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PubMed1997

Suppression of acetylcholine-induced relaxation by local anesthetics and vascular NO-cyclic GMP system.

BACKGROUND: Local anesthetics have been demonstrated to attenuate acetylcholine-induced relaxation of vascular smooth muscle, but the mechanism responsible has not been elucidated. The present study was undertaken to ascertain whether this effect of local anesthetics is due to suppression of the vascular nitric oxide (NO)-cyclic GMP (cGMP) system. METHODS: Isolated rat aortae were cut into helical strips and mounted in bathing solution to measure isometric tension changes. They were precontracted with phenylephrine (0.3 microM) then exposed to cumulative concentrations of relaxants including acetylcholine, sodium nitroprusside (SNP) and papaverine, in the absence or presence of local anesthetics. Aortae for cGMP measurements were cut longitudinally into pairs of strips and bathed in the solution without tension. In the absence or presence of anesthetics, they were stimulated with acetylcholine or SNP, and the cGMP content of each strip was radioimmunoassayed. RESULTS: Acetylcholine-induced, endothelium-dependent relaxation of phenylephrine-precontracted aortae was attenuated by lidocaine (30-300 microM), tetracaine (10-30 microM), bupivacaine (10-100 microM) and ropivacaine (30-100 microM). SNP-induced relaxation was attenuated by lidocaine (300 microM), tetracaine (30 microM), bupivacaine (10-100 microM) and ropivacaine (30-100 microM). Papaverine-induced relaxation was attenuated by lidocaine (300 microM), bupivacaine (30-100 microM) and ropivacaine (30-100 microM), and augmented by tetracaine (30 microM). Cyclic GMP levels in acetylcholine-stimulated aortae were reduced significantly by lidocaine (300 microM), tetracaine (100 microM) and bupivacaine (300 microM) treatment, but not by ropivacaine (300 microM). SNP-stimulated cGMP levels were reduced by tetracaine (100 microM) but not by any other anesthetics at the concentrations tested. CONCLUSION: We conclude that lidocaine, tetracaine and bupivacaine suppress acetylcholine-stimulated formation of cGMP. However, the attenuation of acetylcholine-induced relaxation by local anesthetics is not totally ascribable to reduced cGMP levels.

Acetylcholine↗

PubMed2005

Pre-anesthetic presence of an injured dam influences pups' locomotor behavior during emergence from anesthesia in rats.

BACKGROUND: Pre-anesthetic mother-infant interaction is an important factor for smooth emergence of pediatric anesthesia. In many mammalian species, disruptions of the mother-infant relationship cause psychological and behavioral changes. This study was to investigate whether or not pre-anesthetic presence of an injured dam has an impact on locomotor behavior of rat pups. METHODS: We used a video-tracking system to test the effects of pre-anesthetic relations between pups and their dams on pups' locomotor behavior during emergence from general anesthesia, in 40 3-week-old Sprague-Dawley male rats. Pups were divided into two groups: pups housed with a dam (n = 20) and those housed with an injured dam (n = 20). Pups were anesthetized with 1.2% halothane for 30 min. At emergence, we recorded their locomotor behavior for 15 min. RESULTS: Pre-anesthetic manipulation to dams significantly increased the distance traveled by pups. However, the manipulation did not cause any difference in the maximum velocity. CONCLUSION: Pre-anesthetic presence of an injured dam influenced pups' locomotor behavior at emergence from anesthesia.

Anesthesia Recovery Period↗

PubMed2006

Volatile anesthetics evoke prolonged changes in the proteome of the left ventricule myocardium: defining a molecular basis of cardioprotection?

