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At least 19 recordsLinked to original sources
PubMed1988

Modulation of the benzodiazepine/gamma-aminobutyric acid receptor chloride channel complex by inhalation anesthetics.

Inhalation anesthetics, such as diethyl ether, halothane, and enflurane, increase 36Cl- uptake into rat cerebral cortical synaptoneurosomes in a concentration-dependent, picrotoxin-sensitive fashion. At concentrations consistent with those that stimulate 36Cl- uptake, inhalation anesthetics also inhibit the binding of t-[35S]butylbicyclophosphorothionate ([35S]TBPS) to well-washed cortical membranes. Scatchard analysis of [35S]TBPS binding indicates that these agents reduce the apparent affinity of this radioligand and have little effect on the Bmax. The ability of inhalation anesthetics to directly stimulate 36Cl- uptake and inhibit [35S]TBPS binding is a property shared by nonvolatile anesthetics. Nonetheless, there are differences between nonvolatile agents (such as barbiturates and alcohols) and inhalation anesthetics, because the former compounds augment muscimol (a GABAmimetic) stimulated 36Cl- uptake, whereas the latter group (such as ether and enflurane) inhibit this effect. These findings demonstrate that therapeutically relevant concentrations of inhalation anesthetics perturb the benzodiazepine/gamma-aminobutyric acid receptor chloride channel complex, and suggest this oligomeric protein may be a common mediator of some aspects of anesthetic action.

Anesthesia, Inhalation↗
PubMed1986

The postoperative adverse effects of inhalational anesthetics.

Inhalational general anesthetics can contribute to postoperative morbidity (Table II). Postoperative effects of inhalational anesthetics on the central nervous system are speculative. The "toxic" effects of these agents during the postoperative period are most often an extension of their pharmacologic and physiochemical properties. Inhalational anesthetics may produce a number of varied changes in mental status after surgery such as headache, emergence excitement, and delirium. It is very important for health professionals to be aware of the risk of perioperative myocardial infarction in patients with preexisting heart disease if early detection and treatment are to occur. Relative to the common postoperative problems of atelectasis, pneumonia, and aspiration, inhalational agents may have a contributory role especially in patients with preexisting pulmonary disease. Postoperative nausea and vomiting are other common problems in which inhalational agents may have a role in their development. Although extensively investigated, suspected halothane hepatoxicity is a very rare complication if it exists at all. The renal effects of inhalational anesthetics are usually mild and transitory, although the use of methoxyflurane can produce direct nephrotoxicity. The evidence to support a clinically significant direct immunosuppressant effect of inhalational anesthetics after surgery is inconclusive. A concensus exists that any minor, short-lived effects are in all probability overshadowed by the nonspecific stress of surgery itself. By reducing this stress, anesthetics undoubtedly have a protective effect. There are probably no major mutagenic or carcinogenic effects of inhalational anesthetics under normal conditions. Inhalational anesthetics should be avoided during pregnancy because of their teratogenic potential and their effects on the uterus.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1976

Clinical significance of the biotransformation of inhalation anesthetics.

Inhalation anesthetics, a class of drugs formerly believed to be biologically inert, are now recognized to undergo considerable biotransformation. The viscerotoxicity of certain anesthetics on kidney and liver can be explained in terms of metabolism. The entity of "halothane hepatitis" remains mechanistically and diagnostically a mystery, but if it exists, it could be due to abnormalities of biotransformation.

Anesthesia, Inhalation↗
PubMed1990

Endothelium-derived relaxing factor is not responsible for inhibition of hypoxic pulmonary vasoconstriction by inhalational anesthetics.

