Linked Life Data

2403507

Source:http://linkedlifedata.com/resource/pubmed/id/2403507

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1990-2-1
pubmed:abstractText
The mechanisms responsible for renal insufficiency in septic shock (SS) have not been well characterized. We therefore investigated renal hemodynamics and the renal excretion of prostaglandin E2 (PGE2) in a nonhuman primate model of severe, low systemic vascular resistance (SVR) SS. In 18 cynomolgus monkeys, SS was induced by an infusion of 3 x 10(10) live Escherichia coli per kg; five saline-treated animals served as nonseptic controls. Systemic and renal hemodynamics, and urine PGE2 concentrations were determined over the 3 h after the induction of sepsis. The septic group demonstrated a significant (p less than .001) and sustained depression in both mean arterial pressure and SVR. Septic animals also had significantly lower effective renal plasma flow (ERPF) (p less than .01) and glomerular filtration rate (GFR) (p less than .01) compared to controls. Furthermore, the renal hemodynamic response to SS was biphasic, with significant increases in ERPF and GFR in the second hour postsepsis, followed by a pronounced decrease in the third postseptic hour. The septic group also demonstrated an increase in the renal excretion of PGE2 (p less than .001) that was temporally associated with the transient recovery in renal hemodynamics during the second postseptic hour. These sepsis-induced renal alterations may be important in the pathogenesis of renal insufficiency complicating clinical SS.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0090-3493
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
52-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Renal hemodynamics and prostaglandin E2 excretion in a nonhuman primate model of septic shock.
pubmed:affiliation
Critical Care Medicine Department, National Institutes of Health, Bethesda, MD.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.