| pubmed-article:5648829 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C0004461 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C0028778 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C0004745 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C0037473 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C1749549 | lld:lifeskim |
| pubmed-article:5648829 | lifeskim:mentions | umls-concept:C1140675 | lld:lifeskim |
| pubmed-article:5648829 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:5648829 | pubmed:dateCreated | 1968-7-3 | lld:pubmed |
| pubmed-article:5648829 | pubmed:abstractText | Sodium pentobarbital and sodium thiopental decrease both the peak initial (Na) and late steady-state (K) currents and reduce the maximum sodium and potassium conductance increases in voltage-clamped lobster giant axons. These barbiturates also slow the rate at which the sodium conductance turns on, and shift the normalized sodium conductance vs. voltage curves in the direction of depolarization along the voltage axis. Since pentobarbital (pK(a) = 8.0) blocks the action potential more effectively at pH 8.5 than at pH 6.7, the anionic form of the drug appears to be active. The data suggest that these drugs affect the axon membrane directly, rather than secondarily through effects on intermediary metabolism. It is suggested that penetration of the lipid layer of the membrane by the nonpolar portion of the barbiturate molecules may cause the decrease in membrane conductances, while electrostatic interactions involving the anionic group on the barbiturate, divalent cations, and "fixed charges" in the membrane could account for the slowing of the rate of sodium conductance turn-on and the shift of the normalized conductance curves along the voltage axis. | lld:pubmed |
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| pubmed-article:5648829 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:5648829 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:5648829 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:5648829 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:5648829 | pubmed:issn | 0022-1295 | lld:pubmed |
| pubmed-article:5648829 | pubmed:author | pubmed-author:BlausteinM... | lld:pubmed |
| pubmed-article:5648829 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:5648829 | pubmed:volume | 51 | lld:pubmed |
| pubmed-article:5648829 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:5648829 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:5648829 | pubmed:pagination | 293-307 | lld:pubmed |
| pubmed-article:5648829 | pubmed:dateRevised | 2010-6-22 | lld:pubmed |
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| pubmed-article:5648829 | pubmed:year | 1968 | lld:pubmed |
| pubmed-article:5648829 | pubmed:articleTitle | Barbiturates block sodium and potassium conductance increases in voltage-clamped lobster axons. | lld:pubmed |
| pubmed-article:5648829 | pubmed:publicationType | Journal Article | lld:pubmed |
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