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Joe Henry Steinbach - One of the best experts on this subject based on the ideXlab platform.
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Halothane Blocks Sensory Neurons Low-Voltage-activated Calcium Current
1991Co-Authors: M Takenoshita, Joe Henry SteinbachAbstract:Makoto Takenoshita” and Joe Henry Steinbach Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110 Although volatile anesthetic agents have been used clini- cally for many years, the mechanisms by which they act on the nervous system to produce anesthesia are not known. A possible site of action is the voltage-gated calcium-se- lective channel (Kmjevic and Puil, 1988). Accordingly, the action of the Halogenated alkane anesthetic halothane on voltage-dependent Ca currents in neonatal rat sensory neu- rons was examined using whole-cell patch-clamp record- ings. Halothane reversibly reduced the low-voltage-activat- ed Ca current with an EC, of about 100 @t. Similar effects were seen using a Halogenated Ether anesthetic (isoflurane) and in sensory neurons from adult rats. At higher concen- trations, both halothane and isoflurane reduced the high- voltage-activated Ca current. Because low-voltage-activat- ed Ca current has been postulated to be involved in the control of neuronal excitability and bursting (Llinas, 1988), this block may explain some of the clinical actions of volatile anesthetics. The mechanisms by which volatile anesthetics produce clinical anesthesia are not understood. It is clear that at clinically rel- evant concentrations they have relatively little effect on con- duction in peripheral axons, so it has been suggested that they act on some aspect of synaptic transmission (Larrabee and Pos- temak, 1952; Richards, 1983). More recent work has indicated that some voltage-gated membrane channels may be affected. In particular, neuronal voltage-dependent calcium currents have been implicated as a possible site ofaction. It has been suggested that volatile anesthetics depress evoked transmitter release by reducing Ca entry (Takenoshita and Takahashi, 1987), and mea- surements of evoked quanta1 content at Ia synapses onto mo- tomeurons show a reduction (Kullmann et al., 1989). Further- more, halothane has been found to reduce voltage-gated Ca current in hippocampal neurons (Krnjevic and Puil, 1988). There are several classes of voltage-gated Ca currents (Bean, 1989); the most distinct are the low-voltage-activated (LVA, or “T”) current and the high-voltage-activated (HVA, or “N” and/or
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Halothane blocks low-voltage-activated calcium current in rat sensory neurons
The Journal of Neuroscience, 1991Co-Authors: M Takenoshita, Joe Henry SteinbachAbstract:Although volatile anesthetic agents have been used clinically for many years, the mechanisms by which they act on the nervous system to produce anesthesia are not known. A possible site of action is the voltage-gated calcium-selective channel (Krnjevic and Puil, 1988). Accordingly, the action of the Halogenated alkane anesthetic halothane on voltage-dependent Ca currents in neonatal rat sensory neurons was examined using whole-cell patch-clamp recordings. Halothane reversibly reduced the low-voltage-activated Ca current with an EC50 of about 100 microM. Similar effects were seen using a Halogenated Ether anesthetic (isoflurane) and in sensory neurons from adult rats. At higher concentrations, both halothane and isoflurane reduced the high-voltage- activated Ca current. Because low-voltage-activated Ca current. Because low-voltage-activated Ca current has been postulated to be involved in the control of neuronal excitability and bursting (Llinas, 1988), this block may explain some of the clinical actions of volatile anesthetics.
M Takenoshita - One of the best experts on this subject based on the ideXlab platform.
