Linked Life Data

16150837

Source:http://linkedlifedata.com/resource/pubmed/id/16150837

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-14
pubmed:abstractText
Myocardial endotoxin tolerance may be induced in both males and females; however, it remains unknown whether there are mechanistic and threshold differences between the sexes. We hypothesized that endogenous estrogen mediates a higher threshold for endotoxin (ETX)-induced protection in females. Adult proestrus and ovariectomized (OVX) female rats were preconditioned (PC) with intraperitoneal injections of 125 (PC+125) or 500 (PC+500) microg/kg Salmonella typhimurium LPS (ETX) or normal saline (PC-). Twenty-four hours later, injury dose ETX (500 microg/kg) was injected. After 6 h, myocardial function was measured via Langendorff. p38 MAPK and JNK activation and TNF-alpha, IL-1, and IL-6 expression were evaluated. ETX injury significantly decreased left ventricular developed pressure in PC- groups vs. controls. PC+500 regimen protected against ETX injury, resulting in normal cardiac function. PC+125 regimen protected OVX but not proestrus females, which had diminished myocardial function. Activated JNK and TNF-alpha increased in PC- but were diminished in PC+500 animals. Importantly, activated JNK and TNF increased in PC+125 proestrus females, whereas PC+125 OVX females displayed decreases in these molecules. There were no differences in p38 MAPK activation or expression of IL-1 or IL-6. These results demonstrate that proestrus females require a higher stimulus (PC+500) to achieve myocardial protection against ETX injury. Removal of endogenous estrogen (OVX) lowered the preconditioning threshold (PC+125), resulting in protection after lesser injury. Additionally, myocardial JNK and TNF expression was decreased in OVX PC+125 females, which correlated with myocardial function differences. Therefore, we conclude that endogenous estrogen mediates a higher threshold for ETX tolerance in female myocardium.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
290
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R27-33
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16150837-Animals, pubmed-meshheading:16150837-Cardiotonic Agents, pubmed-meshheading:16150837-Enzyme Activation, pubmed-meshheading:16150837-Estrogens, pubmed-meshheading:16150837-Female, pubmed-meshheading:16150837-Heart, pubmed-meshheading:16150837-Interleukin-1, pubmed-meshheading:16150837-Interleukin-6, pubmed-meshheading:16150837-Lipopolysaccharides, pubmed-meshheading:16150837-MAP Kinase Kinase 4, pubmed-meshheading:16150837-Myocardium, pubmed-meshheading:16150837-Ovariectomy, pubmed-meshheading:16150837-Rats, pubmed-meshheading:16150837-Rats, Sprague-Dawley, pubmed-meshheading:16150837-Salmonella typhimurium, pubmed-meshheading:16150837-Tumor Necrosis Factor-alpha, pubmed-meshheading:16150837-Ventricular Function, Left, pubmed-meshheading:16150837-p38 Mitogen-Activated Protein Kinases
pubmed:year
2006
pubmed:articleTitle
Endogenous estrogen mediates a higher threshold for endotoxin-induced myocardial protection in females.
pubmed:affiliation
545 Barnhill Dr., Emerson 215, Indiana University Medical Center, Indianapolis, IN 46202, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural