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PubMed1995

Effects of volatile anesthetics on acetylcholine-induced relaxation in the rabbit mesenteric resistance artery.

BACKGROUND: Vascular endothelium plays an important role in the regulation of vascular tone. Volatile anesthetics have been shown to attenuate endothelium-mediated relaxation in conductance arteries, such as aorta. However, significant differences in volatile anesthetic pharmacology between these large vessels and the small vessels that regulate systemic vascular resistance and blood flow have been documented, yet little is known about volatile anesthetic action on endothelial function in resistance arteries. Furthermore, endothelium-dependent relaxation mediated by factors other than endothelium-derived relaxing factor (EDRF) has recently been recognized, and there is no information available regarding volatile anesthetic action on non-EDRF-mediated endothelium-dependent relaxation. METHODS: Employing isometric tension recording and microelectrode methods, the authors first characterized the endothelium-dependent relaxing and hyperpolarizing actions of acetylcholine (ACh) in rabbit small mesenteric arteries, and tested the sensitivities of these actions to EDRF pathway inhibitors and K+ channel blockers. They then examined the effects of the volatile anesthetics isoflurane, enflurane, and sevoflurane on ACh-induced endothelium-dependent relaxation that was sensitive to EDRF inhibitors and that which was resistant to the EDRF inhibitors but sensitive to blockers of ACh-induced hyperpolarization. The effects of the volatile anesthetics on endothelium-independent sodium nitroprusside (SNP)-induced relaxation were also studied. RESULTS: Acetylcholine concentration-dependently caused both endothelium-dependent relaxation and hyperpolarization of vascular smooth muscle. The relaxation elicited by low concentrations of ACh (< or = 0.1 microM) was almost completely abolished by the EDRF inhibitors NG-nitro-L-arginine (LNNA), oxyhemoglobin (HbO2), and methylene blue (MB). The relaxation elicited by higher concentrations of ACh (> or = 0.3 microM) was only attenuated by the EDRF inhibitors. The remaining relaxation, as well as the ACh-induced hyperpolarization that was also resistant to EDRF inhibitors, were both specifically blocked by tetraethylammonium (TEA > or = 10 mM). Sodium nitroprusside, a NO donor, produced dose-dependent relaxation, but not hyperpolarization, in the endothelium-denuded (E[-]) strips, and the relaxation was inhibited by MB and HbO2, but not TEA (> or = 10 mM). One MAC isoflurane, enflurane, and sevoflurane inhibited both ACh relaxation that was sensitive to the EDRF inhibitors and the ACh relaxation resistant to the EDRF inhibitors and sensitive to TEA, but not SNP relaxation (in the E[-] strips). An additional finding was that the anesthetics all significantly inhibited norepinephrine (NE) contractions in the presence and absence of the endothelium or after exposure to the EDRF inhibitors. CONCLUSIONS: The results confirm that ACh has a hyperpolarizing action in rabbit small mesenteric resistance arteries that is independent of EDRF inhibitors but blocked by the K+ channel blocker TEA. The ACh relaxation in these resistance arteries thus appears to consist of distinct EDRF-mediated and hyperpolarization-mediated components. Isoflurane, enflurane, and sevoflurane inhibited both components of the ACh-induced relaxation in these small arteries, indicating a more global depression of endothelial function or ACh signaling in endothelial cells, rather than a specific effect on the EDRF pathway. All these anesthetics exerted vasodilating action in the presence of NE, the primary neurotransmitter of the sympathetic nervous system, which plays a major role in maintaining vasomotor tone in vivo. This strongly indicates that the vasodilating action of these anesthetics probably dominates over their inhibitory action on the EDRF pathway and, presumably, contributes to their known hypotensive effects in vivo. Finally, the vasodilating action of these anesthetics is, at least in part, independent from endothelium.

Acetylcholine↗
PubMed1999

Inhibition of nitric oxide metabolism enhances the hypnotic-anesthetic action of the alpha2-adrenoceptor agonist dexmedetomidine in vivo.