BACKGROUND: Volatile anesthetics can alter cardiac gene and protein expression. Of those underlying molecular changes in gene and protein expression in the myocardium after exposure to volatile anesthetics that have been identified, some of them have been related to cardioprotection. METHODS: We used two-dimensional gel electrophoresis and mass spectrometry to identify changes in the protein expression of the left ventricle myocardium of anesthesized rats. We maintained anesthesia for 3 h using isoflurane, sevoflurane or desflurane, respectively, at 1.0 minimum alveolar concentration (MAC) and dissected the left ventricular myocardium either immediately or 72 h after the end of anesthesia. RESULTS: We found changes of at least twofold in 106 proteins of the more than 1.600 protein spots discriminated in each gel. These differentially expressed proteins are associated with functions in glycolysis, mitochondrial respiration and stress response. No obvious difference could be observed between the patterns of differential expression of the three volatile anesthetics. CONCLUSION: We provide the first study of post-anesthetic protein expression profiles associated with three common volatile anesthetics. These volatile anesthetics promote a distinct change in the myocardial protein expression profile, whereby changes in the expression pattern still exist 72 h after anesthesia. These proteome changes are closely related to cardioprotection and ischemic preconditioning, indicating a common functional signaling of volatile anesthestics.

Anesthetics, Inhalation↗

PubMed1985

Catabolism of exogenous and endogenous sphingomyelin and phosphatidylcholine by homogenates and subcellular fractions of cultured neuroblastoma cells. Effects of anesthetics.

Cultured murine neuroblastoma cells contain a neutral, Mg2+-stimulated sphingomyelinase and an alkaline phosphatidylcholine-hydrolyzing activity that are enriched in the plasma membrane fraction. The reaction products of sphingomyelin catabolism are phosphocholine and ceramide and those of phosphatidylcholine, glycerophosphocholine and fatty acid. These reactions were studied with endogenous as well as exogenous liposomal substrates. With both exogenous and endogenous substrates, the sphingomyelinase activity was stimulated two- to threefold by Mg2+ and a further three- to fourfold by volatile anesthetic agents. Stimulation was concentration-dependent and corresponded to anesthetic potency: methoxyflurane greater than halothane greater than enflurane. Greater than 80% of the plasma membrane sphingomyelin was hydrolyzed within 2 h in the presence of Mg2+ and anesthetic. In contrast, the activity with exogenous and endogenous phosphatidylcholine was unaffected by Mg2+ or Ca2+ and was markedly inhibited (50-80%) by anesthetic agents. The degree of inhibition was concentration-dependent and corresponded to anesthetic potency. The quantitative importance of choline-containing lipids in cell membranes, the relatively exclusive localization of the neutral Mg2+-stimulated sphingomyelinase in cells of neural origin, the totally different type of hydrolytic attack on phosphatidylcholine, and the reciprocal effects of anesthetics on the hydrolysis of these two lipids strongly suggest important roles for these activities in cell membranes in general and in the neuron in particular.

Anesthetics↗

PubMed1996

Local anesthetics.

BACKGROUND: Dermatology is dependent upon the effects of local anesthetics for diagnostic and therapeutic interventions. A working knowledge of the drugs' actions and interactions is necessary for anyone aspiring to optimize the benefits derived from the use of local anesthetic agents. OBJECTIVE: This article reviews nerve physiology, pharmacology, classification of local anesthetics, adverse reactions (toxic, drug, allergic), local anesthetic use in pregnancy, alternatives to the "-caine" anesthetics, methods for reducing the pain of infiltration, and new agents under development. CONCLUSION: Local anesthetics are safe and effective. With the understanding of the actions and interactions of this class of drugs, maximum patient safety and satisfaction can be achieved.

Anesthesia, Local↗

PubMedDate not supplied

Effects of various anesthetic agents on laryngeal motion during laryngoscopy in normal dogs.

