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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↗
PubMed2004

Pharmacoeconomics of inhaled anesthetic agents: considerations for the pharmacist.

PURPOSE: Types of economic analyses used for inhaled anesthetic agents, factors to consider in calculating the cost of inhaled anesthetics, limitations of pharmacoeconomic studies of these agents, and strategies for controlling inhaled anesthetic costs are discussed. SUMMARY: Inhaled anesthetic agents comprise a substantial component of drug budgets. Calculation of the cost of administering an inhaled anesthetic should take into consideration the cost per mL, potency, waste, concentration and duration of gas delivery, fresh gas flow rate, molecular weight, and density. The use of newer inhaled anesthetic agents with low solubility in blood and tissue provides a more rapid recovery from anesthesia than older, more soluble agents, and also provides the same level of control of depth of anesthesia at a lower fresh gas flow rate and possibly a lower cost than older agents at a higher fresh gas flow rate. A more rapid recovery may facilitate fast-track recovery and yield cost savings if it allows the completion of additional surgical cases or allows a reduction in personnel overtime expenses. Interpretation of pharmacoeconomic studies of inhaled anesthetics requires an appreciation of the limitations in methodology and ability to extrapolate results from one setting to another. Pharmacists' efforts to reduce anesthetic waste and collaborate with anesthesiologists to improve the use of these agents can help contain costs, but improving scheduling and efficiency in the operating room has a greater potential to reduce operating room costs. CONCLUSION: Much can be done to control costs of anesthetic agents without compromising availability of these agents and patient care.

Administration, Inhalation↗
PubMed2006

Inhaled anesthetic agents.

PURPOSE: The pharmacology, bioavailability and pharmacokinetics, indications, clinical efficacy, adverse effects and toxicities, and dosage and administration of the inhaled anesthetics are reviewed. SUMMARY: The inhaled anesthetics include desflurane, enflurane, halothane, isoflurane, and sevoflurane and are thought to enhance inhibitory postsynaptic channel activity and inhibit excitatory synaptic activity. The mechanism of action of inhaled anesthetics has not been completely defined. A number of factors can influence the pharmacokinetics of inhaled anesthetics, including solubility in blood, cardiac output, tissue equilibration, extent of tissue perfusion, metabolism, and age. All of the available inhaled anesthetics are effective for inducing or maintaining anesthesia or both. Most clinical trials of inhaled anesthetics have evaluated differences in induction and emergence from anesthesia by comparing (1) times to loss of reflex, extubation, and response to verbal commands; orientation to time and place; and ability to sit up without assistance, (2) need for post-surgical analgesia, and (3) time to discharge as measures of efficacy. Adverse effects and toxicities of the inhaled anesthetics include nephrotoxicity, hepatotoxicity, cardiac arrhythmias, neurotoxicity, postoperative nausea and vomiting, respiratory depression and irritation, malignant hyperthermia, and postanesthesia agitation. Safety issues surrounding these gases include occupational exposure and intraoperative fires within the delivery systems used with inhaled anesthetics. Drugs used for anesthesia during surgery can account for 5-13% of a hospital's drug budget. CONCLUSION: The inhaled anesthetics have been shown to be both safe and effective in inducing and maintaining anesthesia. These agents differ in potency, adverse-effect profile, and cost. Newer anesthetic gases, such as sevoflurane and desflurane, appear to have more favorable physico-chemical properties. These factors, as well as patient characteristics and duration and type of procedure, must be considered when selecting an inhaled anesthetic.

Anesthetics, Inhalation↗
PubMed1981

Interfacial preference of anesthetic action upon the phase transition of phospholipid bilayers and partition equilibrium of inhalation anesthetics between membrane and deuterium oxide.

