Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-5-10
pubmed:abstractText
The hypothesis that glutamate dilates pial arterioles of newborn pigs through the production of carbon monoxide (CO) was addressed. Anesthesized newborn pigs were equipped with cranial windows to measure pial arteriolar responses to stimuli. Heme oxygenase (HO) inhibitors added topically inhibited dilation to glutamate and to specific glutamate receptor agonists. The initial dilation to glutamate (10(-5) M) was 22% from baseline without an inhibitor and decreased to 9% with the HO inhibitor chromium mesoporphyrin (CrMP). Inhibition of dilation upon HO inhibition was similar when specific glutamate receptor agonists were employed. RS-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid caused 24% dilation from the baseline without an inhibitor, and the dilation was decreased to 1% with tin protoporphyrin (SnPP). (RS)-2-amino-3-(3-hydroxy-5-t-butylisoxazol-4-yl)propionic acid (kainate receptors) caused dilation of 18% from baseline without an inhibitor, but only 2% when tin mesoporphyrin was applied. 1-Aminocyclopropanecarboxylic acid (N-methyl-D-aspartate receptors) dilated pial arterioles 33% from baseline in control, but only to 2% in the presence of SnPP. Neither copper mesoporphyrin, which does not inhibit HO, nor light-inactivated CrMP affected the dilations. Furthermore, cerebral microvessels removed from the brain produced CO (stable isotope dilution gas chromatography-mass spectrometry), and this production was dose dependently increased by glutamate and inhibited by metal porphyrin HO inhibitors. These data suggest that dilation of newborn pig pial arterioles to glutamate and specific glutamate receptor agonists involves vascular production of CO. Additional cerebral sources of CO also could be stimulated by glutamate and contribute to the dilation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Monoxide, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase (Decyclizing), http://linkedlifedata.com/resource/pubmed/chemical/Isoxazoles, http://linkedlifedata.com/resource/pubmed/chemical/Mesoporphyrins, http://linkedlifedata.com/resource/pubmed/chemical/Metalloporphyrins, http://linkedlifedata.com/resource/pubmed/chemical/Propionates, http://linkedlifedata.com/resource/pubmed/chemical/Protoporphyrins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, AMPA, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glutamate, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Kainic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, N-Methyl-D-Aspartate, http://linkedlifedata.com/resource/pubmed/chemical/alpha-Amino-3-hydroxy-5-methyl-4-iso..., http://linkedlifedata.com/resource/pubmed/chemical/alpha-amino-3-hydroxy-5-tert-butyl-4..., http://linkedlifedata.com/resource/pubmed/chemical/chromium mesoporphyrin, http://linkedlifedata.com/resource/pubmed/chemical/tin protoporphyrin IX
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
282
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2371-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12003848-Animals, pubmed-meshheading:12003848-Animals, Newborn, pubmed-meshheading:12003848-Arterioles, pubmed-meshheading:12003848-Carbon Monoxide, pubmed-meshheading:12003848-Enzyme Inhibitors, pubmed-meshheading:12003848-Excitatory Amino Acid Agonists, pubmed-meshheading:12003848-Glutamic Acid, pubmed-meshheading:12003848-Heme Oxygenase (Decyclizing), pubmed-meshheading:12003848-Isoxazoles, pubmed-meshheading:12003848-Mesoporphyrins, pubmed-meshheading:12003848-Metalloporphyrins, pubmed-meshheading:12003848-Propionates, pubmed-meshheading:12003848-Protoporphyrins, pubmed-meshheading:12003848-Receptors, AMPA, pubmed-meshheading:12003848-Receptors, Glutamate, pubmed-meshheading:12003848-Receptors, Kainic Acid, pubmed-meshheading:12003848-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:12003848-Swine, pubmed-meshheading:12003848-Vasodilation, pubmed-meshheading:12003848-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
pubmed:year
2002
pubmed:articleTitle
Role of carbon monoxide in glutamate receptor-induced dilation of newborn pig pial arterioles.
pubmed:affiliation
Laboratory for Research in Neonatal Physiology, Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee 38163, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't