OBJECTIVE: To evaluate the effects of various drugs and drug combinations conventionally used for anesthesia on arytenoid cartilage motion during laryngoscopy in normal dogs. STUDY DESIGN: Experimental study. ANIMALS: Six large breed healthy dogs with no previous history of respiratory dysfunction. METHODS: Each dog was randomly assigned to a different injectable anesthetic protocol once weekly for 6 weeks, then in the 7th week all dogs were anesthetized with isoflurane. Videolaryngoscopy was performed and recorded starting immediately after induction until dogs could no longer be safely restrained for endoscopy. Video was digitized and 3 still images of maximal inspiration and expiration from the first 15 seconds (induction) and the last 15 seconds (recovery) were captured and imported into an image analysis software program. The height and area of the laryngeal ostium were measured in pixels. Normalization of the glottal gap area was performed using the formula (normalized glottal gap area (NGGA)=area in pixels/height(2)). ANOVA was performed on the NGGA of images collected at inspiration and expiration during induction and recovery. Fischer's exact test was performed when significance (P<.05) was found. RESULTS: Within each protocol, laryngeal motion (defined as change in NGGA) at induction was not significantly different from laryngeal motion measured at recovery. Additionally, no significant differences were found in arytenoid motion immediately after induction when anesthetic protocols were compared. Arytenoid motion before recovery was significantly greater with thiopental when compared with propofol (P=.046), ketamine+diazepam (P=.0098), acepromazine+thiopental (P=.0021), and acepromazine+propofol (P=.0065). No significant difference in arytenoid motion was seen immediately after induction or before recovery when acepromazine+butorphanol+ isoflurane and thiopental were compared. CONCLUSION: We concluded that intravenous thiopental given to effect is the best choice for assessing laryngeal function in dogs. Dogs premedicated with acepromazine with or without opioids that require further anesthetic restraint for laryngoscopy should be anesthetized with isoflurane administered by mask. CLINICAL RELEVANCE: Misdiagnosis of laryngeal paralysis during laryngoscopy can be avoided by selecting the anesthetic regimens with the least effect on arytenoid motion.

Acepromazine↗

PubMed1980

Interaction of four local anesthetics with phospholipid bilayer membranes: permeability effects and possible mechanisms.

Sodium 22 efflux was measured, at various temperatures, in the presence of different local anesthetics (dibucaine, tetracaine, benzocaine, procaine) in multilamellar liposomes composed of saturated phosphatidylcholines and dicetyl phosphate. These liposomes display a permeability maximum in the temperature region of their respective phase transitions. Local anesthetics cause this permeability maximum to occur at a lower temperature and also increase its magnitude. Binding of the anesthetics to these liposomes displays a biphasic temperature curve with a maximum in the vicinity of the transition temperature. In addition there appears to be a linear relationship between aqueous anesthetic concentrations causing equal permeability effects and corresponding membrane concentrations. All of the anesthetics decrease the cooperativity of the lipid phase transition and this is probably an important factor underlying induced permeability effects. However several observations suggest that additional factors are also important and we have postulated that one such factor is the preferential binding of the anesthetics to phase boundary regions.

Anesthetics, Local↗

PubMed2001

Anesthetics and ion channels: molecular models and sites of action.

The mechanisms of general anesthesia in the central nervous system are finally yielding to molecular examination. As a result of research during the past several decades, a group of ligand-gated ion channels have emerged as plausible targets for general anesthetics. Molecular biology techniques have greatly accelerated attempts to classify ligand-gated ion channel sensitivity to general anesthetics, and have identified the sites of receptor subunits critical for anesthetic modulation using chimeric and mutated receptors. The experimental data have facilitated the construction of tenable molecular models for anesthetic binding sites, which in turn allows structural predictions to be tested. In vivo significance of a putative anesthetic target can now be examined by targeted gene manipulations in mice. In this review, we summarize from a molecular perspective recent advances in our understanding of mechanisms of action of general anesthetics on ligand-gated ion channels.

Anesthetics↗

PubMed1994

Hypothermia modifies anesthetic effect on contractile force and Ca2+ transients in cardiac Purkinje fibers.

