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PubMed2005

Modulation of human 5-hydroxytryptamine type 3AB receptors by volatile anesthetics and n-alcohols.

Functional 5-hydroxytryptamine type 3 (5-HT3) receptors can be formed by 5-HT3A subunits alone or in combination with the 5-HT3B subunit, but only the 5-HT3A receptor has been previously studied with respect to the modulation by volatile anesthetics and n-alcohols. Using two-electrode voltage-clamp, we show for the first time the modulation of heteromeric human (h)5-HT3AB receptors, expressed in Xenopus oocytes, by a series of n-alcohols and halogenated volatile anesthetics. At twice their anesthetic concentration, compounds having a molecular volume of less than 110 A3 enhanced submaximal 5-HT-evoked current. Compounds larger than 110 A3 inhibited submaximal 5-HT-evoked current. In experiments examining 5-HT concentration-response relationships, chloroform and butanol caused a slight decrease in the 5-HT EC50. Sevoflurane and octanol inhibited 5-HT-evoked current at all 5-HT concentrations tested but had no effect upon the 5-HT EC50. Compared with previous data on homomeric h5-HT3A receptors, the presence of the h5-HT3B subunit reduces the enhancement of h5-HT3 receptors by smaller halogenated volatile anesthetics and n-alcohols. In summary, these results suggest that heteromeric h5-HT3AB receptors are modulated by halogenated volatile anesthetics at clinically relevant concentrations, in addition to n-alcohols, suggesting that these receptors may be another physiological target for these compounds. The modulation is dependent upon the molecular volume of the compound, further supporting the concept of an anesthetic binding pocket of limited volume common on other Cys-loop ligand-gated ion channels. Incorporation of the 5-HT3B subunit alters either the anesthetic binding site or the allosteric interactions between anesthetic binding and channel opening.

Alcohols↗
PubMed1994

merA gene expression in aquatic environments measured by mRNA production and Hg(II) volatilization.

The relationship of merA gene expression (specifying the enzyme mercuric reductase) to mercury volatilization in aquatic microbial communities was investigated with samples collected at a mercury-contaminated freshwater pond, Reality Lake, in Oak Ridge, Tenn. Levels of merA mRNA transcripts and the rate of inorganic mercury [Hg(II)] volatilization were related to the concentration of mercury in the water and to heterotrophic activity in field samples and laboratory incubations of pond water in which microbial heterotrophic activity and Hg(II) concentration were manipulated. Levels of merA-specific mRNA and Hg(II) volatilization were influenced more by microbial metabolic activity than by the concentration of mercury. merA-specific transcripts were detected in some samples which did not reduce Hg(II), suggesting that rates of mercury volatilization in environmental samples may not always be proportional to merA expression.

Drug Resistance↗
PubMed1999

Ubiquitin metabolism affects cellular response to volatile anesthetics in yeast.

To investigate the mechanism of action of volatile anesthetics, we are studying mutants of the yeast Saccharomyces cerevisiae that have altered sensitivity to isoflurane, a widely used clinical anesthetic. Several lines of evidence from these studies implicate a role for ubiquitin metabolism in cellular response to volatile anesthetics: (i) mutations in the ZZZ1 gene render cells resistant to isoflurane, and the ZZZ1 gene is identical to BUL1 (binds ubiquitin ligase), which appears to be involved in the ubiquitination pathway; (ii) ZZZ4, which we previously found is involved in anesthetic response, is identical to the DOA1/UFD3 gene, which was identified based on altered degradation of ubiquitinated proteins; (iii) analysis of zzz1Delta zzz4Delta double mutants suggests that these genes encode products involved in the same pathway for anesthetic response since the double mutant is no more resistant to anesthetic than either of the single mutant parents; (iv) ubiquitin ligase (MDP1/RSP5) mutants are altered in their response to isoflurane; and (v) mutants with decreased proteasome activity are resistant to isoflurane. The ZZZ1 and MDP1/RSP5 gene products appear to play important roles in determining effective anesthetic dose in yeast since increased levels of either gene increases isoflurane sensitivity whereas decreased activity decreases sensitivity. Like zzz4 strains, zzz1 mutants are resistant to all five volatile anesthetics tested, suggesting there are similarities in the mechanisms of action of a variety of volatile anesthetics in yeast and that ubiquitin metabolism affects response to all the agents examined.

