Linked Life Data

8752174

Source:http://linkedlifedata.com/resource/pubmed/id/8752174

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
17
pubmed:dateCreated
1996-9-30
pubmed:abstractText
Nitric oxide (NO), a free radical gas implicated in a wide variety of biological reactions, is a novel signaling molecule that may regulate vasodilation, cerebral blood flow, and vascular permeability. This study was performed to determine whether NO mediates the selective increase in brain tumor microvessel permeability after intracarotid infusion of bradykinin in the RG2 rat glioma model. Intracarotid infusion of bradykinin selectively increased the transport of radiolabeled alpha-aminoisobutyric acid and dextran into brain tumors. Transport into normal brain was not increased. The administration of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester, significantly inhibited the increased transport into tumors for both tracers. The inhibitory effect of NG-nitro-L-arginine methyl ester on the response to bradykinin was reversed by L-arginine. The expression of two NO synthase (NOS) isoforms in cultured RG2 glioma cell lines and intracerebral RG2 glioma was examined by immunohistochemistry and Western blot analysis. High levels of expression of neuronal NOS were detected in cultured and intracerebral RG2 cells but not in normal brain tissue, except in rare neuronal cells. The endothelial form of NOS was also expressed in cultured RG2 cells, but not as strongly as neuronal NOS expression. In intracerebral RG2 gliomas, expression of endothelial NOS in the tumor was detected at higher levels than in normal brain. These findings indicate that RG2 rat gliomas express high levels of NOS, which regulate the production of NO, compared with normal brain. We suggest that the selective permeability increase in brain tumor microvessels after bradykinin infusion is mediated by NO. Furthermore, the absence of high levels of NOS in normal brain may account for the attenuated permeability response to bradykinin in normal brain microvessels.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0008-5472
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
56
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4027-31
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8752174-Aminoisobutyric Acids, pubmed-meshheading:8752174-Animals, pubmed-meshheading:8752174-Arginine, pubmed-meshheading:8752174-Blood-Brain Barrier, pubmed-meshheading:8752174-Blotting, Western, pubmed-meshheading:8752174-Bradykinin, pubmed-meshheading:8752174-Brain Neoplasms, pubmed-meshheading:8752174-Capillary Permeability, pubmed-meshheading:8752174-Carbon Radioisotopes, pubmed-meshheading:8752174-Dextrans, pubmed-meshheading:8752174-Enzyme Inhibitors, pubmed-meshheading:8752174-Female, pubmed-meshheading:8752174-Glioma, pubmed-meshheading:8752174-Immunohistochemistry, pubmed-meshheading:8752174-Infusions, Intra-Arterial, pubmed-meshheading:8752174-NG-Nitroarginine Methyl Ester, pubmed-meshheading:8752174-Nitric Oxide, pubmed-meshheading:8752174-Nitric Oxide Synthase, pubmed-meshheading:8752174-Rats, pubmed-meshheading:8752174-Rats, Wistar, pubmed-meshheading:8752174-Tumor Cells, Cultured
pubmed:year
1996
pubmed:articleTitle
Increased brain tumor microvessel permeability after intracarotid bradykinin infusion is mediated by nitric oxide.
pubmed:affiliation
Jonsson Comprehensive Cancer Center, Division of Neurosurgery, University of California, Los Angeles 90095-7039, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.