The half-height linewidth (v 1/2) of the 1H-NMR spectra of dipalmitoylphosphatidylcholine vesicles changes abruptly at the phase transition temperature. In the absence of inhalation anesthetics, proton signals from the choline head group (hydrophilic interface) and acyl-chain tails (lipid core) change at the same temperature of 39.6 degrees C. The present study compared the effect of four inhalation anesthetics, i.e., methoxyflurane, chloroform, halothane and enflurane, upon the ligand-induced phase transition of phosphatidylcholine vesicle membranes at 37 degrees C. The anesthetics showed differential action upon the phase transition of the phospholipid vesicle membranes between the lipid core and the hydrophilic interface. The concentrations of anesthetics which induced the phase transition of the lipid core were about 2-fold greater than those required for the phase transition of the interfacial choline head groups. From the area under the proton signals of inhalation anesthetics in the NMR spectra, the maximum solubilities of methoxyflurane, chloroform and halothane in 2H2O at 37 degrees C were determined to be 0.671 . 10(-4), 2.637 . 10(-4) and 1.398 . 10(-4) (expressed as mole fractions), or 3.35, 13.17 and 6.98 mmol/1000 g 2H2O, respectively. The solubilities of the anesthetic vapor in 2H2O expressed as mole fractions according to Henry's law ere 9.586 . 10(-4), 6.432 . 10(-4) and 2.311 10(-4)/atm (1.013 . 10(5) Pa) partial pressure, respectively. The presence of phospholipid vesicles in 2H2O increased the solubility of the inhalation anesthetics. From difference between solubility in 2H2O and a dipalmitoylphosphatidylcholine vesicle suspension, the partition coefficients of methoxyflurane, chloroform and halothane between the phospholipid vesicle membranes and 2H2O were estimated. These values, calculated from the mole fractions, were 3364, 1660 and 3850, respectively at 37 degrees C.

Anesthetics↗
PubMed1993

Comparing the costs of inhaled anesthetics.

BACKGROUND: The immediate cost of an inhaled anesthetic results from an interplay between four factors: (1) the cost per milliliter of liquid anesthetic, (2) the volume of vapor that results from each milliliter of liquid, (3) the effective potency of the anesthetic (what concentration must be delivered from a vaporizer to provide a clinically appropriate level of anesthesia), and (4) the background flow of the gases that is chosen. A background flow that supplies only the gases/vapors required (taken up) by the patient (a "closed circuit") produces the least cost but also the least control of anesthetic level, whereas a high flow prevents rebreathing (a non-rebreathing system) but produces the greatest cost and control. We define greater "control" as a smaller ratio of delivered to alveolar concentrations. A lower solubility of an anesthetic accords the same level of control at a lower background flow rate than is achieved at a higher background flow rate with a more soluble anesthetic. Thus, a poorly soluble anesthetic may be used with a lower background flow rate than a more soluble anesthetic and may offer greater control and/or decreased cost. METHODS: This report presents a method of determining the cost of inhaled anesthetic use. As an example, the cost of delivering a desflurane anesthetic is compared with that of delivering an isoflurane anesthetic, assuming both provide an alveolar concentration of 1 MAC. The comparison is based on the pharmacokinetic differences of the two anesthetics: taking into account that for a given therapeutic anesthetic concentration (MAC), for desflurane a lower flow rate of background gas is needed to produce similar control (relationship between delivered and alveolar gases) than is needed for isoflurane. RESULTS: The analysis demonstrates that the relative cost of administering the newer and less soluble anesthetic, desflurane, can be less than, greater than, or the same as the cost of administering isoflurane, depending on the background gas inflow rate selected. CONCLUSION: The manner in which inhaled anesthetics are used and their kinetic differences are important determinants of relative cost.

Administration, Inhalation↗
PubMed1987

Does the duration of anesthetic administration affect the pharmacokinetics or metabolism of inhaled anesthetics in humans?

To define the effect of anesthetic duration on the pharmacokinetics of inhaled anesthetics, we determined the pharmacokinetics of isoflurane, enflurane, halothane, and methoxyflurane given simultaneously to seven healthy subjects for exactly 30 min and compared the results with data from a previous study in which these four anesthetics were administered for 120 min. End-tidal and mixed-expired anesthetic concentrations were measured during washin of anesthetic and for 3-9 days of washout. Multiexponential (multicompartment) models were fit by least squares to the alveolar washin and washout curves. We estimated the percentage of anesthetic that was metabolized from total uptake and recovery of anesthetic. Alveolar washout was more rapid after the shorter period of anesthetic administration. However, duration of administration did not affect the time constants determined, the number of compartments identified (i.e., five compartments were identified in both studies), or the percentages of anesthetic metabolized.