Adaptor Proteins, Signal Transducing↗
PubMed1985

Deaths from abuse of volatile substances: a national epidemiological study.

A survey of the United Kingdom detected 282 deaths from abuse of volatile substances during 1971-83. Deaths appeared to have increased in the most recent years, reaching 80 in 1983. Age at death ranged from 11 to 76 years but most deaths (72%) occurred under 20 years. Ninety five per cent of the subjects were male, and in 1983 deaths from volatile substance abuse accounted for 2% of all deaths in males aged 10-19. All areas of the United Kingdom were affected, the rates being highest in Scotland and urban areas. All social classes were affected, though rates were highest in social class V and the armed forces. The volatile substances abused were gas fuels (24%), mainly butane; aerosol sprays (17%); solvents in glues (27%); and other volatile substances, such as cleaning agents (31%). In 51% of cases death was attributed to the direct toxic effects of the substance abused, in 21% to plastic bag asphyxia, in 18% to inhalation of stomach contents, and in 11% to trauma. Deaths associated with the abuse of glues were more likely to be traumatic, but all substances appeared capable of killing directly by their toxic effects, probably by a cardiac mechanism. Only a small proportion of deaths (6%) were due to the abuse of glues among children under 16; hence current attempts to limit access of children to glues will probably have little impact on overall mortality.

Adhesives↗
PubMed1989

Neuropsychological consequences of volatile substance abuse: a population based study of secondary school pupils.

OBJECTIVE: To examine the effects of volatile substance abuse on neuropsychological functioning. DESIGN: A sample of index children and matched controls were identified by a two stage procedure. Firstly, over 5000 secondary school pupils completed a screening questionnaire, and, secondly, a sample of those who acknowledged volatile substance abuse and a matched sample of those who denied the practice were assessed in detail by means of (a) individually conducted interviews and (b) toxicological examination of breath samples (to exclude those intoxicated at the time of testing). SETTING: 16 Local education authority secondary schools in London. SUBJECTS: 160 Pupils aged 13-16: 80 index children who had abused volatile substances to the point of intoxication at least once (confirmed by interview) and 80 controls (confirmed by interview) matched for school year, sex, and ethnic background. MEASUREMENTS AND MAIN RESULTS: Neuropsychological functioning tests provided 35 main outcome measures and were administered blind. Data on educational test performance before substance abuse began were obtained retrospectively. Information on potentially confounding social factors, such as number of siblings, tenure of housing, and parents' socioeconomic and employment state was also obtained. The index children performed significantly less well than the controls in tests of vocabulary, verbal intelligence quotient, full scale intelligence quotient, and a measure of impulsivity. When background social disadvantage was taken into account these differences were no longer significant. There were no significant associations between performance on psychological testing and frequency of abuse, and relations with other aspects of the children's history of abuse were generally weak or unsystematic. Comparisons between the results of these tests and of educational tests taken before substance abuse produced equivocal findings. CONCLUSION: Volatile substance abuse, as commonly practised by secondary school pupils, is unlikely to result in neuropsychological impairment.

Adolescent↗
PubMed2003

Effects of volatile organic compounds, damp, and other environmental exposures in the home on wheezing illness in children.

BACKGROUND: The effects of indoor exposure to volatile organic compounds (VOCs), including formaldehyde, on respiratory health are not clearly understood. The aim of this study was to determine the independent effects of VOCs and other common environmental exposures in the home on the risk and severity of persistent wheezing illness in children. METHODS: Total volatile organic compounds, formaldehyde, nitrogen dioxide, damp (on a four category scale of % wood moisture equivalent), and environmental tobacco smoke (from salivary cotinine) were measured objectively in the homes of 193 children with persistent wheezing illness and 223 controls aged 9-11 years in Nottingham, UK. RESULTS: The risk of wheezing illness was significantly increased only in relation to damp (odds ratio (OR) per increasing category=1.32 (95% confidence interval (CI), 1.00 to 1.75)), and was unrelated to the other exposures measured. Among cases, formaldehyde and damp were associated with more frequent nocturnal symptoms (OR per increasing quartile and category, respectively, 1.45 (1.06 to 1.98) and 1.97 (1.10 to 3.53)), significantly more so in atopic cases, but there was no effect of total volatile organic compounds, nitrogen dioxide, or cotinine. CONCLUSIONS: Domestic volatile organic compounds are not a major determinant of risk or severity of childhood wheezing illness, though formaldehyde may increase symptom severity. Indoor damp increases both the risk and severity of childhood wheezing illness.