Mild hypothermia enhances cardiac contractility, and volatile anesthetics depress contractility. Contractile force (tension) and Ca2+ transients were measured in canine Purkinje fibers at 35 and 25 degrees C with and without halothane and isoflurane to examine how anesthetics attenuate the positive inotropic effect of mild hypothermia. Isometric tension and light emitted from the photoprotein aequorin were used to assess contractility and intracellular Ca2+ transients in fibers stimulated at 40-60 pulses/min. At 35 degrees C, each anesthetic depressed peak tension and peak Ca2+ transients and decreased contractile force duration but, for halothane, increased Ca2+ transient duration. Decreases in tension by both anesthetics at 35 degrees C were converted to marked increases in tension at 25 degrees C, whereas Ca2+ transients were little changed. Removal of anesthetics at 25 degrees C greatly increased tension with a small increase in Ca2+ transients that was much lower than that at 35 degrees C. The curve relating peak contractile force as a function of Ca2+ transients at 25 degrees C during stepwise increases in extracellular CaCl2 was shifted steeper and leftward of the curve at 35 degrees C. These studies suggest that the positive inotropic effect of mild hypothermia is due primarily to increased myofibrillar Ca2+ sensitivity and that anesthetics decrease tension during hypothermia by decreasing myofibrillar Ca2+ sensitivity. Reduced influx of transsarcolemmal or sarcoplasmic reticular Ca2+ may also play a role during mild hypothermia.

Aequorin↗

PubMed1995

Volatile anesthetics inhibit voltage-dependent Ca2+ channels in porcine tracheal smooth muscle cells.

The relaxation of airway smooth muscle by volatile anesthetics is associated with a decreased concentration of intracellular free Ca2+. We hypothesized that inhibition of the entry of extracellular Ca2+ contributes to the relaxation. We therefore examined the effects of halothane, isoflurane, and sevoflurane on macroscopic voltage-activated Ca2+ currents (ICa) in porcine tracheal smooth muscle cells, using the whole cell patch-clamp technique. All three volatile anesthetics significantly inhibited ICa in a dose-dependent manner with no apparent shift in the voltage dependence of induced ICa. The order of inhibitory potencies for ICa was halothane > isoflurane > sevoflurane. When data were plotted as a function of the estimated anesthetic concentrations in the lipid phase, the potencies for inhibition of ICa by the three anesthetics were indistinguishable. We conclude that volatile anesthetics have an inhibitory effect on ICa of porcine tracheal smooth muscle cells at clinically relevant concentrations and that the inhibitory potencies of volatile anesthetics on ICa are closely related to their lipid-phase solubilities.

Anesthetics↗

PubMed1991

Effects of anesthetic agents on systemic critical O2 delivery.

The present study tested the hypothesis that anesthetic agents can alter tissue O2 extraction capabilities in a dog model of progressive hemorrhage. After administration of pentobarbital sodium (25 mg/kg iv) and endotracheal intubation, the dogs were paralyzed with pancuronium bromide, ventilated with room air, and splenectomized. A total of 60 dogs were randomized in 10 groups of 6 dogs each. The first group served as control (C). A second group (P) received a continuous infusion of pentobarbital (4 mg.kg-2.h-2), which was started immediately after the bolus dose. Three groups received enflurane (E), halothane (HL), or isoflurane (I) at the end-tidal concentration of 0.7 minimum alveolar concentration (MAC). The sixth group received halothane at the end-tidal concentration of 1 MAC (HH). Two groups received intravenous alfentanil at relatively low dose (AL) or high dose (AH). The last two groups received intravenous ketamine at either relatively low dose (KL) or high dose (KH). In each group, O2 delivery (Do2) was progressively reduced by hemorrhage. At each step, systemic Do2 and O2 consumption (VO2) were measured separately and the critical point was determined from a plot of Vo2 vs. Do2. The critical O2 extraction ratio (OER) in the control group was 65.0 +/- 7.8%. OER was lower in all anesthetized groups (P, 44.3 +/- 11.8%; E, 47.0 +/- 7.7%; HL, 45.7 +/- 11.2%; I, 44.3 +/- 7.1%; HH, 33.7 +/- 6.0%; AL, 56.5 +/- 9.6%; AH, 43.5 +/- 5.9%; KH, 57.7 +/- 7.1%), except in the KL group (78.3 +/- 10.0%). The effects of halothane and alfentanil on critical OER were dose dependent (P less than 0.05), whereas critical OER was significantly lower in the KH than in the KL group. Moreover, the effects of anesthetic agents on critical Do2 appeared related to their effects on systemic vascular resistance. Anesthetic agents therefore alter O2 extraction by their peripheral vascular effects. However, ketamine, with its unique sympathetic stimulant properties, had a lesser effect on OER than the other anesthetic agents. It could therefore be the anesthetic agent of choice in clinical situations when O2 availability is reduced.