Adult↗
PubMed2002

Acetylcholine receptors do not mediate the immobilization produced by inhaled anesthetics.

UNLABELLED: Acetylcholine receptors transmit excitatory impulses, are broadly distributed throughout the central nervous system, and are particularly sensitive to the depressant effects of inhaled anesthetics. Thus these receptors are potential mediators of the immobility produced by inhaled anesthetics. We tested this potential in rats by giving intraperitoneal atropine, scopolamine, and mecamylamine to block muscarinic (atropine and scopolamine) and neuronal nicotinic (mecamylamine) acetylcholine receptors. Block with scopolamine (up to 100 mg/kg), atropine (10 mg/kg), mecamylamine (up to 4 mg/kg), or atropine (10 mg/kg) plus mecamylamine (up to 4 mg/kg) did not significantly decrease the isoflurane concentration required to suppress movement to noxious stimulation (minimum alveolar anesthetic concentration). We also gave atropine intrathecally, finding that the infusions that did not cause permanent paralysis produced slight or no decreases in the minimum alveolar anesthetic concentration. We conclude that acetylcholine receptors do not seem to play a role as mediators of immobilization by inhaled anesthetics. IMPLICATIONS: Inhaled anesthetics produce two crucial effects: amnesia and immobility in the face of noxious stimulation. Block of muscarinic and neuronal nicotinic acetylcholine receptors in rats does not significantly decrease the isoflurane concentration required to suppress movement to stimulation. Thus, acetylcholine receptors do not seem to play a major role as mediators of the immobilization produced by inhaled anesthetics. Their capacity to mediate other effects of inhaled anesthetics (e.g., amnesia) remains to be tested.

Anesthetics, Inhalation↗
PubMed1993

The impact of streptozotocin-induced diabetes on the minimum alveolar anesthetic concentration (MAC) of inhaled anesthetics in the rat.

We designed experiments to examine the effects of insulin-dependent diabetes mellitus on the anesthetic requirements for volatile anesthetics. A standard tail-clamp technique was used to determine minimum alveolar anesthetic concentrations for halothane, enflurane, and isoflurane in spontaneously breathing rats. Three groups of animals were used: 1) diabetic rats (12 wk after induction of diabetes with streptozotocin, 50 mg/kg, single dose, intravenously), 2) insulin-treated (7 U extended insulin zinc suspension per day, subcutaneously, beginning 5 wk after streptozotocin treatment) diabetic rats, and 3) control rats. The minimum alveolar anesthetic concentration values of the control animals were 1.16 +/- 0.02 vol% for halothane, 2.25 +/- 0.05 vol% for enflurane, and 1.42 +/- 0.04 vol% for isoflurane. Minimum alveolar anesthetic concentration was reduced by 23% for halothane (0.90 +/- 0.06 vol%), by 18% for enflurane (1.85 +/- 0.07 vol%), and by 17% for isoflurane (1.18 +/- 0.04 vol%) in diabetic rats. Insulin treatment restored the anesthetic requirement to control levels for all three anesthetics. These data from the rat model indicate that uncontrolled diabetes lowers anesthetic requirements significantly.

Anesthesia, Inhalation↗
PubMed2006

Inhalational anesthetics as neuroprotectants or chemical preconditioning agents in ischemic brain.

This review will focus on inhalational anesthetic neuroprotection during cerebral ischemia and inhalational anesthetic preconditioning before ischemic brain injury. The limitations and challenges of past and current research in this area will be addressed before reviewing experimental and clinical studies evaluating the effects of inhalational anesthetics before and during cerebral ischemia. Mechanisms underlying volatile anesthetic neuroprotection and preconditioning will also be examined. Lastly, future directions for inhalational anesthetics and ischemic brain injury will be briefly discussed.