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Halothane Blocks Sensory Neurons Low-Voltage-activated Calcium Current
1991Co-Authors: M Takenoshita, Joe Henry SteinbachAbstract:Makoto Takenoshita” and Joe Henry Steinbach Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110 Although volatile anesthetic agents have been used clini- cally for many years, the mechanisms by which they act on the nervous system to produce anesthesia are not known. A possible site of action is the voltage-gated calcium-se- lective channel (Kmjevic and Puil, 1988). Accordingly, the action of the Halogenated alkane anesthetic halothane on voltage-dependent Ca currents in neonatal rat sensory neu- rons was examined using whole-cell patch-clamp record- ings. Halothane reversibly reduced the low-voltage-activat- ed Ca current with an EC, of about 100 @t. Similar effects were seen using a Halogenated Ether anesthetic (isoflurane) and in sensory neurons from adult rats. At higher concen- trations, both halothane and isoflurane reduced the high- voltage-activated Ca current. Because low-voltage-activat- ed Ca current has been postulated to be involved in the control of neuronal excitability and bursting (Llinas, 1988), this block may explain some of the clinical actions of volatile anesthetics. The mechanisms by which volatile anesthetics produce clinical anesthesia are not understood. It is clear that at clinically rel- evant concentrations they have relatively little effect on con- duction in peripheral axons, so it has been suggested that they act on some aspect of synaptic transmission (Larrabee and Pos- temak, 1952; Richards, 1983). More recent work has indicated that some voltage-gated membrane channels may be affected. In particular, neuronal voltage-dependent calcium currents have been implicated as a possible site ofaction. It has been suggested that volatile anesthetics depress evoked transmitter release by reducing Ca entry (Takenoshita and Takahashi, 1987), and mea- surements of evoked quanta1 content at Ia synapses onto mo- tomeurons show a reduction (Kullmann et al., 1989). Further- more, halothane has been found to reduce voltage-gated Ca current in hippocampal neurons (Krnjevic and Puil, 1988). There are several classes of voltage-gated Ca currents (Bean, 1989); the most distinct are the low-voltage-activated (LVA, or “T”) current and the high-voltage-activated (HVA, or “N” and/or
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Halothane blocks low-voltage-activated calcium current in rat sensory neurons
The Journal of Neuroscience, 1991Co-Authors: M Takenoshita, Joe Henry SteinbachAbstract:Although volatile anesthetic agents have been used clinically for many years, the mechanisms by which they act on the nervous system to produce anesthesia are not known. A possible site of action is the voltage-gated calcium-selective channel (Krnjevic and Puil, 1988). Accordingly, the action of the Halogenated alkane anesthetic halothane on voltage-dependent Ca currents in neonatal rat sensory neurons was examined using whole-cell patch-clamp recordings. Halothane reversibly reduced the low-voltage-activated Ca current with an EC50 of about 100 microM. Similar effects were seen using a Halogenated Ether anesthetic (isoflurane) and in sensory neurons from adult rats. At higher concentrations, both halothane and isoflurane reduced the high-voltage- activated Ca current. Because low-voltage-activated Ca current. Because low-voltage-activated Ca current has been postulated to be involved in the control of neuronal excitability and bursting (Llinas, 1988), this block may explain some of the clinical actions of volatile anesthetics.
Sanjay S. Patel - One of the best experts on this subject based on the ideXlab platform.
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Desflurane. A review of its pharmacodynamic and pharmacokinetic properties and its efficacy in general anaesthesia.
Drugs, 1995Co-Authors: Sanjay S. PatelAbstract:Desflurane is a Halogenated Ether inhalation general anaesthetic agent with low solubility in blood and body tissues, and approximately one-fifth the potency ofisoflurane. The pharmacodynamic properties ofdesflurane generally resemble those of isoflurane ; thus, it produces dose-dependent depression of the central nervous and cardiorespiratory systems, and tetanic fade at the neuromuscular junction. The alveolar equilibration ofdesflurane is rapid (90% complete at 30 minutes compared with 73% for isoflurane). Both desflurane and isoflurane are distributed to various tissues to a similar extent. Desflurane is resistant to chemical degradation and undergoes negligible metabolism (10% of that seen with isoflurane). Desflurane 'wash-out'is 2 to 2.5 times faster than that of isoflurane in the first 2 hours after discontinuation of anaesthesia. The low solubility of desflurane facilitates a rapid induction of anaesthesia and precise control of the depth of anaesthesia (during maintenance). Results from a few clinical studies indicate that emergence from desflurane is significantly earlier (by =2 to 6 minutes) than that from propofol anaesthesia, whereas other studies do not concur. In comparison with isoflurane, emergence from desflurane anaesthesia is significantly earlier (by 5 minutes) after ambulatory and =50% earlier (also significant) after nonambulatory surgical procedures. Limited comparative studies with halothane or sevoflurane also suggest an earlier time of emergence from desflurane anaesthesia. Comparative studies of desflurane and propofol, and other inhalation agents, indicate that the times to toleration of oral fluids, sitting and discharge from recovery room are similar, regardless of the general anaesthetic agent administered. However, some limited data in elderly patients (aged >65 years) suggest that this patient group spends a significantly shorter time in the postanaesthesia care unit after desflurane than after isoflurane anaesthesia. Differences, if any, in the recovery of cognitive and psychomotor functions after desflurane or propofol anaesthesia remain unclear. However, in comparison with isoflurane anaesthesia, recovery of these functions (up to 45 minutes postoperatively) occurs earlier after desflurane. Significantly fewer patients are subjectively impaired (i.e. drowsy, clumsy, fatigued or confused) upon recovery from desflurane than from isoflurane anaesthesia. Likewise, significantly fewer adult patients are delirious when recovering from desflurane than from isoflurane anaesthesia, though in paediatric patients delirium is more likely when recovering from desflurane than from halothane anaesthesia. Haemodynamic stability during coronary artery surgery is as well maintained with desflurane as with isoflurane, and the drug does not worsen the adverse postoperative outcomes. Moreover, desflurane appears to be better than isoflurane at blunting the haemodynamic response after sternotomy and other noxious stimuli. The incidence of myocardial ischaemia during coronary artery surgery is similar with either desflurane or isoflurane anaesthesia. Transient airway irritant effects are the most common adverse events during induction of anaesthesia with deseflurane ; therefore, this agent is not recommended for induction of anaesthesia in paediatric patients. The incidence of intraoperative cardiovascular events during desflurane anaesthesia is similar to that reported with isoflurane.
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Desflurane
Drugs, 1995Co-Authors: Sanjay S. PatelAbstract:Synopsis Desflurane is a Halogenated Ether inhalation general anaesthetic agent with low solubility in blood and body tissues, and approximately one-fifth the potency of isoflurane. The pharmacodynamic properties of desflurane generally resemble those of isoflurane; thus, it produces dose-dependent depression of the central nervous and cardiorespiratory systems, and tetanic fade at the neuromuscular junction. The alveolar equilibration of desflurane is rapid (90% complete at 30 minutes compared with 73% for isoflurane). Both desflurane and isoflurane are distributed to various tissues to a similar extent. Desflurane is resistant to chemical degradation and undergoes negligible metabolism (≈10% of that seen with isoflurane). Desflurane ‘wash-out’ is ≈2 to 2.5 times faster than that of isoflurane in the first 2 hours after discontinuation of anaesthesia. The low solubility of desflurane facilitates a rapid induction of anaesthesia and precise control of the depth of anaesthesia (during maintenance). Results from a few clinical studies indicate that emergence from desflurane is significantly earlier (by ≈2 to 6 minutes) than that from propofol anaesthesia, whereas other studies do not concur. In comparison with isoflurane, emergence from desflurane anaesthesia is significantly earlier (by 5 minutes) after ambulatory and ≈50% earlier (also significant) after nonambulatory surgical procedures. Limited comparative studies with halothane or sevoflurane also suggest an earlier time of emergence from desflurane anaesthesia. Comparative studies of desflurane and propofol, and other inhalation agents, indicate that the times to toleration of oral fluids, sitting and discharge from recovery room are similar, regardless of the general anaesthetic agent administered. However, some limited data