol by 26%, and the EC50 of ketamine by 63%. The addition of D-NAME did not change the EC50 values of the three anesthetics. In the presence of L-arginine, the effect of L-NAME on the EC50 of thiopental was reversed. When administered by itself in a concentration range from 0.1 microM to 10 mM, L-NAME did not alter the behavior of the tadpoles. CONCLUSIONS: The results of the present study show that acute inhibition of NOS by L-NAME results in reduced anesthetic requirements of the intravenous anesthetics thiopental, propofol, and ketamine. This interaction of acutely administered L-NAME and intravenous anesthetics indicates that the NO-cyclic guanosine 3',5'-monophosphate system is involved in mediating the anesthetic effect of these compounds.

Anesthetics, Intravenous↗
PubMed2001

Solubilization study of local anesthetics into sodium dodecyl sulfate micelle using anesthetic cation selective electrodes.

The free concentrations of local anesthetic cations in equilibrium with sodium dodecyl sulfate (SDS) micelle which solubilized the anesthetic were determined by using ion-selective electrodes sensitive to local anesthetics, procaine (PC), lidocaine (LC), and mepivacaine (MC). Solubilizate distribution between water and SDS micelle was analyzed by means of the stepwise mass-action model. Association constant, K(1), was found to depend upon the anesthetic concentration, which decreased exponentially as the concentration of free anesthetic increased. Therefore, K(1) should include the interaction function &phi;(A) as K(1)=K(int)exp{-&phi;(A)} where K(int) is an intrinsic association constant. &phi;(A) is an increasing function of the anesthetic concentration, which means that occupation of a solubilization site by a local anesthetic cation makes sequential solubilization more difficult. The binding affinity of an anesthetic with SDS micelle increased in the following order PC<LC<MC.The critical micelle concentration (CMC) of mixed micelle was determined as a function of the concentration of free anesthetic. The CMC decreased with an increasing amount of anesthetics solubilized. All the anesthetic compositions in the micelle calculated thermodynamically from the CMC data were larger than the corresponding ones in the aqueous phase. Although the local anesthetics used here do not form micelles by themselves, the CMC vs composition curve can be regarded as a part of a micellar phase diagram showing the negative azeotropic behavior, which reflects the attractive interaction between the anionic surfactant micelle and the local anesthetic cation.

Journal Article↗
PubMed2002

The use of a uniquely designed anesthetic scavenging hood to reduce operating room anesthetic gas contamination during general anesthesia.

UNLABELLED: Numerous studies have suggested that chronic exposure to trace levels of anesthetic gas is harmful to operating room (OR) personnel. In the delivery of pediatric general anesthesia, an uncuffed endotracheal tube (ETT) is normally used which can result in considerable volatile anesthetic and nitrous oxide contamination of the OR. In this report, we present a method to reduce exposure to these anesthetic gases by means of an anesthetic scavenging hood (ASH). The ASH was used on six pediatric patients undergoing general endotracheal anesthesia via an uncuffed ETT. Measurements of all ambient gas levels were made 6 in. horizontally from the patient's ear and 6 in. from the table surface. The application of the vacuum source to the ASH resulted in a very significant (P < 0.01, paired t-test) decrease in levels of ambient anesthetic gas, with no measurable change in ventilatory variables or changes in body temperature (P > 0.05, paired t-test). Discontinuation of the vacuum force to the ASH resulted in a marked increase in ambient levels of anesthetic gas. We conclude that the ASH is extremely effective in reducing waste anesthetic gas associated with anesthesia administered via an uncuffed ETT. The ASH may be a valuable and cost-effective addition in the OR for both reducing ambient anesthetic waste gas levels and conserving patient heat. IMPLICATIONS: Chronic exposure to trace levels of anesthetic gas is harmful to operating room personnel, especially in the delivery of pediatric general anesthesia via an uncuffed endotracheal tube. The anesthetic scavenging hood is a cost-effective and efficient method to reduce these waste anesthetic gases, and it offers patient heat conservation.

Air Pollution, Indoor↗
PubMed1997

Titration calorimetry of anesthetic-protein interaction: negative enthalpy of binding and anesthetic potency.

