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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2 Pt 2
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pubmed:dateCreated |
1991-3-22
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pubmed:abstractText |
We determined whether the rate of metabolic recovery and electrophysiological deficit after incomplete cerebral ischemia is related to intracellular pH (pHi) achieved at the end of ischemia in a dose-dependent manner. End-ischemic pHi was varied by employing two ischemic durations, 12 and 30 min, and by setting preischemic plasma glucose to approximately 80 or 400 mg/dl. Incomplete global ischemia was produced in anesthetized dogs by transient intracranial hypertension followed by 4 h of reperfusion, and pHi, ATP, and phosphocreatine (PCr) were measured with 31P magnetic resonance spectroscopy. Cerebral blood flow was reduced to approximately 6 ml.min-1.100 g-1 during ischemia. End-ischemic pHi was greater than 5.7 in all animals from various treatment groups except for four of seven dogs treated with 30-min hyperglycemic ischemia. When end-ischemic pHi remained greater than 5.7, there was nearly complete recovery of ATP, PCr, pHi, intracellular bicarbonate concentration [( HCO3-]i), and O2 consumption. Partial recovery of somatosensory-evoked potentials (SEP) occurred in most of these animals. In the 30-min hyperglycemic animals in which pHi fell below 5.5, ATP, PCr, and O2 consumption recovered by only one-half over 60 min of reperfusion and then declined to near-zero levels without SEP recovery. In addition, pHi remained less than 6.0, and [HCO3-]i remained less than 2 mM throughout reperfusion. We conclude that there is an apparent in vivo pHi threshold of approximately 5.5-5.7 during incomplete cerebral ischemia that is associated with an inability to significantly restore pHi and [HCO3-]i and with secondary deterioration of high-energy phosphate levels.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
260
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H532-41
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:1996696-Animals,
pubmed-meshheading:1996696-Brain,
pubmed-meshheading:1996696-Brain Ischemia,
pubmed-meshheading:1996696-Cerebrovascular Circulation,
pubmed-meshheading:1996696-Differential Threshold,
pubmed-meshheading:1996696-Dogs,
pubmed-meshheading:1996696-Energy Metabolism,
pubmed-meshheading:1996696-Evoked Potentials, Somatosensory,
pubmed-meshheading:1996696-Hemodynamics,
pubmed-meshheading:1996696-Hydrogen,
pubmed-meshheading:1996696-Hydrogen-Ion Concentration,
pubmed-meshheading:1996696-Magnetic Resonance Imaging,
pubmed-meshheading:1996696-Phosphates
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pubmed:year |
1991
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pubmed:articleTitle |
Dependence of cerebral energy phosphate and evoked potential recovery on end-ischemic pH.
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pubmed:affiliation |
Department of Anesthesiology/Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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