Anesthesia, Intravenous↗

PubMed1996

Role of mast cells, basophils and their mediators in adverse reactions to general anesthetics and radiocontrast media.

General anesthetics and radiocontrast media (RCM) can cause anaphylactic or anaphylactoid reactions. These are usually underdiagnosed and underreported, but their incidence is apparently rising. Their pathogenesis is complex and not completely understood, but the release of vasoactive mediators from basophils and mast cells plays a central role. The recent development of in vitro techniques to study the release of preformed (histamine and tryptase) and de novo synthesized mediators (PGD2, LTC4, and PAF) from purified basophils and mast cells has made it possible to quantify the mediator-releasing activity of anesthetics such as muscle relaxants, general anesthetics, opioids, and benzodiazepines and RCM on human basophils and mast cells isolated from lung, skin and heart tissues. The majority of general anesthetics and RCM tested induced only the release of preformed mediators (histamine and tryptase), not of the de novo synthesized eicosanoids. There was wide variability in the response of basophils and mast cells from different donors to the same drug or RCM, presumably due to the releasability parameter. Hyperosmolality is probably not the only factor responsible for basophil and mast cell activation by RCM. The in vitro release of histamine induced by anesthetic drugs and RCM was correlated with the release of tryptase. Given the longer half-life of tryptase than histamine in plasma, measurements of plasma tryptase may become a useful diagnostic tool for identifying adverse reactions to anesthetics and RCM.

Anesthetics, General↗

PubMed1983

The influence of molecular form of local anesthetic-type antiarrhythmic agents on reduction of the maximum upstroke velocity of canine cardiac Purkinje fibers.

We studied the local anesthetic effects of the quaternary lidocaine analogues QX-314, QX-572, and QX-222, the tertiary amine lidocaine, its analogues tocainide, 6603, 6211, and the neutral local anesthetic benzocaine to determine if molecular charge of antiarrhythmic agents influences their local anesthetic effects on heart fibers. We used standard microelectrode techniques and canine cardiac Purkinje fibers to compare the effects of stimulation rate, drug concentration, and K+-induced changes in resting membrane potential on the reduction of fast inward sodium current using the maximum rate of rise of the action potential upstroke, Vmax, as an index of changes in peak sodium current. Use-dependent block, defined as a modulation of the reduction in Vmax by local anesthetics due to changes in the stimulation rate, was observed with the permanently charged analogues and was most prominent for agents existing predominantly in the charged form, but was absent for the neutral local anesthetic benzocaine. The development of use-dependent block during rapid stimulation preceded by prolonged periods of quiescence was an exponential process which became more rapid with increasing drug concentration. Recovery from use-dependent block during quiescence was an exponential process that was not influenced by similar drug concentration changes. All local anesthetics caused tonic block, defined as a drug-induced reduction of Vmax from control that attained a constant value at slow stimulation rates (cycle length range 15 seconds to 2 minutes) and was not changed by prolonged (up to 8 minutes) periods of quiescence. These findings suggest that the charged form of lidocaine and its analogues is responsible for use-dependent block of cardiac sodium channels.