Anesthetics, Inhalation↗
PubMed1998

Mucosal blood flow during various intravenous and inhalational anesthetics in the rabbit.

OBJECTIVE: The goal of this study was to compare the effects of nitrous oxide (N2O), isoflurane (ISO), fentanyl (FENT), and propofol (PROP) on the tongue mucosal blood flow (TMBF) in rabbits. STUDY DESIGN: TMBF was measured with a laser Doppler flow meter before and after the administration of 50% N2O (n = 7), 1.0 and 1.5 minimum alveolar concentration ISO (n = 6), 10, 20, and 40 micrograms/kg FENT (n = 8) or 100, 200 and 400 micrograms/kg/min PROP (n = 7). Hemodynamic variables including heart rate, systolic blood pressure (SBP), mean arterial pressure (MAP) and aortic blood flow (AoF) were continuously monitored. Total peripheral resistance (TPR) was calculated as MAP divided by AoF. RESULTS: An increase in TMBF along with reductions in SBP, MAP and TPR were observed in ISO group. In FENT group, TMBF was decreased, whereas other hemodynamic variables showed no change. TMBF in groups N2O and PROP did not change. CONCLUSION: These results indicate that TMBF depends on the anesthetic used.

Anesthetics, Inhalation↗
PubMed2001

Luciferase as a model for the site of inhaled anesthetic action.

UNLABELLED: The in vivo potencies of anesthetics correlate with their capacity to suppress the reaction of luciferin with luciferase. In addition, luciferin has structural resemblances to etomidate. These observations raise the issues of whether luciferin, itself, might affect anesthetic requirement, and whether luciferase resembles the site of anesthetic action. Because the polar luciferin is unlikely to cross the blood-brain barrier (we found that the olive oil/water partition coefficient was 100 +/- 36 x 10(-7)), we studied these issues in rats by measuring the effect of infusion of luciferin in artificial cerebrospinal fluid into the lumbar subarachnoidal space and into the cerebral intraventricular space on the MAC (the minimum alveolar anesthetic concentration required to eliminate movement in response to a noxious stimulus in 50% of tested subjects) of isoflurane. MAC in rats given lumbar intrathecal doses of luciferin estimated to greatly exceed anesthetizing doses of etomidate, did not differ significantly from MAC in rats receiving only artificial cerebrospinal fluid into the lumbar intrathecal space. MAC slightly decreased when doses of luciferin estimated to greatly exceed anesthetizing doses of etomidate were infused intraventricularly (P < 0.05). In contrast to the absent or minimal effects of luciferin, intrathecal or intraventricular infusion of etomidate at similar or smaller doses significantly decreased isoflurane MAC. Luciferin did not affect +-aminobutyric acid type A or acetylcholine receptors expressed in Xenopus oocytes. These results suggest that luciferin has minimal or no anesthetic effects. It also suggests that luciferin/luciferase may not provide a good surrogate for the site at which anesthetics act, if this site is on the surface of neuronal cells. IMPLICATIONS: In proportion to their potencies, anesthetics inhibit luciferin's action on luciferase, and luciferin structurally resembles the anesthetic etomidate. However, in contrast to etomidate, luciferin given intrathecally or into the third cerebral ventricle does not have anesthetic actions, and it does not affect +-aminobutyric acid or acetylcholine receptors in vitro. Luciferase may not provide a good surrogate for the site at which anesthetics act.

Anesthetics, Inhalation↗
PubMed2006

Protein crystallography under xenon and nitrous oxide pressure: comparison with in vivo pharmacology studies and implications for the mechanism of inhaled anesthetic action.