Air Pollution, Indoor↗
PubMed1997

Modeling volatility using state space models.

In time series problems, noise can be divided into two categories: dynamic noise which drives the process, and observational noise which is added in the measurement process, but does not influence future values of the system. In this framework, we show that empirical volatilities (the squared relative returns of prices) exhibit a significant amount of observational noise. To model and predict their time evolution adequately, we estimate state space models that explicitly include observational noise. We obtain relaxation times for shocks in the logarithm of volatility ranging from three weeks (for foreign exchange) to three to five months (for stock indices). In most cases, a two-dimensional hidden state is required to yield residuals that are consistent with white noise. We compare these results with ordinary autoregressive models (without a hidden state) and find that autoregressive models underestimate the relaxation times by about two orders of magnitude since they do not distinguish between observational and dynamic noise. This new interpretation of the dynamics of volatility in terms of relaxators in a state space model carries over to stochastic volatility models and to GARCH models, and is useful for several problems in finance, including risk management and the pricing of derivative securities. Data sets used: Olsen & Associates high frequency DEM/USD foreign exchange rates (8 years). Nikkei 225 index (40 years). Dow Jones Industrial Average (25 years).

Artificial Intelligence↗
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↗
PubMedDate not supplied

Detecting alveolar epithelial injury following volatile anesthetics by (99m)Tc DTPA radioaerosol inhalation lung scan.

BACKGROUND: Many volatile anesthetics have long been thought to affect alveolar epithelial permeability. OBJECTIVE: The purpose of this study was to examine the acute effects of volatile anesthetics on the permeability of the alveolocapillary barrier to (99m)Tc DTPA. METHODS: Twenty-seven patients (24 females, 3 males, age 29-73 years) undergoing operation were enrolled in this study and grouped according to the type of anesthesia received. Group 1 patients were administered 1% halothane. Group 2 patients were given 1.5% isoflurane. Intravenous anesthesia without volatile anesthetics were used for group 3 patients. Before and after anesthesia, (99m)Tc DTPA radioaerosol inhalation lung scans were performed to detect alveolar epithelial injury due to volatile anesthetics. The negative slope of the regression line was designated as the (99m)Tc DTPA pulmonary clearance rate and was expressed in terms of percentage decrease in radioactivity per minute. RESULTS: In group 1, the (99m)Tc DTPA clearance rates were 1.26 +/- 0.34 and 1.29 +/- 0.38 before and after anesthesia, respectively. The difference was not significant (p > 0.05). In group 2, the rates were 0.76 +/- 0.20 and 1.10 +/- 0. 37, before and after anesthesia, respectively. The difference was significant (p < 0.05). In group 3, the clearance rates were 1.07 +/- 0.38 and 1.21 +/- 0.48, before and after anesthesia, respectively. The difference was not significant. CONCLUSIONS: Following isoflurane administration, the more rapid pulmonary clearance of (99m)Tc DTPA indicates that isoflurane increases the permeability of the alveolo-capillary barrier.

Adult↗
PubMed1986

Manipulation of rat brain fatty acid composition alters volatile anesthetic potency.

The molecular mechanism of volatile anesthetic action remains unknown. Attempts to elucidate this mechanism have been complicated by the absence of models in which changes in neuronal cellular properties can be correlated with changes in whole animal anesthetic effect. In this study we describe a model where diet-induced alterations in rat brain fatty acid composition are correlated with alterations in volatile anesthetic potency. Rats maintained on a fat-free diet showed significant depletion of arachidonic acid (20:4 omega 6; 5,8,11,14-eicosatetraenoic acid) and docosahexaenoic acid (22:6 omega 3; 4,7,10,13,16,19,-docosahexaenoic acid) in brain, and a corresponding increase in Mead acid (20: 3 omega 9; 5,8,11-eicosatrienoic acid). These fat-deprived rats were significantly more sensitive to all volatile anesthetics tested than were age-controlled rats on a normal diet. Parenteral supplementation of the fat-deprived animals with linolenic acid (18: 3 omega 3, 9,12,15-octadecatrienoic acid) completely reconstituted the docosahexaenoic acid content of brain without affecting anesthetic sensitivity. In contrast, supplementation of the fat-deprived rats with linoleic acid (18: omega 6; 9,12-octadecadienoic acid) caused a dramatic decrease in anesthetic sensitivity, but only a small change in whole brain arachidonate content. Further analysis revealed that linoleate supplementation of fat-deprived animals resulted in a preferential normalization of the arachidonate content of brain phosphatidylinositol as compared with other brain phosphoglycerides. These results demonstrate for the first time a correlation between changes in membrane composition and anesthetic effect, and indicate that the precise fatty acid composition (perhaps in specific phospholipids) of brain is important in the mechanism of volatile anesthetic action.