Nitric oxide (NO) synthase inhibitors have been demonstrated to increase the anesthetic action of volatile and intravenous anesthetics. This study was designed to test the hypothesis that, comparable to other general anesthetics, the hypnotic-anesthetic action of dexmedetomidine is increased after administration of the NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME). With approval of the local animal care committee, the anesthetic potency of dexmedetomidine or a combination of dexmedetomidine plus 1 mM L-NAME was determined in Xenopus laevis larvae. Anesthesia was defined as loss of righting reflex. Concentration-response curves were calculated by a logistic approach. Additional experiments were performed that exposed the animals to dexmedetomidine in the presence of L-NAME plus L-arginine, as well as D-NAME. In the dexmedetomidine and the dexmedetomidine plus L-NAME groups, the fraction of anesthetized animals increased with increasing concentrations of dexmedetomidine. Calculation of the half-maximal effective concentration (EC50) resulted in a value of 7.8+/-0.6 microM for dexmedetomidine and 3.8+/-0.2 microM for dexmedetomidine plus L-NAME (p<0.05). Addition of L-arginine reversed the potentiating effect of L-NAME. Administration of D-NAME did not affect the EC50 of dexmedetomidine. In a manner comparable to that of other general anesthetics, the anesthetic effect of dexmedetomidine was increased by about 51% by an acute inhibition of the NO metabolism. Together with recent findings that alpha2-adrenoceptor agonists decrease the NO mediated synthesis of cGMP similar to volatile and intravenous anesthetics, the results suggest that the NO/cGMP pathway is an important mediator of the anesthetic action of these compounds.

Adrenergic alpha-Agonists↗
PubMed2004

Identification of cytoskeletal [14C]carboplatin-binding proteins reveals reduced expression and disorganization of actin and filamin in cisplatin-resistant cell lines.

Cisplatin resistant (CP-r) cells often show decreased uptake of cisplatin in association with reduced cell surface proteins and decreased endocytosis. In this report, two major [14C]carboplatin-binding proteins were identified as filamin and actin by photoaffinity labeling and mass spectrometry. Decreased expression of these two proteins was found in two different human CP-r cell lines (KB-CP20 and 7404-CP20), in comparison with their parental cell lines (KB-3-1 and BEL-7404), respectively. Disorganization of beta-actin and filamin 250 and 90 was also detected in these CP-r cells by confocal microscopy. Transfection of a wild-type actin-enhanced green fluorescent protein (EGFP) expression vector into 7404-CP20 cells resulted in a nonfilamentous actin-EGFP distribution compared with a normal distribution in the cisplatin-sensitive BEL-7404 cells, suggesting that cytoskeletal organization is disturbed in the CP-r cells. The identification of actin and filamin as [14C]carboplatin-binding proteins and decreased expression and disorganization of several cytoskeletal proteins in CP-r cells provide a molecular and cellular basis for the known defect in endocytosis in these cells.

Actins↗
PubMed1989

Clinical uses of intravenous anesthetic and analgesic infusions.

Renewed interest in i.v. anesthetic techniques has resulted from the availability of more rapid and shorter-acting i.v. drugs. With recent advances in the area of infusion pump technology, it has become easier to administer i.v. anesthetics and analgesics by continuous infusion techniques. The newer sedative-hypnotic (midazolam, propofol) and analgesic (sufentanil, alfentanil) drugs are better suited pharmacologically to continuous administration techniques than the traditional i.v. agents because they can be more accurately titrated to meet the unique and changing anesthetic needs of the individual patient. With the newer sedative and analgesic drugs, it is now possible to administer i.v. anesthetics in a titrated manner analogous to that which is possible when volatile anesthetics are used. In this way, the drug infusion rate is varied depending on the patient's responses to noxious surgical stimuli. In titrating i.v. drug infusions, consideration must also be given to the age of the patient, pre-existing disease states, potential drug interactions, and proximity to the end of the operative procedure. The availability of rapid and short-acting i.v. drugs like alfentanil and propofol, as well as intermediate-acting muscle relaxants makes it possible to employ total intravenous anesthetic techniques during general surgery. Many non-sedative and non-analgesic i.v. drugs are being investigated in anesthesia for use by continuous infusion techniques, e.g., muscle relaxant, and local anesthetics. Several recent studies have demonstrated the efficacy of continuous infusions of local anesthetics for obstetrical analgesia. The use of continuous local anesthetic infusions makes it possible to achieve improved analgesia (i.e., a more constant degree of analgesia) with lower doses. Improved delivery systems for administering i.v. drugs will make it easier to use continuous infusion techniques in the future. With continued progress in the development of infusion devices and i.v. drugs designed for continuous administration, the use of intravenous anesthetic techniques will become more widespread. In the near future, infusion pumps will likely become standard equipment on all anesthesia machines and anesthesiologists should find these techniques easier to use in their clinical practices.

