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PubMed1996

Interference of volatile anaesthetics with infrared analysis of carbon dioxide and nitrous oxide tested in the Dräger Cicero EM using sevoflurane.

In theory, setting an infrared multi-gas analyser to measure a volatile anaesthetic different from that in the sampled gas mixture may cause interference with carbon dioxide and nitrous oxide readings. The theory was investigated during evaluation of the Dräger Cicero EM anaesthetic workstation for the Medical Devices Agency. Interference occurred as predicted, and was most pronounced when the vapour analyser of the Cicero EM was deliberately and erroneously set to measure isoflurane, but with sevoflurane present in the gas mixture. With 6% sevoflurane in the gas mixture, the carbon dioxide reading decreased from 5% to 3.6%, and the nitrous oxide reading increased from 0% to 8% although, as the apparent isoflurane reading was 9%, the Cicero EM would alert the operator to the problem. However, operators are encouraged to ensure that, when using gas analysers such as that incorporated into the Cicero EM, the analyser is set to measure the correct volatile anaesthetic (the Cicero EM does this automatically when a Vapor vaporizer is attached) and the breathing system does not contain any other volatile anaesthetic agents.

Anesthesiology↗
PubMed1998

Volatile anaesthetics have differential effects on recombinant m1 and m3 muscarinic acetylcholine receptor function.

Muscarinic acetylcholine signalling plays major roles in regulation of consciousness, cognitive functioning, pain perception and circulatory homeostasis. Halothane has been shown to inhibit m1 muscarinic signalling. However, no comparative data are available for desflurane, sevoflurane or isoflurane, nor have the anaesthetic effects on the m3 subtype (which is also prominent in the brain) been studied. Therefore, we have investigated the effects of these compounds on isolated m1 and m3 muscarinic receptor function. Defolliculated Xenopus oocytes expressing recombinant m1 or m3 muscarinic or (for comparison) AT1A angiotensin II receptors were voltage clamped, and Ca(2+)-activated Cl- currents (ICl(Ca)) induced by acetyl-beta-methylcholine (Mch) or angiotensin II were measured in the presence of clinically relevant concentrations of halothane, sevoflurane, desflurane or isoflurane. To determine the site of action of the volatile anaesthetics we compared anaesthetic effects on m1, m3 and AT1A receptor function and studied the effects of volatile anaesthetics on signalling induced by intracellular injection of the second messenger IP3. Desflurane had a biphasic effect on m1 signalling, enhancing at a concentration of 0.46 mmol litre-1 but depressing at 0.92 mmol litre-1. A similar, although not significant, trend was observed with m3 signalling. Isoflurane had no effect on m1 signalling, but profoundly inhibited m3 signalling. Sevoflurane depressed the function of m1 and m3 signalling in a dose-dependent manner. Halothane, similar to its known effect on m1 signalling, dose-dependently depressed m3 function. ICl(Ca) induced by intracellular injections of IP3 were unaffected by all four anaesthetics. Similarly, none of the anaesthetics tested affected AT1A signalling. Absence of interference with AT1A signalling and intracellular pathways suggest that the effects of anaesthetics on muscarinic signalling most likely result from interactions with the m1 or m3 receptor molecule. Multiple interaction sites with different affinities may explain the biphasic response to desflurane. Anaesthetic-specific effects on closely related receptor subtypes suggest defined sites of action for volatile anaesthetics on the receptor protein.

Anesthetics, Inhalation↗
PubMed2001

Prediction of volatile anaesthetic solubility in blood and priming fluids for extracorporeal circulation.

Volatile anaesthetics are often used during cardiopulmonary bypass (CPB). To understand the kinetics of inhaled anaesthetics during CPB, anaesthetists should understand changes in blood solubility caused by fluid use. We set out to predict the solubility of three volatile anaesthetics, desflurane, isoflurane and halothane, during CPB by determining: (i) their solubility in fresh whole blood and eight CPB priming fluids at 37 degrees C; (ii) the effect of temperature on the solubility of these anaesthetics in lactated Ringer's, gelofusin, banked blood and plasma; (iii) their solubility in different mixtures of these four priming fluids at different temperatures; and (iv) their estimated and actual solubility in blood during hypothermic CPB. We calculated solubility using a concept of volume fraction partition coefficient and compared estimated and measured solubilities. For the three anaesthetics tested, solubilities are in the order: fresh whole blood approximately = plasma > banked blood > normal saline approximately = lactated Ringer's approximately = gelofusin approximately = Haemaccel approximately = hydroxyethyl starch > mannitol. The solubilities of the anaesthetics in all priming fluids increased logarithmically at lower temperatures (P<0.05). The volume-fraction estimates of the partition coefficients were within approximately +/-20% of the measured values for all values of solubility. The corresponding estimates of solubility for CPB blood samples were between -36% and +24% of the measured values. During normothermic CPB, blood solubility of volatile anaesthetics would be unchanged when using plasma, slightly reduced when using banked blood and markedly reduced when using crystalloids and colloids.