Anesthetics↗
PubMed1992

Blood flow and tissue oxygen pressures of liver and pancreas in rats: effects of volatile anesthetics and of hemorrhage.

The object of this investigation was to compare the effects of volatile anesthetics and of hemorrhage at comparable arterial blood pressures on splanchnic blood flow (radioactive microspheres) and tissue oxygenation of the liver and pancreas (surface PO2 [PSO2] electrodes). In contrast to earlier studies, we did not use identical minimum alveolar anesthetic concentration multiples as a reference to compare volatile anesthetics; rather, we used the splanchnic perfusion pressure. Under general anesthesia (intravenous chloralose) and controlled ventilation, 12 Sprague-Dawley rats underwent laparotomy to allow access to abdominal organs. Mean arterial pressure was decreased from 84 +/- 3 mm Hg (mean +/- SEM) at control to 50 mm Hg by 1.0 +/- 0.1 vol% halothane, 2.2 +/- 0.2 vol% enflurane, and 2.3 +/- 0.1 vol% isoflurane in a randomized sequence. For hemorrhagic hypotension, blood was withdrawn gradually until a mean arterial pressure of 50 mm Hg was attained. Volatile anesthetics and hemorrhage reduced cardiac output, and hepatic arterial, portal venous, and total hepatic blood flows by comparable degrees. Mean hepatic PSO2 decreased significantly from 30.7 +/- 2.6 mm Hg at control to 17.4 +/- 2 and 17.5 +/- 2 mm Hg during enflurane and isoflurane (each P less than 0.05) anesthesia, respectively. The decrease to 11.5 +/- 2.5 mm Hg was more pronounced during halothane anesthesia. Hemorrhagic hypotension was associated with the lowest hepatic PSO2 (3.4 +/- 1.3 mm Hg) and the highest number of hypoxic (0-5 mm Hg 86%) and anoxic PSO2 values (0 mm Hg 46%). Pancreatic blood flow and oxygenation remained unchanged from control during halothane and enflurane administration, whereas isoflurane increased both variables. Hemorrhagic hypotension slightly reduced pancreatic flow (-8%) but significantly decreased PSO2 from 58 +/- 5 mm Hg at control to 36 +/- 3 mm Hg, with 7% of all measured values in the hypoxic range. Thus, volatile anesthetics preserved pancreatic but not hepatic blood flow and tissue oxygenation in this rat model. Despite comparable effects on perfusion, the PSO2 of the liver and pancreas was the least during hemorrhagic hypotension compared to that with the anesthetics. Because the volative anesthetic-induced hypotension has such a different effect on splanchnic tissue oxygenation compared with hemorrhagic-induced hypotension, the authors conclude that the method of inducing hypotension may have different effects on oxygenation of various tissues.

Anesthetics↗
PubMed1994

Electrophysiologic interaction between class I antiarrhythmic drugs and volatile anesthetics in depressant effects on ventricular activation in a canine myocardial infarction model.

Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarrhythmic drugs depress the ventricular activation in the infarcted myocardium. In the present study, we examined the electrophysiologic interaction between volatile anesthetics (sevoflurane, isoflurane) and class I antiarrhythmic drugs (lidocaine, procainamide) in effects on the ventricular delayed activation in a canine myocardial infarction model. The conduction time of the premature stimulation-induced ventricular excitation was measured in both normal and infarcted zones of the ventricle. An interval from the premature stimulus artifact to the epicardial activation was measured on bipolar electrograms as an index of conduction time, i.e., activation time. In the infarcted zone, the volatile anesthetics and class I antiarrhythmic drugs prolonged the activation time in the infarcted zone, and the combination of the volatile anesthetics and the class I antiarrhythmic drugs markedly prolonged the activation time or blocked the delayed activation. In the normal zone, a similar synergistic interaction was observed, but the effect of these drugs was less compared with that in the infarcted zone. From these results, possible mechanisms to explain the synergistic interaction were discussed.

