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PubMed2001

[Effects of general anesthetics on neuronal nicotinic acetylcholine receptors and their roles in the mechanism of anesthesia].

Neuronal nicotinic acetylcholine receptors (nAchRs) are widely expressed in the central and autonomic nervous systems and have subunit compositions with biophysical and pharmacological properties distinct from those of the receptors at the neuromuscular junction. They are thought to modulate synaptic transmission in the central nervous system (CNS) mainly by regulating the release of neurotransmitters. Although roles of neuronal nAchRs in the CNS are poorly understood, these receptors are involved in cognitive performance, nociception and psychoneurological disorders such as Alzheimer's and Parkinson disease. It is known that both central and peripheral neuronal nAchRs are sensitive to various types of anesthetics. Among those, barbiturates, ketamine, volatile and gaseous anesthetics depress neuronal nAchRs at or below clinical concentrations. Inhibition of neuronal nAchRs by barbiturates is unlikely to contribute to the anesthetic action of barbiturates, since this effect does not correlate with the anesthetic potencies of barbiturate stereoisomers. Relevance of inhibition of these receptors is controversial for anesthetic effects of other anesthetics, because conflicting results have been obtained from comparison of this effect with anesthetic actions of stereoisomers or structurally related compounds. However, it is possible that inhibition of central nAchRs contributes to secondary effects attributed to anesthesia such as impairment in memory and cognitive performance.

Anesthesia↗

PubMed1992

Local anesthetics induce fast Ca2+ efflux through a nonenergized state of the sarcoplasmic reticulum Ca(2+)-ATPase.

The effect of the local anesthetics SKF 525-A, dibucaine, tetracaine, procaine, and benzocaine on sarcoplasmic reticulum vesicles was studied. All the anesthetics tested inhibited the phosphorylation of the Ca(2+)-ATPase by Pi in a competitive manner. Tertiary amine and positively charged anesthetics, in addition to competing with Pi, also decreased the apparent affinity of the ATPase for Mg2+. There was a good correlation between the octanol/water partition coefficients and the inhibitory activity of the different anesthetics. All the anesthetics tested induced a 5- to 10-fold increase in the rate of Ca2+ efflux. This was promoted by the same drug concentration that inhibited the phosphorylation of the ATPase by Pi. The effect on Ca2+ efflux was antagonized by the ligands of the ATPase (Mg2+, K+, Ca2+, MgATP, and ADP) and by the organic polyamines ruthenium red, spermine, spermidine, and putrescine. The natural anion heparin was found to potentiate the effect of the positively charged anesthetics on the rate of Ca2+ efflux. It is concluded that the local anesthetics increase the Ca2+ efflux through a nonenergized state of the Ca(2+)-ATPase, rather than promoting a nonspecific Ca2+ leakage through the membrane.

Anesthetics, Local↗

PubMed2005

Disciplinary actions associated with the administration of local anesthetics against dentists and dental hygienists.

PURPOSE: Research studies have demonstrated the need for and the ability of dental hygienists to provide local anesthetics for pain control and reduction of patient anxiety. Although two-thirds of state dental practice laws allow these services to be performed by dental hygienists, controversy exists between organized dentistry and dental hygiene regarding the administration of local anesthetics by dental hygienists. Some dentists believe the quality of care would be compromised and patient safety jeopardized because dental hygienists do not have adequate background knowledge to prevent complications and recognize emergencies caused by anesthetics. The purpose of this study was to collect quantitative data addressing safety when dental hygienists administer local anesthetics. RESULTS: Eighteen responses were received, for a response rate of 69%. These data showed, over a 10-year period, no reports of disciplinary actions against dental hygienists for the administration of local anesthetics. CONCLUSION: This study affirmed public safety, which should be helpful to states considering statutes to allow the administration of local anesthetics by dental hygienists. Results suggest that properly educated dental hygienists in the states surveyed have administered local anesthetics to patients without harm.

Anesthesia, Dental↗

PubMed1991

[Pollution of the workplace by anesthetic gases. Causes and prevention].