Analgesics↗
PubMed1990

Fundamental properties of local anesthetics. II. Measured octanol:buffer partition coefficients and pKa values of clinically used drugs.

Because local anesthetic molecules interact with ion channel proteins embedded in membranes to effect impulse blockade, and because their clinical potency often depends on both vascular absorption and distribution into the tissue surrounding the site of deposition, the ability to partition into these various compartments is an important determinant of local anesthetic action. Therefore, the hydrophobic nature of local anesthetics used clinically was characterized by the octanol:buffer partition coefficients of their charged (P+) and neutral (Po) species. This was accomplished by previously described optical methods in which direct spectrophotometric measurement of both the pH-dependent distribution coefficient (Q) and of the ionization permit calculation of the pKa and partition coefficients. The rates of alkaline hydrolysis of ester-linked molecules also were measured to assess potential interference of such hydrolysis with the physicochemical assays. Results indicate that the hydrophobicity of a local anesthetic is increased by manipulation of the molecular structure at three sites: (a) the aromatic ring; (b) the intermediate linking group; and (c) the tertiary amine. Po for the agents studied was 10(3)-10(5) times greater than P+. Although there is no systematic relationship between hydrophobicity and pKa, the latter is greater with ester-linked (pKa = 8.59-9.30) than with amide-linked (pKa = 7.92-8.21) local anesthetics. All of the charged species, with the exception of bupivacaine, selectively partition into the aqueous environment (P+ less than 1.0). The temperature dependence of partitioning of the local anesthetics, measured at 25 and 36 degrees C, indicates an entropy-driven hydrophobic uptake. Solutions buffered with bicarbonate and including 5% CO2 showed the same local anesthetic partitioning as that of CO2-free solutions, suggesting that potentiation of impulse blockade by CO2 is not due to increased membrane uptake. Correlations of physicochemical properties of local anesthetics with potencies on isolated nerve confirm that the more potent local anesthetics have greater octanol:buffer partition coefficients, and that the ester-linked local anesthetics are more potent than their amide-linked counterparts having the same hydrophobicities. The correlations of structure with potency also suggest that the extracellular protonated species may contribute to impulse blockade.

Anesthetics, Local↗
PubMed2005

Anesthetics as chemical tools to study the structure and function of nicotinic acetylcholine receptors.

The nicotinic acetylcholine receptor (AChR) is the archetype of the Cys-loop ligand-gated ion channel receptor superfamily. Noncompetitive antagonists inhibit the AChR without interacting directly with agonist sites. Among noncompetitive antagonists, general and local anesthetics have been used for decades to study the structure and function of muscle- as well as neuronal-type AChRs. In this review, we address and update all information regarding the characterization of binding sites and the mechanism of action for n-alkanols, barbiturates, inhalational and dissociative general anesthetics, as well as for tertiary and quaternary local anesthetics. The experimental evidence outlined in this review suggest that: (1) several neuronal-type AChRs might be targets for the pharmacological action of distinct anesthetics; (2) the molecular components of a specific anesthetic locus on a certain receptor type are different from the structural determinants of the site for the same anesthetic on a different receptor type; (3) there are unique binding sites for distinct anesthetics in the same receptor; (4) the affinity of a specific anesthetic depends on the AChR conformational state; (5) anesthetics may inhibit AChRs by different mechanisms including open-channel-blocking, augmenting the desensitization process, and/or inactivating the opening of resting receptors; and (6) some anesthetics may potentiate AChR activity.