Anesthetic potency increases at lower temperatures. In contrast, the transfer enthalpy of volatile anesthetics from water to macromolecules is usually positive. The transfer decreases at lower temperature. It was proposed that a few selective proteins bind volatile anesthetics with negative delta H, and these proteins are involved in signal transduction. There has been no report on direct estimation of binding delta H of anesthetics to proteins. This study used isothermal titration calorimetry to analyze chloroform binding to bovine serum albumin. The calorimetrically measured delta H cal was -10.37 kJ.mol-1. Thus the negative delta H of anesthetic binding is not limited to signal transduction proteins. The binding was saturable following Fermi-Dirac statistics and is characterized by the Langmuir adsorption isotherms, which is interfacial. The high-affinity association constant, K, was 2150 +/- 132 M-1 (KD = 0.47 mM) with the maximum binding number, Bmax = 3.7 +/- 0.2. The low-affinity K was 189 +/- 3.8 M-1 (KD = 5.29 mM), with a Bmax of 13.2 +/- 0.3. Anesthetic potency is a function of the activity of anesthetic molecules, not the concentration. Because the sign of delta H determines the temperature dependence of distribution of anesthetic molecules, it is irrelevant to the temperature dependence of anesthetic potency.

Anesthetics↗
PubMed1990

Effects of general anesthetics on the bacterial luciferase enzyme from Vibrio harveyi: an anesthetic target site with differential sensitivity.

The effects of a diverse range of 36 general anesthetics and anesthetic-like compounds on a highly purified preparation of the bacterial luciferase enzyme from Vibrio harveyi have been investigated. Under conditions where the flavin site was saturated, almost all of the anesthetics inhibited the peak enzyme activity and slowed the rate of decay. However, a small number of the more polar agents only inhibited at high concentrations, while stimulating activity at lower concentrations. The inhibition was found to be competitive in nature, with the anesthetics acting by competing for the binding of the aldehyde substrate n-decanal. The anesthetic binding site on the enzyme could accommodate only a single molecule of a large anesthetic but more than one molecule of a small anesthetic, consistent with the site having circumscribed dimensions. The homologous series of n-alcohols and n-alkanes exhibited cutoffs in inhibitory potency, but these cutoffs occurred at very different chain lengths (about C10 for the n-alkanes and C15 for the n-alcohols), mimicking similar cutoffs observed for general anesthetic potencies in animals. Binding constants determined from peak height measurements showed that the inhibitor binding site was predominantly hydrophobic (with a mean delta delta G CH2 of -5.0 kJ/mol), but fluctuations in the binding constants with chain length revealed regions in the binding site with polar characteristics. Binding constants to an intermediate form of the enzyme (intermediate II) were also determined, and these confirmed the principal features of the binding site deduced from the peak height measurements. The long-chain compounds, however, bound considerably tighter to the intermediate II form of the enzyme, and this was shown to account for the biphasic decay kinetics that were observed with these compounds. Overall, there was poor agreement between the EC50 concentrations for inhibiting the luciferase enzyme from V. harveyi and those which induce general anesthesia in animals, with bulky compounds being much less potent, and moderately long chain alcohols being much more potent, as luciferase inhibitors than as general anesthetics.

Alcohols↗
PubMed2004

Possible mechanism of irreversible nerve injury caused by local anesthetics: detergent properties of local anesthetics and membrane disruption.

BACKGROUND: Irreversible nerve injury may result from neural membrane lysis due to the detergent properties of local anesthetics. This study aimed to investigate whether local anesthetics display the same properties as detergents and whether they disrupt the model membrane at high concentrations. METHODS: Concentrations at which dodecyltrimethylammonium chloride and four local anesthetic (dibucaine, tetracaine, lidocaine, and procaine) molecules exhibit self-aggregation in aqueous solutions were measured using an anesthetic cation-sensitive electrode. Light-scattering measurements in a model membrane solution were also performed at increasing drug concentrations. The concentration at which drugs caused membrane disruption was determined as the point at which scattering intensity decreased. Osmotic pressures of anesthetic agents at these concentrations were also determined. RESULTS: Concentrations of dodecyltrimethylammonium chloride, dibucaine, tetracaine, lidocaine, and procaine at which aggregation occurred were 0.15, 0.6, 1.1, 5.3, and 7.6%, respectively. Drug concentrations causing membrane disruption were 0.09% (dodecyltrimethylammonium chloride), 0.5% (dibucaine), 1.0% (tetracaine), 5.0% (lidocaine), 10.2% (procaine), and 20% (glucose), and osmotic pressures at these concentrations were 278, 293, 329, 581, 728, and 1,868 mOsm/kg H2O, respectively. CONCLUSIONS: These results show that all four local anesthetics form molecular aggregations in the same manner as dodecyltrimethylammonium chloride, a common surfactant. At osmotic pressures insufficient to affect the membrane, local anesthetics caused membrane disruption at the same concentrations at which molecular aggregation occurred. This shows that disruption of the model membrane results from the detergent nature of local anesthetics. Nerve membrane solubilization by highly concentrated local anesthetics may cause irreversible neural injury.