Waste anesthetic gas concentrations were measured in areas corresponding to the breathing zones of the anesthetists and operating room nurses for personal exposure (n = 27, time-weighted values) and during special work practices (n = 65). Leaks related to anesthetic machines and high-pressure nitrous oxide components were investigated during (n = 60) and after anesthesia (n = 85). The effect of a local scavenging system on occupational exposure during inhalation induction of anesthesia in children was studied (n = 60). Concentrations of nitrous oxide, halothane, isoflurane, and enflurane were determined by using active dosimeters (SKC 222) and different infrared gas-analyzers. Factors that increase waste anesthetic gas concentrations in operating rooms can be divided into several categories, such as low air conditioning systems, anesthetists' work practices, equipment leakage, including leakage from high-pressure nitrous oxide systems, and inadequate scavenging devices. Equipment leakage is almost invariably present in low-pressure components of the anesthesia machine because so many seals and joints are necessary to permit disassembly for cleaning and replacement. Waste anesthetic gases are also distributed in the exhaled air of patients recovering from anesthesia. To restrict the levels, exposure must be as low as can be achieved with reasonable efforts. Thus, the anesthetic equipment should be designed to avoid leakage, leakage tests should be performed before the use of anesthetic machines, and waste anesthetic gases should be scavenged by central as well as by local systems. Regular and periodic use of a trace gas analyzer permits direct observation of gas leakage and enables anesthetists to modify their work technique in order to reduce avoidable leakage.

Air Pollutants, Occupational↗

PubMed1991

[The ozone layer and its modification by N2O and inhalation anesthetics].

As a result of human activities the ozone layer in the stratosphere, which is necessary for life on earth, has changed. The main causes of ozone destruction are chlorofluorcarbons (CFCs) 11 and 12. Recently, caring anesthetists have wondered if and to what degree N2O and popular potent inhalation anesthetics may also contribute to ozone loss. Having consulted the literature, we attempt to answer that question. The ozone-destroying N2O is chiefly produced by burning fossil elements and nitrogenous fertilizing used in agriculture; the share of medically used N2O lies below 2%. Halothane, enflurane, and isoflurane are halogenated anesthetics that contain ozone-destroying halogens (bromine, chlorine, fluorine) to different extents. Complicated experimental calculations for these volatile anesthetics result in a potential for ozone destruction of 0.36 for halothane and 0.02 for enflurane and isoflurane if the potential for ozone destruction by CFCs is set at 1.0. The lifespan of the inhalation anesthetics in the troposphere is with less than 3 years, dramatically less than that of CFCs (70-140 years). The two most important CFCs, 11 and 12, are considered to be currently produced in a quantity of about 800,000 tons per year. On the other hand, the worldwide production of inhalation anesthetics is said to be only 2,000 tons. In view of the experimental calculations and the low worldwide production, the small greenhouse effect, the shorter lifespan in the troposphere, and the low potential for ozone destruction, the negative effects of medically used N2O and inhalation anesthetics on the ozone layer seem negligible. All in all, the inhalation anesthetics are considered to be responsible for only 0.0005% of the ozone destruction at present.

Air Pollutants↗

PubMed1990

[Effect of local anesthetics on intracellular calcium messenger system].

Local anesthetics have been shown to affect a variety of cellular activities, such as exocytosis, membrane transport, permeability of calcium, and platelet aggregation, among others. Despite the disparate nature of the above phenomena, the calcium ion is essential for all of these cellular processes. Recently, it has been shown that local anesthetics inhibit specific calmodulin-dependent enzymes and protein kinase C-dependent enzymes. Therefore, the mode of action of local anesthetics in the activation of guinea pig neutrophils was examined in this study in order to understand the effect of local anesthetics on the intracellular calcium messenger system. In the presence of calmodulin inhibitors, FMLP-induced chemotaxis and superoxide anion production were strongly suppressed, whereas 1-oleoyl-2-acetylglycerol(OAG)(a direct activator of protein kinase C)-induced superoxide anion production was not affected. In contrast, protein kinase C inhibitors suppressed OAG-induced superoxide anion production but no inhibiting effect on FMLP-induced chemotaxis and superoxide anion production. Local anesthetics suppressed both FMLP- and OAG-induced activation of guinea pig neutrophils. These findings suggest that the inhibiting effect of local anesthetics on the activation of the intracellular calcium messenger system may be part of the pharmacological mechanism of local anesthetics in cellular activities.