Anesthetics↗
PubMed1990

[Let's study pharmacokinetics related to anesthesiology by using computer graphics: inhalation anesthetics].

The pharmacokinetics of inhalation anesthetics has been out of public interest for 20 years. Partition coefficient or solubility of anesthetic, an important determinant of uptake and distribution of inhaled anesthetics, may be the only remains of the pharmacokinetics of inhaled anesthetics. There still, however, are a few evidences which can not be explained by partition coefficient of anesthetic. The authors applied three compartment model to the rise of the blood concentration of anesthetics, i.e., nitrous oxide, enflurane, halothane, and diethyl ether. We revealed that the change in the blood anesthetic concentration may be related to the size of compartments and their time constants. The size of compartments and their time constants may be determined by interaction of partition coefficient of anesthetic and blood distribution to the tissues which may be different with different anesthetic, and may also be different when the blood concentration of anesthetic is different.

Anesthesia, Inhalation↗
PubMed1994

Does general anesthetic-induced desensitization of the Torpedo acetylcholine receptor correlate with lipid disordering?

We have tested the hypothesis that general anesthetics stabilize the desensitized state of the nicotinic acetylcholine receptor by disordering its surrounding lipids. Acetylcholine receptor-rich postsynaptic membranes from the electroplaques of Torpedo were used in this study to obtain the highest possible receptor specific activity in native membranes. We examined 18 general anesthetics, including six inhalation agents, eight 1-alcohols, the enantiomers of 2-octanol, and two intravenous general anesthetics (pentobarbital and ethylcarbamate). The degree of desensitization after preincubation with the general anesthetics was determined by brief exposure to [3H]acetylcholine, making use of the facts that desensitized receptors have much higher affinity than do those in the resting state and that interconversion between the states is slow. All of the general anesthetics desensitized the receptor within minutes, exhibiting steep concentration-response curves with Hill coefficients generally within the range of 2-4. At the highest general anesthetic concentrations, almost all receptors were desensitized. The concentrations that desensitized half of the resting state receptors varied by > 3000-fold. The 2-octanol enantiomers were without stereoselectivity. Membrane order was examined in parallel by using spin-labeled fatty acids doped into the native membranes. The spin label 5-doxylpalmitate reported from the most ordered part of the bilayer near the aqueous interface, whereas 12-doxylstearate reported from the less ordered region nearer the center of the bilayer. The spin label deeper in the membranes was 3 times more sensitive to a given anesthetic than was the other probe. At both depths in the membrane general anesthetics decreased lipid order linearly with increasing concentration. The range of disordering potencies (change in order parameter induced by a unit concentration of general anesthetic in the aqueous phase) was 5333 for 5-doxylpalmitate and 7143 for 12-doxylstearate, but the range of disordering compared at equally desensitizing concentrations was reduced by 875- and 1430-fold, respectively. The average degrees of disordering at concentrations that desensitized half of the resting state receptors were 1.5% and 4.4%, respectively. It is unlikely that changes in membrane order parameter per se cause desensitization, because the associated changes in order parameter can be reproduced by changes in cholesterol content or temperature that do not cause desensitization. We conclude that, although there is a strong association between anesthetic-induced membrane disordering and desensitization, more detailed tests of a mechanistic nature will be necessary to elucidate the mechanisms underlying the Meyer-Overton-type behavior we have observed.

Anesthesia, General↗
PubMed2003

Tolerance to acute isovolemic hemodilution. Effect of anesthetic depth.