Anesthetics↗
PubMed2000

Volatile components of cigarette smoke: effect of acrolein and acetaldehyde on human gingival fibroblasts in vitro.

BACKGROUND: Tobacco and some of its volatile and non-volatile components have been found to affect many types of cells including gingival fibroblasts. Since normal gingival fibroblast functioning is fundamental to the maintenance of the periodontal connective tissue, as well as to wound healing, we examined the effect of acrolein and acetaldehyde, volatile components of cigarette smoke, on proliferation, attachment, and ultrastructure of human gingival fibroblasts (HGFs) in culture. METHODS: Human gingival fibroblast (HGF) strains derived from healthy individuals with non-inflamed gingiva were used in this study. The cells were incubated in the presence of different concentrations of acrolein and acetaldehyde. Cell attachment and proliferation were evaluated after incubation for 3 hours and 5 days, respectively. In addition, the cells were examined with a transmission electron microscope in order to evaluate their morphology. RESULTS: The results show that acrolein and acetaldehyde produced dose-dependent inhibition of HGF attachment and proliferation. The cytotoxic effect was, however, reversible when both substances were removed, after 3 days, from the medium. The main ultrastructural finding for the HGF cytoplasm was the presence of vacuoles and lysosomal structures that became prominent with increasing concentration of acrolein and acetaldehyde. CONCLUSIONS: Our experimental data suggest that acrolein and acetaldehyde, volatile components of tobacco smoke, are detrimental to HGF survival and consequently to the oral connective tissue. According to our morpho-functional evidence, these findings corroborate clinical and epidemiological investigations demonstrating smoke as a risk factor in the development of periodontal disease.

Acetaldehyde↗
PubMed2001

Human gingival fibroblast cytoskeleton is a target for volatile smoke components.

BACKGROUND: Several in vitro investigations have indicated that the particulate phase of cigarette smoke as nicotine affects many cell types including gingival fibroblasts, but few studies have examined the effect of volatile fraction on cellular structures involved in cell functions such as adhesion and proliferation. Since gingival fibroblast survival and reproduction are fundamental to maintaining the oral connective tissue as well as to wound healing, the effects of acrolein and acetaldehyde, volatile fractions of cigarette smoke, on cytoskeleton were examined in human gingival fibroblasts (HGFs) in vitro. METHODS: Human gingival fibroblast (HGF) strains from healthy subjects with non-inflamed gingiva were utilized. The cells were incubated in different concentrations of acrolein and acetaldehyde. Cell adhesion was evaluated after 3 hours. The influence of both substances on cytoskeletal structures, tubulin and vimentin intermediate filaments (VIF), was investigated using indirect immunofluorescence technique. RESULTS: The results show that both substances produced similar effects, resulting in a dose-dependent inhibition of HGF adhesion. Disturbance of HGF cytoskeleton consisted of a disruption of microtubules and vimentin microfilaments with alterations in cell shape. CONCLUSIONS: Our experimental findings suggest that volatile fractions of cigarette smoke such as acrolein and acetaldehyde, because their ability to bind and interact with the cytoskeleton, prevent HGF adhesion. Consequently the maintenance of the oral connective tissue and integrity and remodeling could be impaired. According to our morphological evidence, these findings confirm other clinical and epidemiological investigations reporting that volatile components of cigarette smoke could lead to the initiation and progression of periodontal disease.

Acetaldehyde↗
PubMed2001

Occupational exposure to volatile anaesthetics: epidemiology and approaches to reducing the problem.