Anesthetics, Local↗

PubMed1989

Exposure of rats to inhalational anesthetics alters the hepatobiliary clearance of cholephilic xenobiotics.

Several recent studies indicate that anesthesia-induced alteration of UDP-glucuronic acid concentrations can affect the rate of xenobiotic glucuronidation by UDP-glucuronosyltransferases. Other data demonstrate that the biliary excretion of several cholephilic drugs is depressed in rats anesthetized with diethyl ether. The present study has examined the effect of 2% halothane, 1.5% isoflurane, 2% enflurane and 3% sevoflurane on the clearance and biliary excretion of acetaminophen, digoxin, phenol red and phenol-3,6-dibromphthalein disulfonate. All volatile anesthetics reduced hepatic UDP-glucuronic acid concentrations 50 to 75%. Biliary excretion of acetaminophen as well as the glucuronide and sulfate conjugates was depressed by all anesthetics for about 1 hr, whereas biliary excretion of the glutathione conjugate was increased during this time. Although total clearance, elimination half-life and steady-state volume of distribution were not altered, biliary clearance of acetaminophen was decreased by 39 to 50%. Formation of the glucuronide conjugate of phenol red and its biliary excretion were depressed by all volatile anesthetics; however, total clearance was increased by 15 to 25% during isoflurane or sevoflurane anesthesia. Total clearance and steady-state volume of distribution of digoxin were decreased only in rats exposed to halothane. There were no changes in biliary excretion. Urinary clearance of digoxin was increased by all volatile anesthetics, whereas biliary clearance was decreased by halothane and enflurane. Biliary excretion, clearance and volume of distribution of phenol-3,6-dibromphthalein disulfonate were not altered by the anesthetics. These data indicate that the hepatobiliary elimination of the glucuronidated metabolites is reduced in rats exposed to volatile anesthetics.

Acetaminophen↗

PubMed1989

Effect of anesthetics on calcium stores and membrane order of brain microsomes.

The effects of anesthetic agents from different chemical classes and a nonanesthetic membrane-disordering agent, 2-[2-methoxyethoxy]ethyl-8-[cis-2-n-octylcyclopropyl]octanoate (A2C), on calcium stores of whole brain microsomes and on order of microsomal membranes were compared. Calcium release was determined by measurement of the extramicrosomal calcium concentration and membrane order by the fluorescence polarization of diphenylhexatriene (membrane core) and trimethylammonium-diphenylhexatriene (membrane "surface"). n-Alkanols (methanol, ethanol, propanol, butanol, pentanol, and hexanol), benzyl alcohol (10-100 mM), and diethyl ether (30-300 mM) released calcium from brain microsomes and decreased the surface and interior membrane order of microsomal membranes. Pentobarbital (0.05-1 mM) did not release calcium from microsomes and did not alter the order of brain microsomal membranes. Halogenated anesthetics (halothane, methoxyflurane, and enflurane), 4-phenyl-1-butanol, and A2C decreased membrane order but failed to release calcium from brain microsomes. Comparison of the effects of these agents on microsomal calcium release and order of microsomal membranes revealed that decreases in membrane order are unrelated to the calcium-mobilizing actions of anesthetic compounds. In addition, molecular size appeared to limit ability of anesthetic compounds to release calcium from microsomes. For n-alkanols, benzyl alcohol, and diethyl ether, the ability to release microsomal calcium was correlated with anesthetic potency. Our results demonstrate, for the first time, direct effects of anesthetic agents on intracellular calcium stores of brain tissue and indicate that these stores may be target sites for anesthetics.

Alcohols↗

PubMed1988

Toxicity of local anesthetic agents.

The toxicity of local anesthetic agents can be divided into two categories: (1) systemic toxic reactions due usually to an accidental intravascular injection and (2) local tissue toxicity. The systemic toxicity of local anesthetic agents is primarily characterized by CNS excitation and convulsive activity. The cardiovascular system is more resistant to the toxic actions of local anesthetics. However, local anesthetics can exert a negative chronotropic and inotropic action and cause profound peripheral vasodilation. The combination of cardiac depression and peripheral vascular dilation results in irreversible circulatory collapse. The more potent agents such as bupivacaine appear to be more cardiotoxic and may precipitate ventricular arrhythmias and ventricular fibrillation. Local tissue toxicity is rare following the administration of local anesthetics. However, large doses of chloroprocaine solutions administered intrathecally have been associated with prolonged sensory-motor deficits in a few patients due probably to the low pH and presence of sodium bisulfite in the chloroprocaine solutions. In general, local anesthetic agents are relatively safe if administered properly. However, as with any pharmacological agents, local anesthetics may cause severe toxic reactions due to the improper use of these drugs.