Anesthetics, Local↗

PubMed1999

Local anesthetic anchoring to cardiac sodium channels. Implications into tissue-selective drug targeting.

Local anesthetics inhibit Na+ channels in a variety of tissues, leading to potentially serious side effects when used clinically. We have created a series of novel local anesthetics by connecting benzocaine (BZ) to the sulfhydryl-reactive group methanethiosulfonate (MTS) via variable-length polyethylether linkers (L) (MTS-LX-BZ [X represents 0, 3, 6, or 9]). The application of MTS-LX-BZ agents modified native rat cardiac as well as heterologously expressed human heart (hH1) and rat skeletal muscle (rSkM1) Na+ channels in a manner resembling that of free BZ. Like BZ, the effects of MTS-LX-BZ on rSkM1 channels were completely reversible. In contrast, MTS-LX-BZ modification of heart and mutant rSkM1 channels, containing a pore cysteine at the equivalent location as cardiac Na+ channels (ie, Y401C), persisted after drug washout unless treated with DTT, which suggests anchoring to the pore via a disulfide bond. Anchored MTS-LX-BZ competitively reduced the affinity of cardiac Na+ channels for lidocaine but had minimal effects on mutant channels with disrupted local anesthetic modification properties. These results establish that anchored MTS-LX-BZ compounds interact with the local anesthetic binding site (LABS). Variation in the linker length altered the potency of channel modification by the anchored drugs, thus providing information on the spatial relationship between the anchoring site and the LABS. Our observations demonstrate that local anesthetics can be anchored to the extracellular pore cysteine in cardiac Na+ channels and dynamically interact with the intracellular LABS. These results suggest that nonselective agents, such as local anesthetics, might be made more selective by linking these agents to target-specific anchors.

Anesthetics, Local↗

PubMed2004

Multiple synaptic and membrane sites of anesthetic action in the CA1 region of rat hippocampal slices.

BACKGROUND: Anesthesia is produced by a depression of central nervous system function, however, the sites and mechanisms of action underlying this depression remain poorly defined. The present study compared and contrasted effects produced by five general anesthetics on synaptic circuitry in the CA1 region of hippocampal slices. RESULTS: At clinically relevant and equi-effective concentrations, presynaptic and postsynaptic anesthetic actions were evident at glutamate-mediated excitatory synapses and at GABA-mediated inhibitory synapses. In addition, depressant effects on membrane excitability were observed for CA1 neuron discharge in response to direct current depolarization. Combined actions at several of these sites contributed to CA1 circuit depression, but the relative degree of effect at each site was different for each anesthetic studied. For example, most of propofol's depressant effect (> 70 %) was reversed with a GABA antagonist, but only a minor portion of isoflurane's depression was reversed (< 20 %). Differences were also apparent on glutamate synapses-pentobarbital depressed transmission by > 50 %, but thiopental by only < 25 %. CONCLUSIONS: These results, in as much as they may be relevant to anesthesia, indicate that general anesthetics act at several discrete sites, supporting a multi-site, agent specific theory for anesthetic actions. No single effect site (e.g. GABA synapses) or mechanism of action (e.g. depressed membrane excitability) could account for all of the effects produced for any anesthetic studied.

Action Potentials↗

PubMedDate not supplied

Interaction of muscle relaxants and local anesthetics at the neuromuscular junction.