BACKGROUND: Acceptance of a lower transfusion trigger in the perioperative period requires study of the effects of anesthetic depth on the tolerance to acute isovolemic anemia. Anesthetic agents with negative effects on the cardiovascular system may exert proportionately greater depressant effects on cardiac output response than on tissue oxygen demand, reducing tolerance to acute isovolemic anemia. METHODS: In the first study, animals were anesthetized with halothane (n = 14; 23.8 +/- 4.8 kg, mean +/- SD). In a second study, animals were anesthetized with ketamine (n = 14; 24.3 +/- 4.7 kg). In each study, dogs were randomly allocated to receive either low or high concentrations of anesthetic. Oxygen delivery and oxygen consumption were determined from independent measurements during a stepwise isovolemic hemodilution protocol. In each dog, critical oxygen delivery was determined from a plot of oxygen consumption versus oxygen delivery using a least-sum-of-squares technique. Critical hemoglobin (hemoglobin) was determined from a plot of hemoglobin versus oxygen consumption using the same method. RESULTS: With both agents, the higher anesthetic concentration was associated with decreased oxygen consumption, resulting in a lower critical oxygen delivery. However, critical hemoglobin was significantly higher in the animals receiving the higher anesthetic dosage (1.5 vs. 1.0 minimum alveolar concentration of halothane: 4.1 +/- 1.3 vs. 2.3 +/- 0.5 g/dl, P < 0.05; high- vs. low-dose ketamine: 3.7 +/- 1.4 vs. 2.5 +/- 0.6 g/dl, P < 0.05). This was related to a marked blunting of the cardiac output response to hemodilution in the animals receiving the higher anesthetic dosage. CONCLUSIONS: Increased anesthetic depth with halothane or ketamine resulted in a decreased tolerance to acute anemia, as reflected by a significant increase in critical hemoglobin concentration.

Anemia↗
PubMed1990

Effects of diltiazem, verapamil, and inhalation anesthetics on electrophysiologic properties affecting reentrant supraventricular tachycardia in chronically instrumented dogs.

Paroxysmal supraventricular tachycardia (PSVT) is likely due to reentry involving the atrioventricular (AV) node, AV node with AV bypass pathway, sinus node, or atria. Intravenous diltiazem (DIL) or verapamil (VER) might be used to treat PSVT in anesthetized patients, and either drug could be more or less effective or produce adverse circulatory effects in this circumstance because the available inhalation anesthetics are known to elevate plasma concentrations of acutely administered iv DIL or VER. Because human studies were precluded and there are no reliable animal models for most reentrant PSVT, the authors determined the effects of iv DIL or VER and potent inhalation anesthetics (enflurane, halothane, isoflurane) on supraventricular electrophysiologic (EP) properties affecting the likelihood of reentrant PSVT in chronically instrumented dogs. Measurements of supraventricular EP properties in awake dogs without drugs served as control. DIL and VER were then administered iv to achieve clinically relevant plasma concentrations in awake dogs and EP properties were again measured. Finally, anesthetic effects on EP properties in dogs with DIL or VER were tested at end-tidal concentrations equivalent to 1.2 or 1.6 MAC for enflurane, halothane, or isoflurane. In awake dogs, DIL or VER increased AV node conduction time. Wenckebach point and functional refractoriness, and also reduced the range of premature atrial intervals for and likelihood of producing sinus node interpolation or reentry with atrial extrastimulation (P less than 0.05, ANOVA). AV node conduction time, Wenckebach point, and functional refractoriness were further increased in anesthetized dogs (all agents) with DIL or VER compared with control (P less than 0.05, ANOVA). All anesthetics with DIL or VER abolished sinus node interpolation and reentry. Atrial effective and functional refractory periods were not affected by DIL or VER in awake dogs and were increased by any of the anesthetics in dogs with DIL (P less than 0.05, ANOVA). Atrial refractory periods were little affected by anesthetics with VER. Adverse circulatory effects, including systolic arterial pressure less than 50 mmHg and second-degree (type 1) AV block or sinus arrest with escape rhythms, were most common with VER and any (especially enflurane) of the anesthetics. Finally, anesthetized animals with sinus arrest and escape rhythms (any test condition) could be paced from the atrium at physiologic rates (up to 120 beats/min).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Evidence for direct actions of general anesthetics on an ion channel protein. A new look at a unified mechanism of action.