Inhalational anesthetics inhibit hypoxic pulmonary vasoconstriction (HPV). One mechanism suggested for this action is stimulation of release of endothelium-derived relaxing factor. The present study has tested this hypothesis. These studies were performed in 66 ventilated and perfused isolated rat lungs. There were three study protocols. Study 1 examined the effect of HPV of the inhibition of soluble guanylate cyclase by methylene blue (MB). In the presence or absence of MB, the lungs constricted to hypoxia with pulmonary artery pressure increases of 8.6 +/- 0.2 cmH2O and 11.5 +/- 0.4 cmH2O, respectively, and halothane, enflurane, and isoflurane caused a reversible 50% decrease in the pulmonary pressor response, but acetylcholine (ACh) was vasodilatory in the saline group and vasoconstrictor in the MB group. In Study II a dose-response curve was established for the potent stimulator (Sin 1) of the enzyme guanylate cyclase. In the presence of MB the dose-response curve for Sin 1 was shifted to the right with an increase in the ED50 for Sin 1 from 44 microM for the control to 85 microM for the MB group. In Study III, baseline pulmonary artery pressure was increased with U46619, and the hypoxic pressor response was increased (28.9 +/- 2.5 cmH2O), but halothane again caused a 50% decrease (11.0 +/- 1.8 cmH2O) in the response to hypoxia. In summary, when soluble guanylate cyclase activity is inhibited by MB, the inhibition of hypoxic pulmonary vasoconstriction by halothane, isoflurane, or enflurane was unaltered, and release of endothelium-derived relaxing factor (EDRF) is therefore not an essential mechanism underlying this action.

Animals↗
PubMedDate not supplied

[Proposal of environmental and biological monitoring and health surveillance of the exposed to inhalation anesthetics. Consensus. A Study Group on Occupational Exposure to Inhalation Anesthetics].

The Study Group on Occupational Exposure to Inhalation Anaesthetics of the Lombardy Association of Occupational Health and Industrial Hygiene prepared a document that was discussed during the Congress "Occupational Risks due to Inhalation Anaesthetics", held in Brescia, Italy, on May 12, 1992. The same document was then approved by the Directory Council of the Lombardy Association of Occupational Health and Industrial Hygiene. Data on environmental concentrations of Nitrous Oxide collected from 1989 to 1991 in 269 operating rooms of 47 hospitals in Lombardy are reported. The measured levels are considerably lower than those collected from the same Study Group from 1985 to 1987 in 111 operating rooms. The methodologies for exposure control are discussed, regarding both environmental and biological monitoring. These two techniques are complementary and can be used with standardized methods. The review of the literature on the early effects showed, even with some uncertainty at the current exposure levels, effects on liver and Central Nervous System. Still controversial are the data regarding the reproductive toxicity. Health surveillance programs have been organized in the last 5 years in 18 Lombardy hospitals and they indicate no cases of pathologies due to inhalation anesthetics on 1498 subjects. Operative proposals are suggested on the methodology and the frequency of environmental/biological monitoring and health surveillance. The "technical limit values" reported in the document from the Italian Ministry of Health are also discussed. Finally, research topics are suggested in order to assess the early effects of exposure.

Anesthesia, Inhalation↗
PubMed2003

Glycine receptors mediate part of the immobility produced by inhaled anesthetics.

UNLABELLED: Many inhaled anesthetics potentiate the effect of glycine on inhibitory strychnine-sensitive glycine receptors in vitro, supporting the view that this receptor could mediate the immobility produced by inhaled anesthetics during noxious stimulation (i.e., would underlie minimum alveolar anesthetic concentration [MAC]). There are quantitative differences between anesthetics in their capacity to potentiate glycine's effect in receptor expression systems: halothane (most potentiation), isoflurane (intermediate), and cyclopropane (minimal). If glycine receptors mediate MAC, then their blockade in the spinal cord should increase the MAC of halothane more than that of isoflurane and isoflurane MAC more than cyclopropane MAC; the increases in MAC should be proportional to the receptor potentiation produced in vitro. Rats with chronically implanted intrathecal catheters were anesthetized with halothane, isoflurane, or cyclopropane. During intrathecal infusion of artificial cerebrospinal fluid, MAC was determined. Then MAC was re-determined during an infusion of 3, 12, 24, or 48 (isoflurane only) micro g/min of strychnine (strychnine blocks glycine receptors) in artificial cerebrospinal fluid. Strychnine infusion increased MAC in proportion to the enhancement of glycine receptors found in vitro. The maximum effect was with an infusion of 12 micro g/min. For the combined results at 12 and 24 micro g/min of strychnine, the increase in MAC correlated with the extent of in vitro potentiation (r(2) = 0.82). These results support the hypothesis that glycine receptors mediate part of the immobilization produced by inhaled anesthetics. IMPLICATIONS: In vitro, halothane potentiates glycine's effect on strychnine-sensitive glycine receptors more than isoflurane and isoflurane more than cyclopropane. The present in vivo work indicates that antagonism of the glycine receptor with strychnine increases minimum alveolar anesthetic concentration for halothane more than isoflurane and isoflurane more than cyclopropane. Such results support the notion that glycine receptors may mediate part of the immobility produced by inhaled anesthetics.

Anesthetics, Inhalation↗
PubMed1978

Inhalation anesthetics.

The inhalation anesthetics affect operating room personnel as well as the patient. This occupational exposure is similar in all respects to industrial solvent exposures. Although the extent of the hazard is not yet established, it is clear that only quite low levels of these active chemical should be allowed in the operating room air.

Anesthesia, Inhalation↗
PubMed1996

What is new with inhaled anesthetics: Part 1.

Inhaled anesthetic agents are widely used in the maintenance of general anesthesia. The newer agents, desflurane and sevoflurane, possess pharmacokinetic profiles that are distinctly different from the older inhaled anesthetics. These differences significantly impact the PACU nursing care. This article will focus on the uptake, distribution, and elimination of inhaled anesthetic agents with emphasis being placed on the postanesthesia care of surgical patients receiving these newer agents.

Anesthetics, Inhalation↗
PubMed2003

Blockade of 5-HT2A receptors may mediate or modulate part of the immobility produced by inhaled anesthetics.

UNLABELLED: Many inhaled anesthetics block the in vitro effect of the excitatory neurotransmitter serotonin on the 5-HT2A receptor, supporting the view that this receptor might mediate the capacity of inhaled anesthetics to produce immobility during noxious stimulation (i.e., would underlie MAC, the minimum alveolar concentration required to suppress movement in response to a noxious stimulus in 50% of subjects). In the present investigation in rats, we found that intrathecal administration of the 5HT-2A blocker, ketanserin, can decrease isoflurane MAC. This effect, presumably mediated by blockade of serotonin transmission in the spinal cord, reaches a maximum of 20%-25%. An additional decrease (to 60%) may be obtained by IV infusion of ketanserin, and presumably this decrease results from ketanserin's actions on supraspinal centers. The IV doses of ketanserin that decreased MAC were approximately 100 microg. kg(-1). min(-1) in rats, compared with usual clinical doses of 1.25 microg. kg(-1). min(-1) in humans. These results indicate that 5HT2A receptors are in the neural circuitry influencing isoflurane MAC. These results, together with the blocking action of isoflurane on expressed 5HT2A receptors, strengthen the case for a role for 5HT2A receptors to isoflurane-induced immobility. However, because MAC for isoflurane is predominantly determined in the spinal cord, this result is consistent at most with a minor contribution of these receptors to the immobilizing action of isoflurane. IMPLICATIONS: A subset of serotonin receptors, 5HT2A receptors, may mediate or modulate a minor portion of the immobility produced by inhaled anesthetics.

Anesthetics, Inhalation↗
PubMed2000

CNS penetration by noninvasive viruses following inhalational anesthetics.

The effects of inhalational anesthetics on brain penetration by the neurovirulent noninvasive West Nile virus (WN-25) were studied in mice. WN-25 injected intracerebrally causes encephalitis and kills adult mice, but when injected intraperitoneally (i.p.) it is unable to invade the brain and kill. Under stress conditions, this strain causes encephalitis and death even after i.p. inoculation. In the study described in this paper, we used two inhalational anesthetics, a single short-term exposure to 2% halothane for 10 min in oxygen, or 70% nitrous oxide (N2O) for 30 min in air. Both inhalational anesthetics induced WN-25 encephalitis and death in 33% and 20% of the tested mice, respectively. Exposure of inoculated mice to halothane for prolonged periods or for repeated exposures (two or three times) markedly increased the mortality rate (up to 75%). Exposure to 30% CO2, a known modulator of blood-brain barrier (BBB) activity, was used as a positive control (80% mortality). No death was observed in the control non-exposed injected mice. Virus levels were found to be more than 10(7) plaque-forming units (PFU)/brain in all moribund mice. Additional parameter demonstrating the "stressor-like" nature of inhalation anesthetics was the induction of a significant decrease in weight of the lymphoid organs of inoculated mice. We suggest that inhalational anesthetics induces BBB breaching with subsequent entrance of the noninvasive WN-25 virus into the brain, causing encephalitis and death.

Anesthetics, Inhalation↗
PubMed1990

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

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

Anesthesia, Inhalation↗
PubMed1991

[Initial washout time of inhaled anesthetic agents].

Recovery of inhalation anesthesia is generally considered the inverse of induction. While other factors remain unchanged, the rate of elimination of an inhaled anesthetic agent with a lower solubility such as nitrous oxide (N2O) is faster than one with a high solubility. Therefore, at the end of surgery it is a common practice to discontinue the volatile agent prior to discontinuing N2O. However, the results of our routine monitoring of end-tidal concentrations of anesthetics and physiological gases by employing a mass spectrometer lead us to question the practice. We studied 24 non-premedicated ASA I/II patients requiring endotracheal intubation with an anesthesia time over 2 h. All patients were mechanically ventilated at an appropriate tidal volume and respiratory rate to maintain an ETCO2 of 35-38 mmHg with an anesthetic mixture of 40% O2 and 60% N2O and isoflurane (Forane). At the end of surgery, both N2O and isoflurane were discontinued simultaneously and total oxygen flow was increased to 6 or 10 l/min by random. The exhaled partial pressure of both inhaled anesthetic agents were assessed at the time of anesthetic termination, after 1, 2 min, and then every 2 min up to 20 min or at the time of extubation. The results obtained were plotted against real time using two different scales. Despite the marked difference in their plasma solubilities, these two inhaled anesthetic agents reached to low exhaled partial pressure that had no clinical significance about ten minutes after discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Alpha-2 adrenoreceptors probably do not mediate the immobility produced by inhaled anesthetics.

UNLABELLED: Agonism of alpha-adrenoreceptors has a powerful anesthetic result mediated, in part, by effects on the spinal cord. Alpha-adrenoreceptor agonists (e.g., dexmedetomidine) can decrease the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics (e.g., halothane) to zero, with an apparently additive interaction between halothane and dexmedetomidine. We tested whether the capacity of the inhaled anesthetic isoflurane to produce immobility in the face of noxious stimulation resulted from agonism of alpha-adrenoreceptors. MAC (the concentration required to eliminate movement in response to a noxious stimulus in 50% of subjects) of isoflurane was determined before and after intraperitoneal administration of the alpha-adrenoreceptor antagonists yohimbine and atipamezole. The doses of yohimbine and atipamezole equaled or exceeded those that reverse the ability of agonism of alpha-adrenoreceptors to decrease MAC. Smaller doses of yohimbine or atipamezole slightly increased (by 10%) the MAC of isoflurane, an increase we interpret as the result of blockade of a small amount of tonically active alpha-adrenoreceptor activity. Doses five-fold larger did not change MAC. Doses 10-fold larger decreased MAC. We conclude that alpha-adrenoreceptors do not or minimally mediate the capacity of inhaled anesthetics to produce immobility. IMPLICATIONS: Although stimulation (agonism) of alpha-2 adrenoreceptors can decrease the inhaled anesthetic concentration required to produce immobility in the face of noxious stimulation, blockade of alpha-2 adrenoreceptors minimally affects the concentration. Thus, augmentation of the effect of alpha-2 adrenoreceptors is not an appreciable part of the mechanism whereby inhaled anesthetics produce immobility.

Adrenergic alpha-Antagonists↗
PubMed2002

G protein-coupled receptors as direct targets of inhaled anesthetics.

The molecular pharmacology of inhalational anesthetics remains poorly understood. Despite accumulating evidence suggesting that neuronal membrane proteins are potential targets of inhaled anesthetics, most currently favored membrane protein targets lack any direct evidence for anesthetic binding. We report herein the location of the binding site for the inhaled anesthetic halothane at the amino acid residue level of resolution in the ligand binding cavity in a prototypical G protein-coupled receptor, bovine rhodopsin. Tryptophan fluorescence quenching and direct photoaffinity labeling with [(14)C]halothane suggested an interhelical location of halothane with a stoichiometry of 1 (halothane/rhodopsin molar ratio). Radiosequence analysis of [(14)C]halothane-labeled rhodopsin revealed that halothane contacts an amino acid residue (Trp265) lining the ligand binding cavity in the transmembrane core of the receptor. The predicted functional consequence, competition between halothane and the ligand retinal, was shown here by spectroscopy and is known to exist in vivo. These data suggest that competition with endogenous ligands may be a general mechanism of the action of halothane at this large family of signaling proteins.

Anesthetics, Inhalation↗
PubMedDate not supplied

[Role of inhalation anesthetics in current anesthesiological practice].

Inhalational anesthetic agents represented for long time the sole or mainly anesthetic technique in general anesthesia. In the last twenty years, however, their use has been also related to toxicity among operating room personnel, chronically exposed to the volatile agents. This toxicity could induce the anesthesiologist to give up the volatile anesthetic agents in favour of a total intravenous anesthetic technique. Nevertheless well constructed prospective studies have clearly demonstrated that there is no significant correlation between morbidity index and chronic exposure to inhalational anesthetics. Furthermore a valid air exchange in the operating room, as well as more appropriate anesthesiologic procedures, have significantly reduced the concentration of volatile anesthetic agents in the operating areas. Nowadays inhalational anesthetic agents represent one of the different choices to perform general anesthesia. The anesthesiologist, however, according to patient's physical status and surgical procedure, must choose the anesthetic technique compatible with minimal risk both for patient and operating room personnel.

Abnormalities, Drug-Induced↗
PubMed1989

Simple and inexpensive delivery of halogenated inhalation anesthetics to rodents.

Halogenated inhalation anesthetics offer several advantages over injectable anesthetics for small-animal surgery. Benefits include rapid induction, easy adjustment of anesthetic depth, and a short period of recovery. Although the cost of most inhalation anesthetics is low, present delivery systems are often prohibitively expensive for rodent uses. This report describes a low-cost, portable system that can be used with halothane or isoflurane for general surgery or stereotaxic applications with or without intubation. Also included is a description of rodent nose cones for both general surgery and stereotaxic surgery that allow for simple evacuation of waste gases.

Anesthesia, Inhalation↗
PubMed1996

What is new with inhaled anesthetics: Part 2.

Since the 1800s, inhaled agents have been administered to produce surgical anesthesia. Although inhaled anesthetics are commonly known to produce a state of sleep, they also influence many physiologic processes. This article explores the pharmacodynamics of the inhaled anesthetics used in current anesthesia practice. Equipped with this knowledge, the PACU nurse will be better prepared to anticipate the nursing care needs of patients recovering from inhaled anesthetics.

Anesthetics, Inhalation↗