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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007412,
umls-concept:C0007452,
umls-concept:C0010453,
umls-concept:C0030685,
umls-concept:C0376604,
umls-concept:C0391871,
umls-concept:C0392747,
umls-concept:C0441712,
umls-concept:C0443172,
umls-concept:C0521428,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1963578,
umls-concept:C2603343
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pubmed:issue |
1-2
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pubmed:dateCreated |
1994-8-12
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pubmed:abstractText |
Ischemia-induced changes in neurotransmitter release and their mechanisms were examined using cultured bovine adrenal chromaffin cells. When the cells were incubated in glucose-free media equilibrated with 0% O2/100% N2 (ischemia), ATP content decreased and reached the minimum level within 40 min. Control incubation was done in media equilibrated with 21% O2 in N2. After 10-min incubation under ischemic conditions, basal catecholamine (CA) release was elevated and the elevation persisted up to 90 min. High K(+)-evoked CA release was transiently enhanced at 10 min, but after that, it decreased to reach the minimum level at 60 min. At 10 min, cytosolic free Ca2+ concentration ([Ca2+]i) and 45Ca2+ uptake of the resting cells (basal values) and high K(+)-evoked increases in these two parameters were unchanged, but CA release from permeabilized cells in response to Ca2+ in media was augmented. After 60-min incubation under ischemic conditions, basal [Ca2+]i was elevated: the elevation was observed even in the absence of extracellular Ca2+. In contrast, high K(+)-evoked increases in [Ca2+]i and in 45Ca2+ uptake were suppressed, but basal 45Ca2+ uptake into intact cells and CA release from permeabilized cells were unchanged. These results suggest that in an early phase (10 min) of ischemia, both basal and stimulation-evoked CA release are augmented because of increased sensitivity of exocytotic machinery to Ca2+. In the late phase (60 min), basal CA release is augmented because of an increase in basal [Ca2+]i, which is due to accumulation of Ca2+ derived from intracellular Ca2+ pools: stimulation-evoked CA release is suppressed because of inhibition of stimulation-evoked increase in [Ca2+]i, which is due to functional disturbance of voltage-dependent Ca2+ channels.
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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 |
Apr
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
18
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pubmed:volume |
643
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
266-75
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:8032921-Adenosine Triphosphate,
pubmed-meshheading:8032921-Adrenal Medulla,
pubmed-meshheading:8032921-Analysis of Variance,
pubmed-meshheading:8032921-Animals,
pubmed-meshheading:8032921-Calcium,
pubmed-meshheading:8032921-Catecholamines,
pubmed-meshheading:8032921-Cattle,
pubmed-meshheading:8032921-Cells, Cultured,
pubmed-meshheading:8032921-Ischemia,
pubmed-meshheading:8032921-Kinetics,
pubmed-meshheading:8032921-Models, Biological,
pubmed-meshheading:8032921-Potassium,
pubmed-meshheading:8032921-Probability
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pubmed:year |
1994
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pubmed:articleTitle |
Ischemia-induced changes in catecholamine release and their mechanisms: a study using cultured bovine adrenal chromaffin cells.
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pubmed:affiliation |
Department of Neurosurgery, Kyoto University Faculty of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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