Linked Life Data

7733370

Source:http://linkedlifedata.com/resource/pubmed/id/7733370

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4 Pt 2
pubmed:dateCreated
1995-6-1
pubmed:abstractText
The 1H nuclear magnetic resonance (NMR) signal of tissue myoglobin has provided an opportunity to determine the critical O2 level in saline-perfused myocardium at room temperature. Above the intracellular PO2 of 4 mmHg, the myocardium exhibits no sign of hypoxia. At 4 mmHg, the rate pressure product (RPP) decreases, and the lactate formation rate, measured enzymatically, increases. However, O2 consumption and the 31P-NMR signal of phosphocreatine level remain relatively constant until the cellular PO2 reaches 2 mmHg. The ATP signal intensity dips only when cellular O2 reaches 0.8 mmHg, while pH remains unchanged at 7.2. The sequential nature of the cellular response to limiting O2, starting with alterations in the lactate formation rate and RPP, indicates that NADH, rather than ADP, signals tissue hypoxia. Moreover, the study suggests that the O2 gradient from capillary to cell is larger than that from cytosol to mitochondria.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1675-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Critical intracellular O2 in myocardium as determined by 1H nuclear magnetic resonance signal of myoglobin.
pubmed:affiliation
Biological Chemistry Department, University of California, Davis 95616, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't