Anesthetics, Local↗
PubMed1987

Does the duration of anesthetic administration affect the pharmacokinetics or metabolism of inhaled anesthetics in humans?

To define the effect of anesthetic duration on the pharmacokinetics of inhaled anesthetics, we determined the pharmacokinetics of isoflurane, enflurane, halothane, and methoxyflurane given simultaneously to seven healthy subjects for exactly 30 min and compared the results with data from a previous study in which these four anesthetics were administered for 120 min. End-tidal and mixed-expired anesthetic concentrations were measured during washin of anesthetic and for 3-9 days of washout. Multiexponential (multicompartment) models were fit by least squares to the alveolar washin and washout curves. We estimated the percentage of anesthetic that was metabolized from total uptake and recovery of anesthetic. Alveolar washout was more rapid after the shorter period of anesthetic administration. However, duration of administration did not affect the time constants determined, the number of compartments identified (i.e., five compartments were identified in both studies), or the percentages of anesthetic metabolized.

Adult↗
PubMed2004

Quality of post-anesthetic care in a hospital without a Post-Anesthetic Care Unit. A clinical audit.

AIM: The majority of Italian hospitals are not equipped with a Post- Anesthetic Care Unit. The aim of this study is to evaluate whether it is possible to guarantee post-anesthetic care according to current international quality and safety standards in the absence of such a structure. METHODS: Our hospital is not equipped with a Post-Anesthetic Care Unit and post-anesthetic assistance is assured by the anesthetist and anesthetic nurse themselves. In order to evaluate the quality of the post-anesthetic care a Recovery Chart was devised and strict discharge criteria defined: Recovery Score (modified Aldrete's score) = or >7; systolic blood pressure within 20% of the preoperative values; nausea/vomiting and shivering absent; pain absent/mild. A retrospective audit was conducted in 2 orthopedic operating rooms from January 10, 2000 to January 31, 2001 in order to evaluate major complications, observance of discharge criteria, postanesthetic care time. RESULTS: Incidence of complications was 2.6%. Observance of discharge criteria was 74%. In 26% of cases (69/261 cases) discharge criteria were not completely respected: 14 cases with unstable vital parameters; 46 cases with pain not under control; 6 cases with nausea/vomiting; 3 cases with shivering. In these cases monitoring and treatment was continued on the ward according to the anesthetist's prescriptions. None of these patients died or suffered major complications because of a quick discharge to the ward. Mean post-anesthetic care time was 40+/-18 minutes (median 35 minutes). CONCLUSION: Where the Post- Anaesthetic Care Unit is not available it is virtually impossible to guarantee post-anesthetic care according to current international quality and safety standards, because production pressure can lead the anesthetist to discharge the patient to the ward before he/she is completely stabilized. In these cases the anesthetist must accurately prescribe the necessary postoperative monitoring and treatment (analgesics, antiemetics, fluids, etc.) that must be continued in the surgical ward to guarantee the patient's safety, but it must be underlined that the surgical ward is not the appropriate place to carry on immediate post-anesthetic care.

Anesthesia↗
PubMed1997

Dehydration of Baralyme increases compound A resulting from sevoflurane degradation in a standard anesthetic circuit used to anesthetize swine.