Akathisia, Drug-Induced↗

PubMed1988

Anesthetic action of opiates: correlations of lipid solubility and spectral edge.

The ability of opiates to be a complete anesthetic has been assessed in animals. These studies have investigated the serum levels of opiate required to produce a decrease in anesthetic requirement for a concomitantly administered inhalation anesthetic. A linear dose-response relation has been observed between opiate serum level and reduction in anesthetic requirement up to the level of 50% reduction in minimum alveolar anesthetic concentration (MAC). These studies have not demonstrated the production of one MAC anesthesia by the opiates. Recent EEG studies have provided another means of comparing the central nervous system effects of opiates and inhalation anesthetics. The serum levels of several opiates associated with a 50% reduction (IC50 or 50% inhibitory concentration) in maximal spectral edge frequency (SEF) have been reported. The free, unionized serum levels of each opiate at IC50 in humans or 50% MAC reduction in animals are remarkably similar. We calculated brain lipid opiate content at these serum levels using available physiochemical data. The calculated nanogram and molar brain lipid contents of the drugs fell within a 10-fold range while serum levels varied by 5000-fold. This similarity in membrane lipid content in association with EEG and anesthetic effects suggests that opiate "anesthesia" may involve a membrane effect in addition to the well established receptor interaction.

Anesthesia, Inhalation↗

PubMed1987

Fourier transform infrared studies on phospholipid hydration: phosphate-oriented hydrogen bonding and its attenuation by volatile anesthetics.

Water-phospholipid (dimyristoylphosphatidylcholine) interaction was analyzed in a water-in-oil(benzene) reversed micellar system using Fourier transform infrared spectroscopy, and the effects of inhalation anesthetics (halothane, enflurane, chloroform, and carbon tetrachloride) on the interaction were studied. The O-H stretching frequency, representing water, increased from 3369 cm-1 to a steady 3430 cm-1 when the water/phospholipid mole ratio exceeded 18. The value did not quite reach the frequency of free water of 3490 cm-1 at the water/phospholipid mole ratio of 30. The O-H bending frequency of water did not appear until the water/phospholipid mole ratio exceeded 9. The P=O stretching frequency in the polar head group of unhydrated dimyristoylphosphatidylcholine was 1262 cm-1 and decreased with the addition of water, reaching a steady value of 1238 cm-1 at the water/phospholipid mole ratio of 9. However, the (CH3)3N+ stretching of the choline head, as well as the C-H stretching of the hydrocarbon tail and the C=O stretching of the ester linkage, showed little change by the addition of water. The present results suggest that the primary hydration site of dimyristoylphosphatidylcholine is the phosphate moiety, and up to 18 water molecules are restricted at the polar head group. Apparently, the choline head has a minor role in the hydration of phospholipids despite the positive electrostatic charge. Among the water molecules interacting with the phospholipid head group, about 9 water molecules are strongly bound. The water content in the micelles correlated linearly with the ratio of the absorbance band area between O-H and C=O stretching. The addition of polar anesthetics (halothane, enflurane, and chloroform) increased the O-H stretching frequency and elevated the ratio of the absorbance band area between O-H and C=O stretching, implying that the anesthetics released the structured water molecules bound at the phospholipid-water interface. The anesthetics disrupted the hydrogen bond between the phosphate moiety of the phospholipid and water. Although apolar carbon tetrachloride also released bound water molecules, the magnitude was less than that of the polar anesthetics, as expected. The anesthetics did not affect the C-H stretching or C=O stretching bands, indicating that the disordering action upon the hydrocarbon core of phospholipid membranes is minimal at low water content. These results support our view that the primary site of action of inhalation anesthetics is the membrane-water interface, releasing bound water molecules.

Anesthetics↗

PubMed1987

[Volatile anesthetics and n-alcohols inhibit the uptake of noradrenaline in pheochromocytoma cells].