Anesthetics, Inhalation↗
PubMed2002

Volatile anaesthetics may be the main cause of early but not delayed postoperative vomiting: a randomized controlled trial of factorial design.

BACKGROUND: Despite intensive research, the main causes of postoperative nausea and vomiting (PONV) remain unclear. We sought to quantify the relative importance of operative, anaesthetic and patient-specific risk factors to the development of PONV. METHODS: We conducted a randomized controlled trial of 1180 children and adults at high risk for PONV scheduled for elective surgery. Using a five-way factorial design, we randomly assigned subjects by gender who were undergoing specific operative procedures, to receive various combinations of anaesthetics, opioids, and prophylactic antiemetics. RESULTS: Of the 1180 patients, 355 (30.1% 95% CI (27.5-32.7%)) had at least one episode of postoperative vomiting (PV) within 24 h post-anaesthesia. In the early postoperative period (0-2 h), the leading risk factor for vomiting was the use of volatile anaesthetics, with similar odds ratios (OR (95% CI)) being found for isoflurane (19.8 (7.7-51.2)), enflurane (16.1 (6.2-41.8)) and sevoflurane (14.5 (5.6-37.4)). A dose-response relationship was present for the use of volatile anaesthetics. In contrast, no dose response existed for propofol anaesthesia. In the delayed postoperative period (2-24 h), the main predictors were being a child (5.7 (3.0-10.9)), PONV in the early period (3.4 (2.4-4.7)) and the use of postoperative opioids (2.5 (1.7-3.7)). The influence of the antiemetics was considerably smaller and did not interact with anaesthetic or surgical variables. CONCLUSION: Volatile anaesthetics were the leading cause of early postoperative vomiting. The pro-emetic effect was larger than other risk factors. In patients at high risk for PONV, it would therefore make better sense to avoid inhalational anaesthesia rather than simply to add an antiemetic, which may still be needed to prevent or treat delayed vomiting.

Adolescent↗
PubMed2004

Influence of volatile anaesthetics on hypercapnoeic ventilatory responses in mice with blunted respiratory drive.

BACKGROUND: Subanaesthetic concentrations of volatile anaesthetics significantly affect the respiratory response to hypoxia and hypercapnoeia. Individuals with an inherited blunted respiratory drive are more affected than normal individuals. To test the hypothesis that subjects with blunted hypercapnoeic respiratory drive are diversely affected by different anaesthetics, we studied the effects of three volatile anaesthetics on the control of breathing in C3H/HeJ (C3) mice, characterized by a blunted hypercapnoeic respiratory response. METHODS: Using whole body plethysmography, we assessed respiratory rate (RR) and pressure amplitude in 11 male C3 mice at rest, during anaesthesia with isoflurane, sevoflurane or desflurane, and during recovery. To test respiratory drive, mice were exposed to 8% carbon dioxide. Data were analysed by two-way-analysis of variance with post hoc tests and Bonferroni correction. RESULTS: RR was unaffected during sevoflurane anaesthesia up to 1.0 MAC. Likewise, sevoflurane at 1.5 MAC affected RR less than either isoflurane (P=0.0014) or desflurane (P=0.0048). The increased RR to a carbon dioxide challenge was blocked by all three anaesthetics even at the lowest concentration, and remained depressed during recovery (P<0.0001). Tidal volume was unaffected by all three anaesthetics. CONCLUSIONS: In C3 mice, spontaneous ventilation was less affected during sevoflurane compared with either isoflurane or desflurane anaesthesia. However, the RR response to hypercapnoeia was abolished at 0.5 MAC for all the anaesthetic agents and remained depressed even at the end of recovery. Our data suggest that different volatile anaesthetics have varying effects on the control of breathing frequency but all block the respiratory response to carbon dioxide. Therefore, a genetic predisposition to a blunted carbon dioxide response represents a susceptibility factor that interacts with hypercapnoeic hypoventilation during maintenance of anaesthesia and in the emergence from anaesthesia, regardless of the agent used.