UNLABELLED: In a model anesthetic circuit, dehydration of Baralyme brand carbon dioxide absorbent increases degradation of sevoflurane to CF2=C(CF3)OCH2F, a nephrotoxic vinyl ether called Compound A. In the present study, we quantified this increase using "conditioned" Baralyme in a circle absorbent system to deliver sevoflurane anesthesia to swine. Mimicking continuing oxygen delivery for 2 days after completion of an anesthetic, we directed a conditioning fresh gas flow of 5 L/min retrograde through fresh absorbent in situ in a standard absorbent system for 40 h. The conditioned absorbent was subsequently used (without mixing of the granules) in a standard anesthetic circuit to deliver sevoflurane to swine weighing 78 +/- 2 kg. The initial inflow rate of fresh gas flow was set at 10 L/min with the vaporizer at 8% to achieve the target end-tidal concentration of 3.0%-3.2% sevoflurane in approximately 20 min. The flow was later decreased to 2 L/min, and the vaporizer concentration was decreased to sustain the 3.0%-3.2% value for a total of 2 h (three pigs) or 4 h (eight pigs). Inspired Compound A increased over the first 30 +/- 60 min to a peak concentration of 357 +/- 49 ppm (mean +/- SD), slowly decreasing thereafter to 74 +/- 6 ppm at 4 h. The average concentration over 2 h was 208 +/- 25 ppm, and the average concentration over 4 h was 153 +/- 19 ppm. Pigs were killed 1 or 4 days after anesthesia. The kidneys from pigs anesthetized for both 2 h and 4 h showed mild inflammation but little or no tubular necrosis. These results suggest that dehydration of Baralyme may produce concentrations of Compound A that would have nephrotoxic effects in humans in a shorter time than would be the case with normally hydrated Baralyme. IMPLICATIONS: The vapor known as Compound A can injure the kidney. Dehydration of Baralyme, a standard absorbent of carbon dioxide in inhaled anesthetic delivery systems, can cause a 5- to 10-fold increase in Compound A concentrations produced from the inhaled anesthetic, sevoflurane, given at anesthetizing concentrations in a conventional anesthetic system.

Anesthesia, Closed-Circuit↗
PubMed1991

Saturable binding of anesthetics to nicotinic acetylcholine receptors. A possible mechanism of anesthetic action.

Recent controversies in the existence of saturable binding of general anesthetics in brain tissues prompted a careful examination of specific binding of anesthetics to neural receptors. We examined the binding of both local and general anesthetics using electron spin resonance and radioligand criteria. Our results suggested that the hydrophobic path, most probably through the lipid bilayer, figures importantly in the binding of the uncharged moieties of anesthetics. Competitive interactions by hydrophobic compounds for the high-affinity site in the nicotinic acetylcholine receptor led us to propose a hypothesis that includes a hydrophobic crevice of limited volume as part of the high-affinity site. Association of anesthetic at this crevice is in turn dependent on the anesthetic concentration in the lipid phase of the membrane. The hypothesis provides a mechanism for the saturable interaction of anesthetics with their protein target site in the membrane without violating the correlations expressed by the Meyer-Overton rule of anesthetic action.

Anesthesia↗
PubMed1993

The impact of streptozotocin-induced diabetes on the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics in the rat.

We designed experiments to examine the effects of insulin-dependent diabetes mellitus on the anesthetic requirements for volatile anesthetics. A standard tail-clamp technique was used to determine minimum alveolar anesthetic concentrations for halothane, enflurane, and isoflurane in spontaneously breathing rats. Three groups of animals were used: 1) diabetic rats (12 wk after induction of diabetes with streptozotocin, 50 mg/kg, single dose, intravenously), 2) insulin-treated (7 U extended insulin zinc suspension per day, subcutaneously, beginning 5 wk after streptozotocin treatment) diabetic rats, and 3) control rats. The minimum alveolar anesthetic concentration values of the control animals were 1.16 +/- 0.02 vol% for halothane, 2.25 +/- 0.05 vol% for enflurane, and 1.42 +/- 0.04 vol% for isoflurane. Minimum alveolar anesthetic concentration was reduced by 23% for halothane (0.90 +/- 0.06 vol%), by 18% for enflurane (1.85 +/- 0.07 vol%), and by 17% for isoflurane (1.18 +/- 0.04 vol%) in diabetic rats. Insulin treatment restored the anesthetic requirement to control levels for all three anesthetics. These data from the rat model indicate that uncontrolled diabetes lowers anesthetic requirements significantly.