UNLABELLED: Studies with perfused animal organs did not show a significant inhibition of the norepinephrine uptake by volatile anesthetics However, the uptake of norepinephrine into isolated chromaffin granules proved to be halothane-sensitive , and there is indirect evidence for an inhibition of norepinephrine uptake by halothane in the dog saphenous vein. So far no literature is available on norepinephrine uptake into cultured cells in the presence of volatile anesthetics. The rat pheochromocytoma cell line PC 12, which shares many properties with adrenal medulla cells and also with sympathetic neurons, has been used as a model to study norepinephrine uptake and release. One of its properties in common with sympathetic neurons is the high-affinity uptake system for norepinephrine. Therefore, we have used PC 12 cells as a pharmacologically well-established model system to study the effect of general anesthetics on the uptake of norepinephrine. METHODS: The experiments were performed with monolayers of PC 12 cells on 3 cm petri dishes. The cells were allowed to take up tritiated norepinephrine (0.25 microCI/ml) for 20 min at 36 degrees C in the presence and absence of general anesthetics. RESULTS AND DISCUSSION: The volatile anesthetics halothane, enflurane, isoflurane, and methoxyflurane in clinical relevant concentrations inhibited the high-affinity uptake of tritiated norepinephrine into the PC 12 cells (Fig. 1). We could further show an inhibition of norepinephrine uptake by n-alkanols at concentrations that cause anesthesia in tadpoles. Fig. 2 illustrates that a good correlation (r = 0.997 for the n-alkanols, r = 0.934 for the volatile anesthetics) exists between anesthetic potency and the IC50 for norepinephrine uptake inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Gland Neoplasms↗

PubMed1983

Hepatic injury induced by anesthetic agents in rats.

Recent studies on rats pretreated with phenobarbital indicate that anesthetic agents may produce hepatic injury even when metabolism of the anesthetic is almost negligible. This implies that anesthesia per se may cause hepatic injury. To evaluate this possibility, we determined the amount of hepatic injury produced by halothane, enflurane, isoflurane, thiopental, and fentanyl in rats pretreated with phenobarbital. Anesthetics were administered in doses ranging from 0.04-1.1 MAC (or their equivalent for thiopental or fentanyl) and were given with 10% oxygen for 2 h. Liver specimens taken 24 h later were examined microscopically for hepatic injury. At concentrations of 5-40% of MAC, all anesthetics produced more hepatic injury than did control conditions (i.e., exposure to only 10% oxygen for 2 h). There were no systematic differences among agents, nor did starvation before anesthetic exposure produce a difference among agents. Therefore, mechanisms other than anesthetic metabolism are needed to explain hepatic injury produced by anesthetic agents.

Anesthetics↗

PubMed1981

Waste anesthetic gas exposures to veterinarians and animal technicians.

A survey of veterinarians was conducted in an 11-county region of eastern Colorado to determine the extent of usage of inhalation anesthetics and to measure exposures of veterinarians and their assistants to waste anesthetic gases. The survey indicated that inhalation anesthetics were used in 80.8% of the 210 practices. Exposures to waste anesthetics in veterinary practices were far less than reported in human hospitals. Waste anesthetic concentrations were affected by size of the patient, type of breathing system, and use of scavenging systems. Dilution ventilation had no effect on breathing zone concentrations. The endotracheal tube and occasionally the anesthetic machine were the major sources of leakage of anesthetic gases.

Air Pollutants↗

PubMed1980

Effects of anesthetics on the heart.

General anesthetic agents can be divided on the basis of whether or not they "sensitize" the heart to the arrhythmogenic actions of catecholamines. There appear to be two separate means by which the catecholamines cause ventricular arrhythmias during anesthesia: one is related to a reduction in supraventricular driving rate caused both directly by the anesthetic and reflexly in response to the pressor effect of catecholamine injection; the other action (favoring ventricular fibrillation) is caused by direct anesthetic depression of the intraventricular conducting system. Of the anesthetics used today, halothane has the most pronounced cardiac sensitizing action. The same anesthetics can also be divided according to whether or not they stimulate sympathetic nervous system activity. Those that do (e.g., diethyl ether) abolish the barostatic reflexes. Those that do not (e.g. halothane) reset the barostatic reflexes to favor a reduced level of arterial pressure; they also tend to cause a reduction in sympathetic nervous activity efferent to the heart. Parasympathetic nervous actions are relatively insignificant. All general anesthetics cause myocardial depression at all concentrations that are clinically useful. The mechanism appears to involve a reduction in the Ca2+ available to the contractile elements. Exactly how anesthetics do this is unclear, but these drugs appear to decrease both the Ca2+ influx across the plasma membrane and the Ca2+ content of the sarcoplasmic reticulum.

