Linked Life Data

11045952

Source:http://linkedlifedata.com/resource/pubmed/id/11045952

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-11-17
pubmed:abstractText
This study characterized the effects of fluid percussion brain injury (FPI) on N-methyl-D-aspartate (NMDA)-induced vasodilation and determined the role of nociceptin/orphanin FQ (NOC/oFQ) in such changes as a function of age and time postinsult. FPI elevated cerebrospinal fluid (CSF) NOC/oFQ from 70 +/- 3 to 444 +/- 56 pg/ml ( approximately 10(-10) M) within 1 h and to 1,931 +/- 112 pg/ml within 8 h, whereas values returned to control levels within 168 h in the newborn pig. In contrast, FPI elevated CSF NOC/oFQ from 77 +/- 4 to 202 +/- 16 pg/ml within 1 h and values returned to control levels within 8 h in the juvenile pig. Topical NOC/oFQ (10(-10) M) had no effect on pial artery diameter but attenuated NMDA (10(-8), 10(-6) M)-induced dilation (9 +/- 1 and 16 +/- 1 vs. 5 +/- 1 and 10 +/- 1%) in both age groups. In the newborn, NMDA-induced pial artery dilation was reversed to vasoconstriction within 1 h post-FPI and responses remained impaired for 72 h, but such vasoconstriction was attenuated by pretreatment with [F/G]NOC/oFQ(1-13)-NH(2) (10(-6) M, 1 mg/kg iv), an NOC/oFQ antagonist (9 +/- 1 and 16 +/- 1 vs. -7 +/- 1 and -12 +/- 1 vs -2 +/- 1 and -3 +/- 1% for control, FPI, and FPI pretreated with the NOC/oFQ antagonist). In contrast, in the juvenile, NMDA-induced vasodilation was only attenuated within 1 h post-FPI and returned to control within 8 h. Such dilation was also partially restored by the NOC/oFQ antagonist. These data indicate that NOC/oFQ contributes to impaired NMDA pial artery dilation after FPI. These data suggest that the greater NOC/oFQ release in the newborn versus the juvenile may contribute to age-related differences in FPI effects on excitatory amino acid-induced pial dilation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
279
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2188-95
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11045952-Aging, pubmed-meshheading:11045952-Animals, pubmed-meshheading:11045952-Animals, Newborn, pubmed-meshheading:11045952-Arterioles, pubmed-meshheading:11045952-Blood Pressure, pubmed-meshheading:11045952-Brain Injuries, pubmed-meshheading:11045952-Cerebrovascular Circulation, pubmed-meshheading:11045952-Disease Models, Animal, pubmed-meshheading:11045952-Excitatory Amino Acids, pubmed-meshheading:11045952-Female, pubmed-meshheading:11045952-Glutamic Acid, pubmed-meshheading:11045952-Male, pubmed-meshheading:11045952-N-Methylaspartate, pubmed-meshheading:11045952-Opioid Peptides, pubmed-meshheading:11045952-Peptide Fragments, pubmed-meshheading:11045952-Pia Mater, pubmed-meshheading:11045952-Receptors, Opioid, pubmed-meshheading:11045952-Swine, pubmed-meshheading:11045952-Vasoconstriction, pubmed-meshheading:11045952-Vasodilation, pubmed-meshheading:11045952-Wounds, Nonpenetrating
pubmed:year
2000
pubmed:articleTitle
NOC/oFQ contributes to age-dependent impairment of NMDA-induced cerebrovasodilation after brain injury.
pubmed:affiliation
Departments of Anesthesia and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. armsteaw@mail.med.upenn.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't