Anesthetics, Inhalation↗
PubMed1994

Nitrate, nitrite and volatile N-nitroso compounds in the urine of Schistosoma haematobium and Schistosoma mansoni infected patients.

The present study presents, for the first time, the amounts of nitrate, nitrite and volatile N-nitroso compounds in saliva and urine samples of Schistosoma haematobium and Schistosoma mansoni infected patients. Mid-morning saliva and 24 h urine samples were collected from male patients infected with S.haematobium (n = 129 saliva and 79 urine samples) and S.mansoni (n = 64 saliva and 65 urine samples) and in a comparative control group of healthy individuals (n = 27) from the Nile Delta region of Egypt. Saliva samples were analyzed for the presence of nitrate and nitrite; while urine samples were analyzed for the presence of nitrate, nitrite and volatile N-nitroso compounds. In the control group, N-nitroso-dimethylamine (NDMA) was detected at concentrations (mean +/- SD) of 0.27 +/- 0.47 microgram/day. N-Nitrosopiperidine (NPIP; 0.6 microgram/day) and N-nitrosopyrrolidine (NPYR; 0.4 microgram/day) were also present in one sample. S.mansoni infected subjects showed significantly (P < 0.001) higher levels of 2.9 +/- 2.9 micrograms/day NDMA and a higher frequency of NPIP (in 40/65 samples; 0.4 +/- 0.3 microgram/day) and NPYR occurrence (in 59/65 samples; 0.9 +/- 0.9 microgram/day). Significant further increases in the excretion of volatile N-nitroso compounds were found in S.haematobium-infected patients with mean daily excretion of 19.2 +/- 21 micrograms/day NDMA (in all samples; P < 0.001), 1.6 +/- 2.3 micrograms/day NPIP (in 56/79 samples; P < 0.001) and 1.3 +/- 1.9 micrograms/day NPYR (in 58/79 samples; P < 0.1). The differences either in salivary nitrite/nitrate or in urinary nitrite between the three distinct groups were not significant. However, the urinary excretion of nitrate was elevated from 139 +/- 82 mg/day in the control group to 249 +/- 126 mg/day in S.mansoni infected patients (P < 0.001) and to 174 +/- 176 mg/day in S.haematobium infected subjects (P < 0.005 in comparison to S.mansoni infected group). These results suggest a possible role of N-nitroso compounds in the etiology of schistosome-associated bladder cancer and imply a partial participation of S.mansoni in the multistage process of urinary schistosomiasis-associated bladder carcinogenesis.

Adult↗
PubMed2001

A photoaffinity-labeled green leaf volatile compound 'tricks' highly selective and sensitive insect olfactory receptor neurons.

The sex pheromone of the scarab beetle, Phyllopertha diversa, is emitted by females and specifically detected by olfactory receptor neurons in the male and female antennae. Single sensillum recordings showed that, in contrast to the less sensitive pheromone sensilla in females, olfactory receptor neurons in the male antennae had a low threshold (1 ng), which rivals those of moths. The male and female antennae also possessed olfactory receptor neurons specific for the detection of floral and green leaf volatile compounds. Detectors for the green leaf volatile (Z)-3-hexenyl acetate had a threshold (10 pg) far below the sensitivity of the pheromone-detecting machinery. In addition, these neurons showed a remarkable selectivity even when challenged with related compounds at 10000-fold higher concentrations. Surprisingly, a diazo analog, (Z)-3-hexenyl diazoacetate, elicited slightly higher nervous activity than the natural ligand in the neurons specific and selective for (Z)-3-hexenyl acetate. The inability of the green leaf volatile-detecting machinery to discriminate the photoaffinity-labeled compound from the natural product indicates that the synthetic ligand interacts with odorant-binding protein, odorant receptor and odorant-degrading enzyme as does the cognate ligand.

Acetates↗
PubMed1985

Dynamic headspace analyses of residual volatiles in pharmaceuticals.

Pharmaceutical preparations may be assayed for volatile organic compounds by purging them with a stream of inert carrier gas and collecting the organics onto a suitable sorbent material, from which they may be backflushed to a gas chromatograph. Compared to solvent extraction, the process offers advantages of increased sensitivity, ease of automation, and elimination of the solvent peak. Examples are given of three major sources of volatiles in pharmaceuticals, with the development of a method for quantitating the volatiles using an internal standard.

Benzene↗
PubMed1987

Capillary chromatographic analysis of volatile organic compounds in the indoor environment.

