Linked Life Data

9364193

Source:http://linkedlifedata.com/resource/pubmed/id/9364193

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
1997-12-9
pubmed:abstractText
In a model of volume-controlled hemorrhagic shock in rats, invariably leading to death within 30 min of bleeding termination, the intravenous (i.v.) bolus injection of ACTH-(1-24) at the dose of 0.16 mg/kg restored cardiovascular and respiratory functions and greatly prolonged survival. I.v. or intracerebroventricular (i.c.v.) treatment with NG-nitro-L-arginine methylester (L-NAME), a non-isoform-selective inhibitor of nitric oxide synthases (NOSs), at the doses of 2.5-10 mg/kg i.v. or 0.015-0.135 mg/kg i.c.v., as well as i.v. treatment with S-methylisothiourea (SMT), a selective inhibitor of the inducible isoform of NOS, at the doses of 0.001-3 mg/kg, dose-dependently improved cardiovascular and respiratory functions and potentiated the effect of a subthreshold dose (0.02 mg/kg) of ACTH-(1-24). On the other hand, either intraperitoneal or i.c.v. pretreatment with L-arginine, the substrate of NOSs, prevented the effect of ACTH-(1-24). These data suggest that inhibition of NO overproduction is involved in the mechanism of action of ACTH-(1-24) in shock reversal.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
61
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1889-97
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Inhibition of nitric oxide synthases enhances the effect of ACTH in hemorrhagic shock.
pubmed:affiliation
Department of Biomedical Sciences, University of Modena, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't