BACKGROUND: Ion permeation through the nicotinic acetylcholine receptor channel is inhibited by general anesthetics. This inhibition could be mediated either by binding of anesthetic molecules to the channel protein itself or by the effects of anesthetics on the lipid environment of the protein. METHODS: Patch clamp recording techniques were used to investigate the effects of ether and propofol on acetylcholine receptor channels in outside-out patches from BC3H-1 cells. The kinetic and conductance properties of single channels were measured. A rapid perfusion system was used to make rapid changes in anesthetic concentration during patch clamp recording to determine the kinetics of inhibition by anesthetics. RESULTS: Ether, isoflurane (results from previous studies), and propofol produce distinct kinetic patterns of single acetylcholine receptor channel activity. Ether reduces the apparent current amplitude of channels, isoflurane induces flickering channel activity and propofol merely decreases the open time of the channel. The kinetics of inhibition are also different for these anesthetics. Ether (< 40 microseconds) is faster than isoflurane (300-600 microseconds) which is faster than propofol (> or = 2 ms). CONCLUSIONS: These diverse patterns can be interpreted in terms of a unitary mechanism in which the anesthetics interact directly with the channel protein. Each anesthetic is considered to bind to a site on the protein (perhaps, but not necessarily within the pore of the channel) and interrupt the flow of ions through the pore. Anesthetics have access to this inhibitory binding site even when the gate of the channel is closed. The pattern of channel activity induced by an anesthetic is determined by the frequency and duration of binding events.

Cells, Cultured↗
PubMed1988

Cardiovascular responses to V1-vasopressinergic antagonism in conscious versus anesthetized rats.

Experiments were performed to compare the possible effect of endogenous arginine vasopressin on renal hemodynamics between anesthetized, surgically stressed rats and conscious rats. Animals were instrumented with arterial and venous catheters as well as with a pulsed Doppler flow probe on the left renal artery. The rats were studied under the following conditions: (1) conscious and unrestrained; (2) anesthetized only; (3) anesthetized with minor surgical stress; and (4) anesthetized with major surgical stress. Two anesthetic agents were also compared, a mixture of ketamine (110 mg/kg i.m.) and acepromazine (1 mg/kg i.m.), and sodium pentobarbital (50 mg/kg i.p.). Baseline mean arterial blood pressure was significantly higher in pentobarbital-anesthetized rats following surgical stress compared with conscious animals, but blood pressure was not affected by ketamine-acepromazine anesthesia. After baseline measurements of blood pressure, heart rate, and renal blood flow, a specific V1-vasopressinergic antagonist (d(CH2)5Tyr(Me) arginine vasopressin, 10 mg/kg i.v.) was administered to each group. Mean arterial blood pressure, heart rate, and renal blood flow were monitored for an additional 15 min. Mean arterial blood pressure and renal blood flow decreased after V1 antagonism in ketamine-acepromazine-anesthetized rats with major surgical stress, but were not affected in pentobarbital-anesthetized animals. Heart rate and renal vascular resistance were not affected following V1 blockade with either anesthetic agent. These data suggest that arginine vasopressin plays a role in maintaining blood pressure and renal perfusion in ketamine-acepromazine-anesthetized rats following surgical stress, but does not have a significant effect on renal hemodynamics under pentobarbital anesthesia.

Acepromazine↗
PubMed1976

Exposure to anesthetic gases and ethanol during work in operating rooms.