The wide variety of volatile organic compounds found in the indoor environment can present a difficult chromatographic problem for the analyst. Capillary-column gas chromatography is required to achieve adequate separation. Thermal desorption/capillary gas chromatography/mass spectrometry is usually the preferred method for broad spectrum analysis of the volatile organics detected indoors. Cryogenic trapping is required for capillary gas chromatographic analysis of the more volatile components.

Air Pollutants↗
PubMed1990

Determination of volatile organics in drinking water with USEPA method 524.2 and the ion trap detector.

New drinking water regulations require the monitoring of eight volatile organic compounds that have established maximum contaminant levels (MCLs) and 51 other volatile organics for which MCLs are not established. A laboratory analytical method (Method 524.2) for the determination of 58 of these compounds is investigated, and precision and accuracy data are obtained. The method uses a standard inert gas purge extraction, isolation of the volatile organics on a three-stage solid-phase trap, thermal desorption into a gas chromatograph, separation with a fused-silica capillary column, and identification and measurement with a relatively low cost, benchtop ion trap detector that functions as a mass spectrometer. At a concentration of 2 micrograms/L (2 parts per billion), the grand mean measurement accuracy for 54 compounds was 95% of the true value with a mean relative standard deviation (RSD) of 4%. At 0.2 micrograms/L (200 parts per trillion), the grand mean measurement accuracy for 52 compounds was 95% of the true value with a mean RSD of 3%.

Gas Chromatography-Mass Spectrometry↗
PubMedDate not supplied

Identification limits for volatile organic compounds in the blood by purge-and-trap GC-FTIR.

An analysis method for volatile organic compounds in blood based on purge-and-trap extraction coupled with gas chromatography-Fourier transform infrared spectroscopy (GC-FTIR) was developed. The sample volume was 5 mL, and the internal standard was diethyl ketone. The chromatographic separation was carried out on a PoraPLOT Q capillary column, and the effluent was first directed to the FTIR and then to a flame ionization detector (FID). FTIR identification limits were measured for 27 volatile organic compounds; the criteria for the limit were that the first hit-list position should be obtained against the Sadtler library, which contains 3240 spectra, and that the correlation value should exceed 0.5. It was required that the peak be seen by FID but not necessarily by a Gram-Schmidt chromatogram. The FTIR identification limits, ranging from 0.01 mg/L for ethyl acetate, methylethyl ketone, and sevoflurane to 24 mg/L for methanol, generally allowed the detection of volatile-substance exposure at a lower level than is acutely toxic. Quantitative calibration data were presented for selected substances, based on the FID response, which shows that the method is also amenable to quantitative analysis. The throughput of the method without additional automation is five samples per day, the purge-and-trap stage being the limiting factor.

Flame Ionization↗
PubMed2005

A dissection of volatility in yeast.

It has been suggested that volatility, the proportion of mutations which change an amino acid, can be used to infer the level of natural selection acting upon a gene. This conjecture is supported by a correlation between volatility and the rate of nonsynonymous substitution (dN), or the ratio of nonsynonymous and synonymous substitution rates, in a variety of organisms. These organisms include yeast, in which the correlations are quite strong. Here we show that these correlations are a by-product of a correlation between synonymous codon bias toward translationally optimal codons and dN. Although this analysis suggests that volatility is not a good measure of the selection, we suggest that it might be possible to infer something about the level of natural selection, from a single genome sequence, using translational codon bias.

Base Sequence↗
PubMed2001

Volatile profiles and lipid oxidation of irradiated cooked chicken meat from laying hens fed diets containing conjugated linoleic acid.

The objective of this study was to determine the influence of dietary conjugated linoleic acid (CLA) on lipid oxidation, volatile profiles, and sensory characteristics of irradiated cooked chicken meat. Forty-eight 27-wk-old White Leghorn hens were fed a diet containing 0, 1.25, 2.5, or 5.0% CLA. After 12 wk of feeding trial, hens were slaughtered, and boneless, skinless breast and thigh muscles were separated. Meats of three birds from a dietary treatment were pooled and ground together through a 9-mm and a 3-mm plate, and patties were prepared. Patties were individually packaged and cooked in a water bath at 85 C for 15 min. After cooling to room temperature, patties were repackaged in oxygen-permeable or oxygen-impermeable bags, irradiated at 0 or 3 kiloGray (kGy) with an electron beam irradiator, and analyzed for lipid oxidation, volatile profiles, and sensory characteristics at 0 and 5 d of storage at 4 C. Cooked meat patties from hens fed CLA diets had lower TBA-reactive substances values and produced less hexanal and pentanal than the control. The irradiated and nonirradiated cooked chicken meat with aerobic packaging developed severe lipid oxidation during the 5-d storage at 4 C. Irradiation accelerated lipid oxidation in aerobic-packaged cooked chicken meat, but its effect was not as significant as that of the packaging. No odor differences were found among the cooked chicken meats from the different dietary CLA treatments. The increased storage stability of cooked meat from hens fed CLA diets was caused by the increased saturated fatty acids and CLA content in meat lipids. Tissue CLA was stable from oxidative changes and had minimal effect on volatile production in irradiated and nonirradiated cooked chicken meat during storage.