Anesthetics↗

PubMed1980

The possible role of catecholamines in the protective effect of general anesthetics against kidney lesions in rats subjected to hemorrhagic hypotension.

Dibenamine, 15 mg/kg, injected i.p. in rats anesthetized with ketamine, 60 min before bleeding for 60 min against 40 mm Hg, significantly reduced the severity of kidney lesions. The maximum bleeding volume was reduced by 14%. Adrenalectomy also reduced the bleeding volume but all animals died within 24 hr. In unanesthetized rats bled against 40 mm Hg, plasma adrenaline and nor-adrenaline rose approximately tenfold as compared with unbled animals. Comparable marked increases in plasma adrenaline and somewhat smaller increases in plasma nor-adrenaline were observed after bleeding rats anesthetized with ketamine and ethylurethane, anesthetics which protect only slightly against the occurrence of kidney lesions. The rise in plasma adrenaline and nor-adrenaline was significantly lower after bleeding rats anesthetized with the highly protective anesthetics Na-pentobarbital, halothane and methoxyflurane. If, however, rats anesthetized with Na-pentobartical were bled for 40 min against 25 mm Hg, a situation in which the occurrence of kidney lesions is not prevented, the plasma concentration of both catecholamines was as high as in unanesthetized rats bled against 40 mm Hg. It is concluded that vasoconstriction due to the release of catecholamines is an important factor in the generation of kidney lesions during hypotension in rats and that the protective effect of a number of general anesthetics largely depends on their ability to suppress the release of catecholamines.

Adrenalectomy↗

PubMed1995

Local anesthetic use by dentists in Ontario.

A mail survey to obtain data on the annual use of local anesthetics in dentistry was sent to each of the 6,271 certified dentists in Ontario in 1993. The survey asked dentists to identify the different types and total amounts of local anesthetics used in their practice yearly. A total of 2,426 dentists responded to the survey. Based on extrapolation of the data collected, it is estimated that more than 11,000,000 cartridges of local anesthetic are administered annually by dentists in Ontario. The distribution of use of specific types of local anesthetics and vasoconstrictors was also determined. Lidocaine with 1:100,000 epinephrine accounted for 23.4 per cent of all cartridges used, followed by articaine with 1:200,000 epinephrine (19.9 per cent), articaine with 1:100,000 epinephrine (17.9 per cent), prilocaine with 1:200,000 epinephrine (16.4 per cent), mepivacaine with 1:20,000 levonordefrin (6.4 per cent), and mepivacaine plain (6.3 per cent). Other anesthetics were used to a lesser degree. Further analysis revealed no statistically-significant differences in the use of local anesthetics among dentists who responded to the survey and non-responders. The results of this survey document the current use of local anesthetics in dentistry.

Anesthesia, Dental↗

PubMed1995

[Is there a receptor for volatile anesthetics?].

Because of the presence of inequality of the effect of volatile anesthetics on various neurotransmission systems, a specific receptor is proposed. Nonetheless, the differences are only of the magnitude, and almost all synapses are equally affected. The outstanding features of the action of volatile anesthetics are this wide range of the target, and the steep dose-response curve. The steep dose-response curve indicates that various synapses respond to anesthetics with high cooperativity. When a string of amino acids folds into biologically meaningful structure by enclosing hydrophobic areas inside, some hydrophobic parts are left at the protein-water interface. These hydrophobic patches become the binding site for anesthetics. Because of the wide difference in the structures of anesthetics, it is difficult to assume a specific binding site of lock-and-key type for all anesthetics with all synaptic proteins. Presumably volatile anesthetics bind most hydrophobic patches nonselectively. The affinity to each patch may differ, and the relative specificity to each synapse may ensue. To define these areas as a receptor is a matter of opinion.

Anesthetics, Inhalation↗