Anesthesia, Inhalation↗
PubMed1981

Interfacial preference of anesthetic action upon the phase transition of phospholipid bilayers and partition equilibrium of inhalation anesthetics between membrane and deuterium oxide.

The half-height linewidth (v 1/2) of the 1H-NMR spectra of dipalmitoylphosphatidylcholine vesicles changes abruptly at the phase transition temperature. In the absence of inhalation anesthetics, proton signals from the choline head group (hydrophilic interface) and acyl-chain tails (lipid core) change at the same temperature of 39.6 degrees C. The present study compared the effect of four inhalation anesthetics, i.e., methoxyflurane, chloroform, halothane and enflurane, upon the ligand-induced phase transition of phosphatidylcholine vesicle membranes at 37 degrees C. The anesthetics showed differential action upon the phase transition of the phospholipid vesicle membranes between the lipid core and the hydrophilic interface. The concentrations of anesthetics which induced the phase transition of the lipid core were about 2-fold greater than those required for the phase transition of the interfacial choline head groups. From the area under the proton signals of inhalation anesthetics in the NMR spectra, the maximum solubilities of methoxyflurane, chloroform and halothane in 2H2O at 37 degrees C were determined to be 0.671 . 10(-4), 2.637 . 10(-4) and 1.398 . 10(-4) (expressed as mole fractions), or 3.35, 13.17 and 6.98 mmol/1000 g 2H2O, respectively. The solubilities of the anesthetic vapor in 2H2O expressed as mole fractions according to Henry's law ere 9.586 . 10(-4), 6.432 . 10(-4) and 2.311 10(-4)/atm (1.013 . 10(5) Pa) partial pressure, respectively. The presence of phospholipid vesicles in 2H2O increased the solubility of the inhalation anesthetics. From difference between solubility in 2H2O and a dipalmitoylphosphatidylcholine vesicle suspension, the partition coefficients of methoxyflurane, chloroform and halothane between the phospholipid vesicle membranes and 2H2O were estimated. These values, calculated from the mole fractions, were 3364, 1660 and 3850, respectively at 37 degrees C.

Anesthetics↗
PubMed2006

Temperature dependence of thermodynamic activity in volatile anesthetics: correlation between anesthetic potency and activity.

Temperature dependence of the saturated concentration and the activity coefficient of anesthetics (1-propanol, diethyl ether, chloroform, and halothane) in water were evaluated using vapor pressure and H NMR measurement. We found that these physical values (quantities) correlate with anesthetic potencies estimated according to the thermodynamic equilibrium model. The anesthetic potency for hydrophilic anesthetic (diethyl ether) decreased with decreasing temperature because of the temperature specificity of this saturated concentration. In contrast, potencies of hydrophobic anesthetics (chloroform and halothane) increased with decreasing temperature because of the temperature specificity of those activity coefficients. By assuming that anesthetics interact with hydrated water of cell membranes, the temperature dependence of anesthetic potencies in vivo is qualitatively explicable.

Anesthetics↗
PubMed1997

The response of anesthetic agent monitors to trifluoromethane warns of the presence of carbon monoxide from anesthetic breakdown.

OBJECTIVE: Trifluoromethane and CO are produced simultaneously during the breakdown of isoflurane and desflurane by dry CO2 absorbents. Trifluoromethane interferes with anesthetic agent monitoring, and the interference can be used as a marker to indicate anesthetic breakdown with CO production. This study tests representative types of gas monitors to determine their ability to provide a clinically useful warning of CO production in circle breathing systems. METHODS: Isoflurane and desflurane were reacted with dry Baralyme at 45 degrees C. Standardized samples of breakdown products were created from mixtures of reacted and unreacted gases to simulate the partial degrees of reaction which might result during clinical episodes of anesthetic breakdown using 1% or 2% isoflurane and 6% or 12% desflurane. These mixtures were measured by the monitors tested, and the indication of the wrong agent or a mixture of agents due to the presence of trifluoromethane was recorded and related to the CO concentration in the gas mixtures. RESULTS: When presented with trifluoromethane from anesthetic breakdown, monochromatic infrared monitors displayed inappropriately large amounts of isoflurane or desflurane. Agent identifying infrared and Raman scattering monitors varied in their sensitivity to trifluoromethane. Mass spectrometers measuring enflurane at mass to charge = 69 were most sensitive to trifluoromethane. CONCLUSION: Monochromatic infrared monitors were unable to indicate anesthetic breakdown via interference by trifluoromethane, but did indicate falsely elevated anesthetic concentrations. Agent identifying infrared and Raman monitors provided warning of desflurane breakdown via the interference of trifluoromethane by displaying the wrong agent or mixed agents, but may not be sensitive enough to warn of isoflurane breakdown Some mass spectrometers provided the most sensitive warnings to anesthetic breakdown via trifluoromethane, but additional data processing by some patients monitor units reduced their overall effectiveness.