The concentration of halothane and ethanol in operating rooms was measured during 37 routine operations performed in nine different departments of surgery at six different hospitals. The time-weighted halothane concentrations in the respiratory zones of anesthetic and surgical nurses were 0.3--34.0 ppm (time-weighted average 7.2 ppm) and 0.1--9.2 ppm (time-weighted average 2.5 ppm), respectively, in the different operating departments. The corresponding ethanol concentrations were 0.3--36.5 ppm (time-weighted average 12.5 ppm) for anesthetic nurses and 1.5--46.6 ppm (time-weighted average 15.3 ppm) for surgical nurses. The anesthetic technique influences the exposure of the operating staff to anesthetic gases, but it does not affect exposure to ethanol. In controlled experiments volunteers were exposed to low concentrations of halothane or ethanol. About 60% of both substances was retained. The content of ethanol in the end-expired air approached zero within a few minutes after the end of exposure, while low residual concentrations of halothane were demonstrable for more than 1 h. Although exposure to ethanol is insignificant in relation to the metabolic capacity of the body, ethanol indicates the presence of volatile disinfectant components, and its spread through the room atmosphere should be kept in mind when the ventilation of operating rooms is designed. The effective elimination of airborne pollutants in operating rooms calls for good general ventilation in conjunction with local exhaust close to the sources of anesthetic gas leakage. General ventilation mainly affects the concentration of substances well-mixed with the room atmosphere, such as volatile disinfectant components and anesthetic vapor that has spread beyond the actual work zones of the medical staff. For a significant reduction in the concentration of anesthetic gases in the respiratory zones of the medical staff, the gases must be vented at the source of leakage. Since airborne anesthetics occur not only in operating rooms, general ventilation has to meet certain minimum requirements also in anesthetic induction rooms and recovery rooms. Operating rooms and anesthetic induction rooms must also be supplied with local exhaust systems.

Air Conditioning↗
PubMed2005

Efficacy of intraoral topical anesthetics in children.

OBJECTIVES: The literature reports mixed results regarding the efficacy of intraoral topical anesthetics. Only a few studies have been performed in children. Some non-placebo controlled studies have been carried out to compare the efficacy in reducing children's injection pain between different topical anesthetics METHODS: In a randomized, double blind, placebo controlled study with split-mouth design 104 children were enrolled to evaluate the efficacy of four topical anesthetics (Gingicain Spray, Gingicaine Topical Anesthetic, Legecain-Solution, EMLA Crème) when used prior to buccal injections within the conservative treatment of carious upper primary molars. The heart rate change and a Face Pain Scale were used as primary variables. The Visual Analog Scale, the modified Children's Hospital Pain Scale and the Sound-Eyes-Motor Scale were also evaluated. RESULTS: There was no significant difference between the placebo and any corresponding topical anesthetic with regard to the primary variables (HRC and FPS). A significant difference was found in favour of Gingicain Spray and Gingicaine Topical Anesthetic according to secondary variables (VAS, S(E)MS). CONCLUSION: While the secondary variables point to a benefit of the topical anesthetics Gingicain Spray and Gingicaine Topical Anesthetic compared to placebo, the results of the primary variables showed no differences in effectiveness of topical anesthetics and their corresponding placebos.

Administration, Topical↗
PubMed2000

Dual effects of intravenous anesthetics on the function of norepinephrine transporters.

BACKGROUND: Norepinephrine transporters (NETs) terminate the neuronal transmission of norepinephrine, which is released from noradrenergic neurons. To investigate the interaction with NET, the authors examined the effects of short- and long-term treatment with anesthetics on the activity and mRNA level of NET. METHODS: To assay [3H]norepinephrine uptake, bovine adrenal medullary cells in culture were incubated with [3H]norepinephrine in the presence of intravenous anesthetics, including propofol, thiamylal, and diazepam. To study the direct interaction between the anesthetics and NET, the effect of propofol on the binding of [3H]desipramine to the plasma membrane was examined. To study the long-term effect of anesthetics, [3H]norepinephrine uptake by cells pretreated with propofol for 6-24 h and [3H]desipramine binding after pretreatment for 12 h were measured. Simultaneously, we examined the effect of anesthetics on the expression of NET mRNA using the reverse transcriptase-polymerase chain reaction. RESULTS: All of the intravenous anesthetics inhibited [3H]norepinephrine uptake in a concentration-dependent manner. The active concentrations of propofol (1-3 microm) and thiamylal (< or = 30 microm) were similar to those encountered clinically. The kinetic analysis revealed that all the anesthetics noncompetitively inhibited [3H]norepinephrine uptake. Propofol inhibited [3H]desipramine binding with a potency similar to that observed in [3H]norepinephrine uptake. Scatchard analysis showed that propofol competitively inhibited [3H]desipramine binding. On the other hand, long-term treatment of cells with propofol (10 microm) enhanced the NET functional activity and [3H]desipramine binding, and also increased the level of NET mRNA. CONCLUSIONS: These results suggest that intravenous anesthetics have a dual effect on NET; short-term treatment causes inhibition, whereas long-term treatment leads to up-regulation. The interaction of intravenous anesthetics with NET may modulate the neuronal transmission of norepinephrine during anesthesia.