Animal Feed↗
PubMed2002

Delta opioid agonists and volatile anesthetics facilitate cardioprotection via potentiation of K(ATP) channel opening.

Opioids and volatile anesthetics produce marked cardioprotective effects against myocardial infarction via the activation of ATP-sensitive potassium (K(ATP)) channels, however, the effect of combined treatment with both drugs is unknown. We examined the hypothesis that opioids and volatile anesthetics potentiate cardiac K(ATP) channel opening, thereby enhancing cardioprotection. Rats were treated with the delta opioid agonists, TAN-67 or BW373U86, or isoflurane, together or alone with and without diazoxide, a mitochondrial K(ATP) channel opener. Glibenclamide, a non-selective K(ATP) channel blocker, was used to further characterize the signaling mechanism involved. Myocardial infarct size (IS) was determined by tetrazolium staining and was expressed as a percent of the area at risk (AAR). High doses of TAN-67 (10 mg/kg), diazoxide (10 mg/kg), and isoflurane (1 MAC) produced a significant reduction in IS compared with the control group (30+/-3%, 36+/-5%, and 42+/-2 vs. 58+/-2%, respectively), whereas lower doses of the drugs had no effect except for the low dose of isoflurane (0.5 MAC). The combination of TAN-67 and diazoxide or isoflurane and diazoxide resulted in a marked reduction in IS compared with controls in the presence of high (9+/-3% and 14+/-3%) and low (17+/-7% and 31+/-7%) dose combinations, respectively. The combination of TAN-67 or BW373U86 and isoflurane also caused a striking reduction in IS/AAR (16+/-7% and 7+/-2%, respectively). To date, this is the first demonstration that opioids and volatile anesthetics work in conjunction to confer protection against myocardial infarction through potentiation of cardiac K(ATP) channel opening.

Adenosine Triphosphate↗
PubMed1998

Drug-specific effects of volatile anesthetics on Ca2+ sensitization in airway smooth muscle.

UNLABELLED: Halothane directly relaxes airway smooth muscle, partly by decreasing the Ca2+ sensitivity during membrane receptor stimulation. The effects of other volatile anesthetics on Ca2+ sensitivity are unclear. In the current study, we compared the ability of halothane, sevoflurane, and isoflurane to inhibit increases in Ca2+ sensitivity during muscarinic receptor stimulation. Beta-escin-permeabilized canine tracheal smooth muscle strips were used. Anesthetics were applied during contractions induced by 3 microM acetylcholine and 10 microM guanosine 5'-triphosphate at a constant cytosolic Ca2+ concentration of 0.3 microM. Effects were evaluated as a percent relaxation from initial force corrected for time. Halothane significantly decreased force at both low (0.76 minimum alveolar anesthetic concentration [MAC]) and high (1.8 MAC) concentrations in a concentration-dependent manner. Sevoflurane also decreased force, significantly so at a high concentration (1.7 MAC). Isoflurane did not significantly affect force even at a high concentration (1.7 MAC). Halothane's relaxing effect was significantly greater than that of the other two anesthetics at each corresponding MAC concentration. Among these three volatile anesthetics compared at equipotent anesthetic concentrations, halothane was the most potent in reducing Ca2+ sensitivity during muscarinic receptor stimulation in canine tracheal smooth muscle. This may contribute to halothane's greater relaxing effect compared with isoflurane at the same MAC concentrations in intact airway smooth muscle. IMPLICATIONS: In this study, we showed that three volatile anesthetics (halothane, sevoflurane, and isoflurane) compared at equipotent anesthetic concentrations differed in their ability to inhibit Ca2+ sensitivity during muscarinic receptor stimulation in airway smooth muscle. The potency order was halothane > sevoflurane > or = isoflurane.

Acetylcholine↗
PubMed1999

Minimum alveolar anesthetic concentration of volatile anesthetics in normal and cardiomyopathic hamsters.

