Linked Life Data

8067426

Source:http://linkedlifedata.com/resource/pubmed/id/8067426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 2
pubmed:dateCreated
1994-9-21
pubmed:abstractText
Isolated resistance arteries from the gracilis muscle of rats were simultaneously perfused and superfused with physiological salt solution (PSS) equilibrated with control (21% O2) and reduced (15, 10, 5, or 0% O2) concentrations of O2. The vessels exhibited a significant dilation in response to reduced PO2, which could be inhibited by selective perfusion of the lumen with 21% O2 PSS, endothelial removal, and 1 microM indomethacin, but was unaffected by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (10 microM). Contraction of the arteries in response to 50 mM K+ was inhibited by 0% O2, whereas agonist (norepinephrine and serotonin)-induced contractions and pressure-induced myogenic responses were insensitive to reduced PO2. These results suggest that 1) skeletal muscle resistance arteries are intrinsically sensitive to reduced PO2 independent of parenchymal cell influences, 2) inhibition of resting tone in these vessels is mediated by an endothelium-derived product of the cyclooxygenase pathway, and 3) various forms of contractile activation are not equally sensitive to inhibition by reduced PO2 in extraparenchymal resistance arteries of skeletal muscle.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H706-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Response of extraparenchymal resistance arteries of rat skeletal muscle to reduced PO2.
pubmed:affiliation
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't