In contrast with most inhalational anesthetics, the anesthetic gases xenon (Xe) and nitrous oxide (N(2)O) act by blocking the N-methyl-d-aspartate (NMDA) receptor. Using x-ray crystallography, we examined the binding characteristics of these two gases on two soluble proteins as structural models: urate oxidase, which is a prototype of a variety of intracellular globular proteins, and annexin V, which has structural and functional characteristics that allow it to be considered as a prototype for the NMDA receptor. The structure of these proteins complexed with Xe and N(2)O were determined. One N(2)O molecule or one Xe atom binds to the same main site in both proteins. A second subsite is observed for N(2)O in each case. The gas-binding sites are always hydrophobic flexible cavities buried within the monomer. Comparison of the effects of Xe and N(2)O on urate oxidase and annexin V reveals an interesting relationship with the in vivo pharmacological effects of these gases, the ratio of the gas-binding sites' volume expansion and the ratio of the narcotic potency being similar. Given these data, we propose that alterations of cytosolic globular protein functions by general anesthetics would be responsible for the early stages of anesthesia such as amnesia and hypnosis and that additional alterations of ion-channel membrane receptor functions are required for deeper effects that progress to "surgical" anesthesia.

Anesthetics↗
PubMed1997

Inhalational anesthetic effects on rat cerebellar nitric oxide and cyclic guanosine monophosphate production.

BACKGROUND: Inhalational anesthetics interact with the nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway in the central nervous system (CNS) and attenuate excitatory neurotransmitter-induced cGMP concentration. The site of anesthetic action on the NO-cGMP pathway in the CNS remains controversial. This study investigated the effect of inhalational anesthetics on N-methyl-D-aspartate (NMDA)-stimulated NO synthase activity and cyclic cGMP production in rat cerebellum slices. METHODS: The interaction of inhalational anesthetics with NO synthase activation and cGMP concentration was determined in cerebellum slices of 10-day-old rats. Nitric oxide synthase activity in cerebellum slices was assessed by measuring the conversion of L-[3H]arginine to L-[3H]citrulline. The cGMP content of cerebellum slices was measured by radioimmunoassay. RESULTS: Isoflurane at 1.5% and 3% enhanced the NMDA-stimulated NO synthase activity by two times while halothane at 1.5% and 3% produced no significant effect. However, the NMDA-stimulated cGMP production was inhibited by both anesthetic agents. The anesthetic inhibition of cGMP accumulation was not significantly altered by a mixture of superoxide dismutase and catalase or by glycine, a coagonist of the NMDA receptor. CONCLUSIONS: The enhancement of NMDA-induced NO synthase activity by isoflurane and the inhibition of NMDA-stimulated cGMP production by halothane and isoflurane suggests that inhalational anesthetics interfere with the neuronal NO-cGMP pathway. This inhibitory effect of anesthetics on cGMP accumulation is not due to either their interaction with the glycine binding site of the NMDA receptor or to the action of superoxide anions.

Anesthetics, Inhalation↗
PubMed1995

Inhalational anesthetics do not alter nitric oxide synthase activity.

Inhalational anesthetics inhibit the nitric oxide (NO)-soluble guanylate cyclase signaling pathway in vascular and neuronal tissues and it has been proposed that this inhibition is due to several mechanisms, which include a direct inhibition of NO synthase. To determine the direct interaction of anesthetics with NO synthase, the effects of halothane, isoflurane and enflurane on NO synthase activity of bovine and rat brains and cultured bovine aortic endothelial cells were investigated. Halothane and enflurane at 1% to 3% concentrations produced no significant effect on crude bovine brain NO synthase activity, as measured by the conversion of L-[3H]arginine to L-[3H]citrulline. Similarly, crude rat brain NO synthase activity was not affected by exposure to 1% to 4% halothane or isoflurane. The effects of inhalational anesthetics on the crude bovine brain NO synthase activity were not altered when assayed at two different temperatures (22 degrees C and 37 degrees C). Halothane and isoflurane produced no significant effects on the activity of partially purified rat brain NO synthase at different concentrations of L-[3H]arginine in the reaction mixture. Partially purified endothelial NO synthase, when equilibrated with halothane or isoflurane (0.5-2%), exhibited no significant alteration in enzyme activity. This study suggests that the effects of inhalational anesthetics on NO synthesis in rat and bovine brains and in vascular endothelial cells are not due to their direct interaction with NO synthase.

Amino Acid Oxidoreductases↗