UNLABELLED: Minimum alveolar anesthetic concentrations (MAC) values of volatile anesthetics in cardiovascular diseases remain unknown. We determined MAC values of volatile anesthetics in spontaneously breathing normal and cardiomyopathic hamsters exposed to increasing (0.1%-0.3% steps) concentrations of halothane, isoflurane, sevoflurane, or desflurane (n = 30 in each group) using the tail-clamp technique. MAC values and their 95% confidence interval were calculated using logistic regression. In normal hamsters, inspired MAC values were: halothane 1.15% (1.10%-1.20%), isoflurane 1.62% (1.54%-1.69%), sevoflurane 2.31% (2.22%-2.40%), and desflurane 7.48% (7.30%-7.67%). In cardiomyopathic hamsters, they were: halothane 0.89% (0.83%-0.95%), isoflurane 1.39% (1.30%-1.47%), sevoflurane 2.00% (1.85%-2.15%), and desflurane 6.97% (6.77%-7.17%). Thus, MAC values of halothane, isoflurane, sevoflurane, and desflurane were reduced by 23% (P < 0.05), 14% (P < 0.05), 13% (P < 0.05), and 7% (P < 0.05), respectively in cardiomyopathic hamsters. IMPLICATIONS: Minimum alveolar anesthetic concentrations of volatile anesthetics were significantly lower in cardiomyopathic hamsters than in normal hamsters.

Anesthetics, Inhalation↗
PubMed1987

Comparison of the effects of volatile anesthetics on brain glucose metabolism in rats.

The objective of this investigation was to compare the effects of the commonly used volatile anesthetics on concentrations of plasma and cerebral glucose and cerebral intermediary metabolites. Fasted male Long-Evans rats were anesthetized with a volatile anesthetic and, after tracheostomy and paralysis, were mechanically ventilated. Each of three groups received one MAC concentration of anesthesia with halothane, enflurane, or isoflurane. At the end of 60-75 min of anesthesia, blood was sampled for arterial blood gas and plasma glucose analysis, and the brain was rapidly sampled and frozen for analysis of energy metabolites. Physiologic variables were maintained as follows: PaCO2 30-40 mmHg, pHa 7.20-7.40, PaO2 greater than 60 mmHg, MAP greater than 60 mmHg, and rectal temperature 37.5-38.5 degrees C. Mean plasma glucose concentrations in the three groups were as follows (muMol/ml +/- SEM): halothane, 7.45 /- .62; enflurane, 6.95 +/- .22; isoflurane, 10.11 +/- 1.00. Mean brain glucose concentrations in the three groups were (muMol/gm wet weight): halothane, 2.04 +/- .20; enflurane, 2.07 +/- .26; isoflurane, 3.04 +/- .31. Plasma and brain glucose levels were significantly increased in the isoflurane group compared to the other two groups (P less than .05) with no differences occurring in the brain/plasma glucose ratio among the three groups. No differences were present between groups in brain lactate, pyruvate, fructose diphosphate, malate, alpha-ketoglutarate, phosphocreatine, or adenine nucleotides. Thus, at one MAC concentration, major differences between volatile anesthetics on brain energy availability are not present, although isoflurane raised cerebral glucose levels.

Animals↗
PubMed1989

Effect of volatile anesthetics on synaptic transmission in the rat hippocampus.

The synaptic effects of halothane, isoflurane, and enflurane were examined in the rat hippocampus in vivo and compared with the effects of ketamine and urethane. Actions of the agents on excitatory amino acid-mediated neurotransmission were studied by observing evoked responses and long-term potentiation in the stratum pyramidale of CA1 with stimulation of the contralateral CA3 region. Long-term potentiation is a long-lasting increase in synaptic efficacy, which follows a brief stimulus train. It has been shown to be established through activation of the NMDA subclass of excitatory amino acid receptors and is thought to be involved in memory processing. Volatile anesthetics had no effect on evoked excitatory responses or on long-term potentiation. Actions of the anesthetics on inhibitory processes in the hippocampus were studied by pairing stimuli at a range of interpulse intervals. The first stimulus activated inhibitory processes that caused the response to the second stimulus to be smaller than the initial response, a phenomenon termed paired pulse depression. Paired pulse depression was significantly prolonged by the volatile anesthetics compared with that under urethane or ketamine. These results indicate that the mechanism of action of the volatile anesthetics at the hippocampal CA1 synapse does not involve amino acid-mediated excitation but does involve enhancement of inhibition.

Animals↗