in elderly patients (aged >65 years) suggest that this patient group spends a significantly shorter time in the postanaesthesia care unit after desflurane than after isoflurane anaesthesia. Differences, if any, in the recovery of cognitive and psychomotor functions after desflurane or propofol anaesthesia remain unclear. However, in comparison with isoflurane anaesthesia, recovery of these functions (up to 45 minutes post-operatively) occurs earlier after desflurane. Significantly fewer patients are subjectively impaired (i.e. drowsy, clumsy, fatigued or confused) upon recovery from desflurane than from isoflurane anaesthesia. Likewise, significantly fewer adult patients are delirious when recovering from desflurane than from isoflurane anaesthesia, though in paediatric patients delirium is more likely when recovering from desflurane than from halothane anaesthesia. Haemodynamic stability during coronary artery surgery is as well maintained with desflurane as with isoflurane, and the drug does not worsen the adverse postoperative outcomes. Moreover, desflurane appears to be better than isoflurane at blunting the haemodynamic response after sternotomy and other noxious stimuli. The incidence of myocardial ischaemia during coronary artery surgery is similar with either desflurane or isoflurane anaesthesia. Transient airway irritant effects are the most common adverse events during induction of anaesthesia with deseflurane; therefore, this agent is not recommended for induction of anaesthesia in paediatric patients. The incidence of intraoperative cardiovascular events during desflurane anaesthesia is similar to that reported with isoflurane. The incidence of postoperative nausea and vomit-ing after desflurane anaesthesia is higher than after propofol but similar to that after other inhalation agents. Hepatic or renal function is not adversely affected after desflurane anaesthesia. Overall, although desflurane is generally not well tolerated during induction of anaesthesia, it embodies many of the desirable feature s of an ideal agent, which include stability to chemical degradation, low solubility in blood and body tissues, negligible metabolism and low potential for hepato-renal toxicity. These favourable physical and pharmacokinetic characteristics should present desflurane as a valuable inhalation anaesthetic agent for the maintenance of general anaesthesia in ambulatory surgery (complementary to intravenous induction with propofol) as well as in nonambulatory surgical procedures. Pharmacodynamic Properties Desflurane is a Halogenated Ether inhalation general anaesthetic agent with low solubility in blood and body tissues and low potency [minimum alveolar concentration (MAC) value ranging from 4.58 to 7.25%, depending on the stimulus used]. It is approximately one-fifth as potent as isoflurane. The cerebrovascular and cardiorespiratory effects of desflurane essentially parallel those of isoflurane. It produces dose-dependent decreases in cerebrovascular resistance and cerebral metabolic rate of oxygen consumption, increases in intracranial pressure at 0.5 to 1.5 MAC doses and impairment of cerebral autoregulation. Desflurane suppresses EEG activity at ≥1.24 MAC, and it is not epileptogenic either at deep anaesthetic levels or under hypocapnic conditions. There is a dose-dependent suppression of somatosensory-evoked potentials at 0.5 to >1.5 MAC in healthy volunteers, while sub-MAC concentrations suppress intermediate-latency auditory-evoked responses. Cardiac output is maintained in humans despite dose-dependent depression of cardiovascular function and myocardial contractility during desflurane anaesthesia with controlled ventilation. Tachycardia may be more prominent with desflurane than isoflurane at >1.0 MAC. Adequate myocardial tissue perfusion is maintained despite a decline in perfusion pressure during desflurane anaesthesia. Prolonged anaesthesia (up to 7 hours) appears to result in cardiovascular, but not cerebral, tolerance in humans. Desflurane, like isoflurane, is a coronary vasodilator, but it does not appear to induce the ‘coronary steal’ phenomenon in a canine model. A rapid increase in end-tidal concentrations of desflurane (at ≥1.0 MAC) in patients and healthy volunteers results in transient sympathetic-mediated cardiovascular stimulation which is significantly more pronounced than that observed with isoflurane. This sympathoexcitation is absent with sevoflurane. Dose-dependent respiratory depressant effects of desflurane (at ≤1.24 MAC), such as decrease in tidal volume and increase in ventilation rate, are similar to those of isoflurane. Desflurane produces neuromuscular relaxation and therefore potentiates skeletal muscle relaxation induced by neuromuscular blocking agents. Pharmacokinetic Properties Equilibration between inspired and tissue concentrations of desflurane is rapid compared with that of other inhalation anaesthetic agents. Alveolar equilibration of desflurane is ≈90% complete in healthy volunteers within 30 minutes compared with isoflurane (73%) or halothane (58%). The estimated tissue distribution of desflurane is generally similar to that of isoflurane. Desflurane is eliminated ≈2 to 2.5 times more quickly than isoflurane or halothane in the first 2 hours after discontinuation of anaesthesia. Pulmonary clearance of desflurane is 4.11 L/min ( vs 3.94 L/min for isoflurane and halothane) and total body clearance is 4.60 L/min ( vs 4.00 and 3.94 L/min for isoflurane and halothane, respectively). Desflurane is resistant to in vitro degradation in moist soda lime at ≤60°C, although there is slight degradation at 80°C (0.45% per hour). Desflurane undergoes negligible metabolism (≈10% that of isoflurane) in vivo , although the precise mechanism is unknown. Clinical Evaluation A number of studies in ambulatory patients report a statistically significant earlier emergence from desflurane than from propofol or isoflurane anaesthesia (≈2 to 6 and 5 minutes earlier, respectively), although some studies have not found this difference between desflurane and propofol anaesthesia. Emergence from desflurane anaesthesia in this group of patients appears to be significantly more rapid than emergence from sevoflurane or halothane anaesthesia. The times to toleration of oral fluids, sitting and readiness for discharge from the recovery room are comparable, regardless of the general anaesthetic administered. In the early postoperative period up to 90 minutes, psychomotor and cognitive functions are less impaired after desflurane than after isoflurane ambulatory anaesthesia, whereas such differences are less apparent when desflurane is compared with propofol. Generally, these functions return to their baseline levels within 2 hours postoperatively regardless of the anaesthetic background. Subjective impairment (i.e. drowsiness, clumsiness, fatigue or confusion) is significantly less upon recovery from desflurane than from isoflurane anaesthesia. Emergence from nonambulatory anaesthesia with desflurane is ≈50% significantly earlier than that with isoflurane. In addition, up to 45 minutes postoperatively, cognitive and psychomotor function recovery occurs earlier after desflurane than after isoflurane anaesthesia, although this difference is not apparent 60 minutes after cessation of administration. Elderly patients (aged >65 years) recovering from nonambulatory desflurane anaesthesia tend to spend a shorter time in the postanaesthesia care unit compared with those who received isoflurane anaesthesia (80 vs 128 minutes). Desflurane does not worsen the adverse postoperative outcomes after coronary artery surgery, and haemodynamic stability during desflurane anaesthesia is similar to that during isoflurane or opioid anaesthesia. Compared with isoflurane, desflurane is better at blunting the haemodynamic response after sternotomy and other noxious stimuli. There is no difference between desflurane and isoflurane anaesthesia with respect to the incidence of ECG changes indicative of myocardial ischaemia during coronary artery surgery. However, when desflurane is compared with opioid anaesthesia, conflicting results with respect to the incidence of myocardial ischaemia upon induction, but not during maintenance of anaesthesia, were reported. Changes in the depth of anaesthesia in response to surgical stimuli are more rapidly controlled with desflurane than with isoflurane. Limited data suggest that desflurane (1 to 4.5%) in oxygen provides well tolerated and effective obstetric analgesia during vaginal delivery. Likewise, caesarean section surgery can be performed without excessive uterine bleeding when desflurane 3% (end-tidal concentration) is administered. Tolerability The pungency of desflurane is reflected in its transient airway irritant effects during induction of anaesthesia at concentrations >6%. These effects (commonly seen in adults) include coughing, excitatory effects, breath-holding, excessive secretions and laryngospasm. The airway irritant effects are not well tolerated by paediatric patients, in whom excitatory effects (51 %) and coughing (29%) are the most commonly reported reflexes. Other adverse events include apnoea, pharyngitis and oxyhaemoglobin desaturation (SpO_2
Thérèse Zeegers-huyskens - One of the best experts on this subject based on the ideXlab platform.
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Theoretical studies of the interaction between enflurane and water
Journal of Molecular Modeling, 2013Co-Authors: Wiktor Zierkiewicz, Danuta Michalska, Thérèse Zeegers-huyskensAbstract:Increase of the atmospheric concentration of Halogenated organic compounds is partially responsible for a change of the global climate. In this work we have investigated the interaction between Halogenated Ether and water, which is one of the most important constituent of the atmosphere. The structures of the complexes formed by the two most stable conformers of enflurane (a volatile anaesthetic) with one and two water molecules were calculated by means of the counterpoise CP-corrected gradient optimization at the MP2/6–311++G(d,p) level. In these complexes the CH…O_w hydrogen bonds are formed, with the H…O_w distances varying between 2.23 and 2.32 Å. A small contraction of the CH bonds and the blue shifts of the ν(CH) stretching vibrations are predicted. There is also a weak interaction between one of the F atoms and the H atom of water, with the H_w…F distances between 2.41 and 2.87 Å. The CCSD(T)/CBS calculated stabilization energies in these complexes are between −5.89 and −4.66 kcal mol^−1, while the enthalpies of formation are between −4.35 and −3.22 kcal mol^−1. The Cl halogen bonding between enflurane and water has been found in two complexes. The intermolecular (Cl···O) distance is smaller than the sum of the corresponding van der Waals radii. The CCSD(T)/CBS stabilization energies for these complexes are about −2 kcal mol^−1. Figure Complex between enflurane and water molecules
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Theoretical studies of the interaction between enflurane and water
Journal of Molecular Modeling, 2012Co-Authors: Wiktor Zierkiewicz, Danuta Michalska, Thérèse Zeegers-huyskensAbstract:Increase of the atmospheric concentration of Halogenated organic compounds is partially responsible for a change of the global climate. In this work we have investigated the interaction between Halogenated Ether and water, which is one of the most important constituent of the atmosphere. The structures of the complexes formed by the two most stable conformers of enflurane (a volatile anaesthetic) with one and two water molecules were calculated by means of the counterpoise CP-corrected gradient optimization at the MP2/6–311++G(d,p) level. In these complexes the CH…Ow hydrogen bonds are formed, with the H…Ow distances varying between 2.23 and 2.32 A. A small contraction of the CH bonds and the blue shifts of the ν(CH) stretching vibrations are predicted. There is also a weak interaction between one of the F atoms and the H atom of water, with the Hw…F distances between 2.41 and 2.87 A. The CCSD(T)/CBS calculated stabilization energies in these complexes are between −5.89 and −4.66 kcal mol−1, while the enthalpies of formation are between −4.35 and −3.22 kcal mol−1. The Cl halogen bonding between enflurane and water has been found in two complexes. The intermolecular (Cl···O) distance is smaller than the sum of the corresponding van der Waals radii. The CCSD(T)/CBS stabilization energies for these complexes are about −2 kcal mol−1.
James K Hardy - One of the best experts on this subject based on the ideXlab platform.
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membrane extraction for the determination of Halogenated Ether priority pollutants in water
Journal of Environmental Science and Health Part A-toxic\ hazardous Substances & Environmental Engineering, 1999Co-Authors: David Mark Frantz, James K HardyAbstract:Abstract A method is described for the solvent‐free extraction, concentration, and determination of the Halogenated Ether base/neutral priority pollutants in water. Samples are collected by permeation through a silicone polycarbonate membrane followed by trapping onto a Tenax‐TA sampling tube. These samples were thermally desorbed and allowed to directly pass into a gas Chromatograph (GC) equipped with a flame ionization detector (FID) for subsequent separation and quantitation. Concentrations in the parts per billion (μg/L) were found for all the compounds studied. A linear relationship was obtained for concentrations ranging between approximately 8 and 300 parts per billion (ppb). The method can be used as an alternative to current preconcentration methods or for continuous monitoring of wastewater streams. It also offers the advantages of eliminating the need for costly solvents which in turn may contribute to sample contamination, and also lowering the number of analysis steps while still providing ac...
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permeation sampling of Halogenated Ether priority pollutants
Journal of Environmental Science and Health Part A-toxic\ hazardous Substances & Environmental Engineering, 1998Co-Authors: David Mark Frantz, James K HardyAbstract:Abstract A method for the determination of five Halogenated Ether priority pollutants using time‐weighted‐average concentrations is described. These compounds permeate through a silicone polycarbonate membrane and are trapped onto a Tenax TA™ adsorbent. Compounds of interest are solvent desorbed by acetone, followed by separation and quantitation by gas chromatography‐mass spectrometry (GC‐MS). A linear relationship was found between the amount of Halogenated Ether trapped onto the Tenax adsorbent and the product of the concentration of Ether in solution and the exposure time. Concentrations ranged from 0.04 to 7.2 mg/L for a twenty‐four hour exposure. The temperature of solution was found to alter the pollutant permeation rate. This sampler offers the advantages of providing time‐weighted‐average concentrations with a relatively simple sampling method.