The effects on neuromuscular (NM) function of combinations of relaxants (d-tubocurarine, pancuronium, and succinylcholine) and local anesthetics (cocaine, procaine, lidocaine, etidocaine, and a quaternized derivative of procaine, procaine methobromide) were investigated using the rat's phrenic nerve--hemidiaphragm preparation. Combinations of ineffective concentrations of NM blocking agents with ineffective concentrations of local anesthetics caused a greater than 90% NM block. Preliminary administration of ineffective concentrations of local anesthetics significantly ( p less than 0.001) decreased the ED50 of NM blocking agents. The administration of ineffective concentrations of NM blocking agents caused a similar decrease of the ED50 of local anesthetics. Concentrations of d-tubocurarine and pancuronium which alone produced partial NM block had additive effects. These findings suggest that the interaction of NM blocking agents and local anesthetics consists of true potentiation caused by the different sites of action of the two types of compounds at the NM junction. The degree of potentiation may be enough to cause clinically significant NM block in patients who at the same time receive high enough doses of both agents. In vitro the NM block caused by the combinations of local anesthetics and NM blocking agents can be reversed by 4-aminopyridine.

Anesthetics, Local↗

PubMed1990

Hepatic circulation and oxygen supply-uptake relationships after hepatic ischemic insult during anesthesia with volatile anesthetics and fentanyl in miniature pigs.

The objective of the present study was to quantitate the effects of several anesthetics on hepatic circulation, oxygenation, and function after hepatic ischemic insult and during reperfusion. We examined the effects of different anesthetics on hepatic circulation, oxygenation, and function after hepatic ischemic insult in 28 miniature pigs weighing 20-27 kg. The preparation allowed a stepwise decrease followed by a complete cessation for 1 h of hepatic blood and oxygen supply. Immediately after the unclamping of both vessels supplying the liver and restoration of the hepatic circulation, systemic mean arterial pressure decreased to approximately 75% of preischemic values in animals anesthetized with pentobarbital and fentanyl and to 60% of preischemic values in pigs anesthetized with halothane, enflurane, or isoflurane. Total hepatic blood flow immediately returned to preischemic values without significant difference between the groups. Subsequently, hepatic oxygen delivery returned to 75%-95% of preischemic values. Hepatic oxygen uptake returned to 50%-60% of preischemic values in animals anesthetized with pentobarbital and with volatile anesthetics and up to 80% and then later to baseline values with fentanyl anesthesia. Lactate uptake by the liver returned to preischemic values only in animals given fentanyl or isoflurane but remained at approximately 50% of preischemic values during enflurane and 20%-40% during halothane and pentobarbital anesthesia. Thus, the study indicates that both isoflurane and fentanyl anesthesia provide more protection from ischemic insult than do halothane, enflurane, or pentobarbital anesthesia.

Anesthetics↗

PubMed1991

What solvent best represents the site of action of inhaled anesthetics in humans, rats, and dogs?

The correlation between the potency of inhaled anesthetics and their solubility in a hydrophobic phase provides an opportunity to define better the characteristics of the anesthetic site of action. The correlation implies that inhaled anesthetics act in a hydrophobic site and that the solvent used has properties representative of the true site of anesthetic action. We sought to characterize this site more accurately by testing for the solvent that provided the best correlation for a diverse group of anesthetics. We determined the solubility of halothane, enflurane, cyclopropane, fluroxene, isoflurane, sevoflurane, and desflurane in benzene, olive oil, Intralipid, n-octanol, and lecithin. We used established MAC values for rats, dogs, and humans for all but sevoflurane and desflurane, for which we determined MAC in rats to be 2.80% +/- 0.24% (mean +/- standard deviation) and 7.71% +/- 0.65%, respectively. Lecithin gave the lowest coefficient of variation for the product of potency (MAC) x solubility, but the difference was statistically significant only for a comparison of the products for lecithin and olive oil. The values for lecithin were within the range of values produced by biological variation. More important, the correlation of log MAC and log solubility had an average slope of unity (-1.04 +/- 0.07) for lecithin, but a slope differing from unity for benzene (-0.82 +/- 0.05) and olive oil (-0.87 +/- 0.05). We conclude that lecithin is probably more representative of the site of action of these anesthetics than the other solvents.

Anesthesia, Inhalation↗