Adrenal Medulla↗
PubMed2006

[Anesthetic protection against hepatic injury].

In this review article, hepatocyte injury by volatile anesthetics, effects of anesthetics on hepatic perfusion, protection offered by either ischemic preconditioning or anesthetic preconditioning against hepatic ischemia-reperfusion injury and effects of anesthetics on sepsis-induced hepatic injury are discussed. Halothane poses significant risk of immunologically-mediated hepatocyte injury and disturbances of hepatic blood supply. Other modern volatile anesthetics such as isoflurane, sevoflurane and desflurane seem to have only minor risks. Several animal studies demonstrate that volatile anesthetics offer more protection against ischemia-reperfusion injury than intravenous anesthetics. On the contrary, intravenous anesthetics may be more protective against sepsis-induced hepatic injury than volatile anesthetics.

Anesthetics↗
PubMed2001

Determination of the hydrophobicity of local anesthetic agents.

Hydrophobicity, a term used to describe a fundamental physicochemical property of local anesthetics, was in the past obtained by octanol/buffer partitioning. It has been suggested that the octanol method, despite its obvious advantages, also has some drawbacks. HPLC has become an attractive alternative for the measurement of hydrophobicity and has been applied to local anesthetics recently. However, the methods in current use for measuring the hydrophobicity of local anesthetics suffer from a number of limitations and remain obscure. This study introduces a new HPLC method for measuring the hydrophobicity of eight local anesthetics in current clinical use. Using a C(18) derivatized polystyrene-divinylbenzene stationary phase HPLC column, the log k'(w) values of local anesthetics were determined by measuring the capacity factor k'(i) in the process of chromatographic separation using a hydrophobic stationary phase and a hydrophilic mobile phase. A rapid reversed-phase HPLC method was developed to directly measure log k'(w) of eight local anesthetics. A high correlation between log k'(w) and hydrophobicity (log P(oct)) from the traditional shake-flask method was obtained for the local anesthetics, demonstrating the reliability of the method. The results reveal an improved method for measuring the hydrophobicity of the local anesthetic agents in the unionized form. This simple, sensitive and reproducible approach may serve as a valuable tool for describing the physicochemical properties of novel local anesthetics.

Alkanes↗
PubMed2003

[Anesthesia in the breast feeding period. Excretion of anesthetic agents and adjuvants into breast milk and potential pharmacological side-effects on the suckling infant].

Whenever an anesthetic is needed during the breast feeding period, potential pharmacological side-effects imposed on the infant by any kind of anesthetic agent used during both general and regional anesthesia are in contrast to the potential beneficial effects of breast feeding for the infant and the mother. Despite an increasing knowledge and understanding of the mechanisms of excretion of drugs and their metabolites through breast milk, information about most anesthetic drugs are still either inconclusive or contradictory. Often it is impossible to decide whether a certain substance that is potentially excreted through breast milk might be harmless or harmful for the breast-fed infant. In addition to that only few anesthetic agents and drugs used in conjunction with an anesthetic are officially approved for use during pregnancy and the period of breast feeding and for medico-legal reasons pharmaceutical companies generally advise against the use of any of those drugs during this period. However, based on the knowledge of pharmacological properties of commonly used anesthetic agents it is reasonable to assume that continuing breast feeding in the immediate postoperative period after a single anesthetic can be considered safe for the infant since no adverse effects caused by or secondary to the single use of those drugs can be expected. Provided there is a careful choice of anesthetic drugs, there is no need to consider that a single general or regional anesthetic is an indication to stop breast feeding. Even planned elective surgical procedures do not need to be postponed. No scientifically based interval between surgery under general or regional anesthesia and resumption of breast feeding can be recommended. Instead current opinion is that breast feeding can be resumed as soon as the mother feels physically and mentally capable to do so.

Adjuvants, Anesthesia↗