Do Anesthetics Fluidize Membranes?

Ueda, I.; Hirakawa, Masahisa; Arakawa, Kasumi; Kamaya, Hiroshi

doi:10.1097/00000542-198601000-00010

Cited by 39 publications

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“…[24][25][26] interpretation of the nervous system. No gross or microscopic abnormalities were observed in the central, In spite of these acute narcotic effects, this study demonstrates that subchronic exposure of rats to ETBE peripheral, or autonomic nervous systems of rats exposed to 5000 ppm ETBE.…”

Section: Clinical Observations and Ophthalmological Neuropathology Evmentioning

confidence: 99%

Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

et al. 1997

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Section: Clinical Observations and Ophthalmological Neuropathology Evmentioning

confidence: 99%

Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

et al. 1997

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“…Recent investigations show that anaesthetics and organic solvents affect both the enzymes and the lipid part of the membrane (Ueda et al 1986;Korpola & Tahti 1987;Edelfors & Ravn-Jonsen 1989;1990). Korpola & Tahti (1987) found that several solvents affect the ATPase activity of the synaptosomal membrane.…”

mentioning

confidence: 99%

Effect of Organic Solvents on Nervous Cell Membrane as Measured by Changes in the (Ca²⁺/Mg²⁺) ATPase Activity and Fluidity of Synaptosomal Membrane

Edelfors

Ravn-Jonsen

1992

Pharmacology & Toxicology

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The effect of various solvents on the central nervous system was studied by using rat brain synaptosomal membranes as an in vitro model. The activity of (Ca2+/Mg2+) ATPase and the membrane fluidity was determined. The alteration of the ATPase activity depended on the physio-chemical characteristics of the solvent in question. Incubation with aliphatic alkanes caused a stimulation of the ATPase activity whereas mixed hydrocarbons as kerosene, white spirit and gasoline inhibited the enzyme. Incubation with chlorinated hydrocarbons caused a biphasic response dependent on the concentration. Oxygen-containing hydrocarbons exhibited various effects as found after incubation with hydrocarbons. The different effects of the solvents on the ATPase activity suggest that the lipophilicity of the solvents is one of more parameters affecting the membrane. Furthermore, the biphasic response following the incubation with chlorinated hydrocarbons indicates that more mechanisms are involved in the enzyme effect. The membrane fluidity is increased with higher concentrations of the solvents. From the results it is concluded that the ATPase activity depends not only on the membrane fluidity and volume, but also on the hydrophilic vicinity of the enzyme molecule.

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“…These ideas included anaesthetic-induced volume expansion of the cell membrane [48], increased fluidity of the cell membrane [49] and increased lateral surface pressure [50,51]. Another impetus for these hypotheses stemmed from the dramatic findings that animals under conditions of increased hydrostatic or barometric pressure were resistant to the effects of volatile anaesthetics [52,53].…”

Section: The Lipid Bilayer As the Site – The Meyer-overton Correlationmentioning

confidence: 99%

Anaesthetic mechanisms: update on the challenge of unravelling the mystery of anaesthesia

Lugli

Yost

Kindler

2009

European Journal of Anaesthesiology

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General anaesthesia is administered each day to thousands of patients worldwide. Although more than 160 years have passed since the first successful public demonstration of anaesthesia, a detailed understanding of the anaesthetic mechanism of action of these drugs is still lacking. An important early observation was the Meyer-Overton correlation, which associated the potency of an anaesthetic with its lipid solubility. This work focuses attention on the lipid membrane as a likely location for anaesthetic action. With the advent of cellular electrophysiology and molecular biology techniques, tools to dissect the components of the lipid membrane have led, in recent years, to the widespread acceptance of proteins, namely receptors and ion channels, as more likely targets for the anaesthetic effect. Yet these accumulated data have not produced a comprehensive explanation for how these drugs produce CNS depression. In this review, we follow the story of anaesthesia mechanisms research from its historical roots to the intensely neurophysiologic inquiries regarding it today. We will also describe recent findings that identify specific neuroanatomical locations mediating the actions of some anaesthetic agents.

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Do Anesthetics Fluidize Membranes?

Cited by 39 publications

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Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

Effect of Organic Solvents on Nervous Cell Membrane as Measured by Changes in the (Ca²⁺/Mg²⁺) ATPase Activity and Fluidity of Synaptosomal Membrane

Anaesthetic mechanisms: update on the challenge of unravelling the mystery of anaesthesia

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Do Anesthetics Fluidize Membranes?

Cited by 39 publications

References 0 publications

Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

Neurotoxicological Evaluation of Ethyl Tertiary-Butyl Ether Following Subchronic (90-day) Inhalation in the Fischer 344 Rat

Effect of Organic Solvents on Nervous Cell Membrane as Measured by Changes in the (Ca2+/Mg2+) ATPase Activity and Fluidity of Synaptosomal Membrane

Anaesthetic mechanisms: update on the challenge of unravelling the mystery of anaesthesia

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Effect of Organic Solvents on Nervous Cell Membrane as Measured by Changes in the (Ca²⁺/Mg²⁺) ATPase Activity and Fluidity of Synaptosomal Membrane