Adenosine Decreases the Minimum Alveolar Concentration of Halothane in Dogs

Seitz, P; Riet, M. ter; Rush, William; Merrell, W. J.

doi:10.1097/00000542-199011000-00029

Cited by 37 publications

(20 citation statements)

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“…Administration of adenosine decreases MAC of halothane in dogs,86 and intrathecal administration of the adenosine agonist R-phenylisopropyl-adenosine (R-PIA) decreases halothane MAC in rats 87. However, aminophylline, an adenosine receptor blocker, does not increase halothane MAC in dogs,88 rats,88 or humans 89.…”

Section: Relevance Of Plausible Specific Targets (Alphabetical Order)mentioning

confidence: 99%

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Eger

Raines

Shafer³

et al. 2008

Anesthesia &Amp; Analgesia

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A paradox arises from present information concerning the mechanism(s) by which inhaled anesthetics produce immobility in the face of noxious stimulation. Several findings, such as additivity, suggest a common site at which inhaled anesthetics act to produce immobility. However, two decades of focused investigation have not identified a ligand- or voltage-gated channel that alone is sufficient to mediate immobility. Indeed, most putative targets provide minimal or no mediation. For example, opioid, 5-HT3, gamma-aminobutyric acid type A and glutamate receptors, and potassium and calcium channels appear to be irrelevant or play only minor roles. Furthermore, no combination of actions on ligand- or voltage-gated channels seems sufficient. A few plausible targets (e.g., sodium channels) merit further study, but there remains the possibility that immobilization results from a nonspecific mechanism.

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Section: Relevance Of Plausible Specific Targets (Alphabetical Order)mentioning

confidence: 99%

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Eger

Raines

Shafer³

et al. 2008

Anesthesia &Amp; Analgesia

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“…The animal data suggesting adenosine receptormediated antinociception are being reviewed elsewhere in this issue. In brief, abundant studies in rodents have demonstrated a delay in withdrawal tests for noxious stimuli [Sawynok and Sweeney, 1989;Sawynok, 1998], in normal tissue and in tissues compromised by peripheral inflammation [Karlsten et al, 1992a], peripheral and central nerve injury [Lee and Yaksh, 1996;Sjölund et al, 1996Sjölund et al, , 1997Sjölund et al, , 1998Cui et al, 1997Cui et al, , 1998], or during anesthesia [Birch et al, 1988;Seitz et al, 1990]. However, there are difficulties in translating these experimental data into the clinic.…”

Section: Experimental Backgroundmentioning

confidence: 99%

Adenosine and pain relief: A clinical overview

Segerdahl¹,

Sollevi²

1998

Drug Dev. Res.

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This overview summarizes the current clinical state of knowledge in the field of adenosine‐mediated pain reduction, also including a condensed experimental background of relevance for clinical implementation. Clinical investigations have been systematically performed and include experimental pain models in volunteers, as well as studies in acute perioperative pain and in chronic neuropathic pain. Adenosine has been administered as a low‐dose intravenous infusion and as an intrathecal injection. Effects on pain and on signs of hyperexcitability in the nervous system have been investigated, both after administration of adenosine alone and in combination with well‐known analgesic agents. The different modes of adenosine administration demonstrate reduced pain, primarily in modalities that involve mechanisms of hyperexcitability of the central nervous system, i.e., central sensitization. Because this phenomenon is an important factor in chronic pain conditions, the promising results of pain relief in patients with neuropathic pain suggest that this is especially relevant for future development and research. In addition, the potential use of adenosine in combination with other pain‐modulating agents deserves further evaluation. Drug Dev. Res. 45:151–158, 1998. © 1998 Wiley‐Liss, Inc.

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“…The ␣ 2 -adrenergic receptor seems to play a role in antinociceptive responses as well as in the state of arousal (Bol et al, 1999). In fact, agonists and/or antagonists that work through these GPCRs have been reported to significantly alter anesthetic requirements in humans and animals (Segal et al, 1988;Seitz et al, 1990;Glass et al, 1997;Ishizawa et al, 2000a). Although this might include unrelated, parallel effects on the central nervous system, recent studies show that inhaled anesthetics can interfere with GPCR signaling in vitro (Durieux, 1995;Honemann et al, 1998;Schotten et al, 1998), suggesting direct anesthetic effects.…”

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confidence: 99%

G Protein-Coupled Receptors as Direct Targets of Inhaled Anesthetics

et al. 2002

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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 proteincoupled 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.

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Adenosine Decreases the Minimum Alveolar Concentration of Halothane in Dogs

Cited by 37 publications

References 0 publications

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?

Adenosine and pain relief: A clinical overview

G Protein-Coupled Receptors as Direct Targets of Inhaled Anesthetics

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