Long term occupational exposure to trace concentrations of volatile anaesthetics is thought to have adverse effects on the health of exposed personnel. In contrast with halothane--an agent likely to cause mutagenic effects and proven to be teratogenic--isoflurane and enflurane have not so far been proved to have adverse effects on the health of personnel exposed long term. Data on the newer agents sevoflurane and desflurane are limited. Since possible health hazards from long term exposure to inhalational anaesthetics cannot yet be definitively excluded, many Western countries have established limits for exposure. These usually range from 2 to 10 ppm as a time-weighted average over the time of exposure. A number of investigations have demonstrated that, in operating theatres with modern climate control and waste anaesthetic gas scavenging systems, occupational exposure is unlikely to exceed threshold limits. However, occupational exposure from the use of volatile agents in operating theatres with poor air control--especially during bronchoscopy procedures in paediatric patients--remains a source of concern. This also holds true for both postanaesthesia care units (PACU) and intensive care units (ICU) lacking proper air conditioning and waste gas scavengers. To minimise occupational exposure to volatile anaesthetics, all measures must be taken to provide climate control and properly working scavenging devices, and ensure sufficient personal skill of the anaesthetist, e.g. during inhalational mask induction. Furthermore, low-flow anaesthesia should be used whenever possible. The sole use of intravenous drugs such as propofol instead of volatile agents, were this possible, would eliminate occupational exposure, but may result in environmental pollution by toxic metabolites (e.g. phenol).

Anesthetics, Inhalation↗
PubMed2000

Tandem pore domain K channels: an important site of volatile anesthetic action?

Despite over 150 years of clinical use, the mechanism and molecular elements by which volatile anesthetics produce unconsciousness are not established. Although enhanced activity of inhibitory neurotransmitter systems (GABAA) and depression of excitatory neurotransmitter systems (NMDA) probably contribute to the anesthetic state, the role of other ion channels families have also been studied. Potassium channels represent the largest group of mammalian ion channels and their activity to reduce neuronal excitability makes them viable candidates as sites of anesthetic action. Several studies from the 1970's and 80's identified volatile anesthetic enhancement of neuronal potassium currents. More recently, a new family of K channels with a unique structure (tandem pore domains) that may be responsible for baseline or background K currents have been isolated and some members of this family can be activated by volatile anesthetics. These emerging findings suggest a new molecular mechanism by which volatile anesthetics may mediate central nervous system depression.

Action Potentials↗
PubMed2004

Preconditioning of the myocardium by volatile anesthetics.

Cardiovascular disease continues to be a major health problem. Tremendous efforts have been invested in clinical and laboratory research in the hopes of decreasing the risk of patients with cardiovascular disease undergoing cardiac and non-cardiac surgeries. A powerful endogenous mechanism of cardioprotection, termed ischemic preconditioning, was reported in a laboratory setting whereby the myocardium can be preconditioned by a brief ischemic episode and protected against a subsequent prolonged ischemic attack. Since this initial observation, several pharmacological agents have been demonstrated to mimic ischemic preconditioning. These include opioids, potassium channel openers such as pinacidil and diazoxide, and adenosine agonists. Recently, volatile anesthetics were found to be powerful cardiac preconditioning agents. Infarct size reduction as the result of anesthetic-induced preconditioning paralleled that of ischemic preconditioning. The use of volatile anesthetics as preconditioning agents in high-risk patients undergoing cardiac and non-cardiac surgeries can potentially result in the reduction of morbidity and disability in this class of patients. However, to fully realize the potential use of this novel property of volatile anesthetics, the underlying mechanism of anesthetic-induced preconditioning would need to be elucidated. This review highlights the major recent findings on the cardioprotective effects of volatile anesthetics.

Anesthetics, Inhalation↗
PubMed1991

Volatile substance abuse.

Volatile substance abuse has been reported in the literature over the past 20 years or so, and has apparently increased as countries have become more industrialised. This review attempts to clarify trends in volatile substance abuse, problems associated with this behaviour and possible solutions. Data sources included a Medline Search on volatile substance abuse over the last five years, Commonwealth publications, recent State and Territory inhouse publications, three research monographs from the National Institute on Drug Abuse (NIDA) and an article library from the author's workplace. Some 250 articles and monographs were identified, reviewed and categorised into sections relating to epidemiology (including mortality), physiological effects and responses to the problem. Articles were used for reference where they reflected the most up-to-date information or where they were seen as authoritative statements. While the body of knowledge concerning volatile substance abuse has improved, little progress has been made in finding effective solutions to the problem. The fact that users are typically young and that there is a real risk of sudden death associated with even initial use suggests that continuing research is needed to develop innovative approaches to the problem.

Aerosol Propellants↗