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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001969,
umls-concept:C0004745,
umls-concept:C0005486,
umls-concept:C0006104,
umls-concept:C0011065,
umls-concept:C0024467,
umls-concept:C0038454,
umls-concept:C0080103,
umls-concept:C0439831,
umls-concept:C1274040,
umls-concept:C1517945,
umls-concept:C1880497,
umls-concept:C1996904,
umls-concept:C2699787
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pubmed:issue |
2-4
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pubmed:dateCreated |
1993-5-19
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pubmed:abstractText |
In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Barbiturates,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Ethanol,
http://linkedlifedata.com/resource/pubmed/chemical/Magnesium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium
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pubmed:status |
MEDLINE
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pubmed:issn |
1015-3845
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
122-35
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1844545-Alcoholic Intoxication,
pubmed-meshheading:1844545-Animals,
pubmed-meshheading:1844545-Barbiturates,
pubmed-meshheading:1844545-Brain,
pubmed-meshheading:1844545-Calcium,
pubmed-meshheading:1844545-Cerebrovascular Disorders,
pubmed-meshheading:1844545-Energy Metabolism,
pubmed-meshheading:1844545-Ethanol,
pubmed-meshheading:1844545-Hydrogen-Ion Concentration,
pubmed-meshheading:1844545-Ischemic Attack, Transient,
pubmed-meshheading:1844545-Magnesium,
pubmed-meshheading:1844545-Magnetic Resonance Spectroscopy,
pubmed-meshheading:1844545-Male,
pubmed-meshheading:1844545-Potassium,
pubmed-meshheading:1844545-Rats,
pubmed-meshheading:1844545-Rats, Wistar
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pubmed:articleTitle |
Alcohol intoxication results in rapid loss in free magnesium in brain and disturbances in brain bioenergetics: relation to cerebrovasospasm, alcohol-induced strokes, and barbiturate anesthesia-induced deaths.
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pubmed:affiliation |
Department of Physiology, SUNY Health Science Center, Brooklyn.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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