Air Pollutants, Occupational↗
PubMed1998

The effect of adenosine triphosphate on sevoflurane requirements for minimum alveolar anesthetic concentration and minimum alveolar anesthetic concentration-awake.

UNLABELLED: We evaluated the effects of i.v. adenosine triphosphate (ATP) on sevoflurane minimum alveolar anesthetic concentration (MAC) and MAC-Awake. The study group included healthy patients 20-60 yr of age. The study groups for MAC-Awake determination included 49 patients who were scheduled for elective surgery. The study groups for MAC determination included 53 patients scheduled for elective surgery involving a skin incision. These patients were randomly assigned to two groups, an ATP group and a control group. The ATP group received 100 micrograms.kg-1.min-1 ATP i.v., and the control group received no medication. The ATP group and the control group were compared with regard to MAC-Awake (anesthetic concentration achieving 50% probability of eye opening in response to a verbal command) and MAC (anesthetic concentration achieving 50% probability of no movement in response to skin incision). The MAC-Awake was 0.7% +/- 0.1% in the control group (mean +/- SD) and 0.7% +/- 0.1% in the ATP group. MAC was 1.9% +/- 0.1% in the control group and 2.1% +/- 0.2% in the ATP group. The differences in MAC and MAC-Awake between the two groups were not statistically significant. We conclude that ATP infusion (100 micrograms.kg-1.min-1) has no effect on sevoflurane MAC and MAC-Awake. IMPLICATIONS: We found that an i.v. adenosine triphosphate infusion (100 micrograms.kg-1.min-1) has no effect on sevoflurane minimum alveolar anesthetic concentration (anesthetic concentration achieving 50% probability of no movement in response to skin incision) and minimum alveolar anesthetic concentration-Awake (anesthetic concentration achieving 50% probability of eye opening in response to a verbal command) in humans.

Adenosine Triphosphate↗
PubMed2000

Inhaled anesthetics have hyperalgesic effects at 0.1 minimum alveolar anesthetic concentration.

UNLABELLED: We investigated the hyperalgesic (antianalgesic) effect of the inhaled anesthetics isoflurane, halothane, nitrous oxide, and diethyl ether, or the nonimmobilizer 1, 2-dichlorohexafluorocyclobutane at subanesthetic partial pressures (or, for the nonimmobilizer, subanesthetic partial pressures predicted from lipid solubility) in rats. Hyperalgesia was assessed as a decrease in the time to withdrawal of a rat hind paw exposed to heat. All four anesthetics, including nitrous oxide and diethyl ether, produced hyperalgesia at low partial pressures, with a maximal effect at 0.1 minimum alveolar anesthetic concentration (MAC) required to prevent response to movement in 50% of animals, and analgesia (an increased time to withdrawal of the hind paw) at 0. 4 to 0.8 MAC. The nonimmobilizer had neither analgesic nor hyperalgesia effects. We propose that inhaled anesthetics with a higher MAC-Awake (the MAC-fraction that suppresses appropriate responsiveness to command), such as nitrous oxide and diethyl ether, can be used as analgesics because patients are conscious at higher anesthetic partial pressures, including those which have analgesic effects, whereas anesthetics with a lower MAC-Awake do not produce analgesic effects at concentrations that permit consciousness. IMPLICATIONS: The inhaled anesthetics isoflurane, halothane, nitrous oxide, and diethyl ether produce antianalgesia at subanesthetic concentrations, with a maximal effect at approximately one-tenth the concentration required for anesthesia. This effect may enhance perception of pain when such small concentrations are reached during recovery from anesthesia.

Anesthetics, Inhalation↗