Linked Life Data

15782912

Source:http://linkedlifedata.com/resource/pubmed/id/15782912

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-3-23
pubmed:abstractText
Previous studies demonstrated that bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary vasoconstriction leading to pulmonary hypertension (PHS, ascites) in broilers. The lungs of broilers are constantly challenged with LPS that can trigger pulmonary vasoconstriction. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure (PAP), whereas others fail to exhibit any response to the same supramaximal dose of LPS. In the present study we evaluated the impact of a variety of factors on the magnitude of the PAP response of male broilers to LPS, including: (1) the role of the initial PAP (low vs. high initial PAP); (2) the source of the LPS (Salmonella typhimurium vs. Escherichia coli); (3) the dose of LPS (0.02, 0.1, and 0.5 mg/kg of BW); and (4) the role of micro-particle selection for improved pulmonary vascular capacity (cellulose survivors vs. saline-injected controls). Broilers in the low initial PAP group (21 +/- 0.34 mmHg, mean +/- SEM) did not differ in their pulmonary hypertensive response to LPS compared with broilers in the high initial PAP group (29 +/- 0.55 mmHg, mean +/- SEM). Lipopolysaccharide from S. typhimurium elicited pulmonary hypertensive responses qualitatively similar to those elicited by E. coli LPS. A detailed evaluation revealed that an LPS dose of 0.1 mg/kg of BW elicits a maximal pulmonary hypertensive response in male broilers, and broilers selected by micro-particle injection for a robust pulmonary vascular capacity did not differ in their pulmonary hypertensive response to LPS compared with unselected broilers. This research confirms that the variable pulmonary hypertensive responses among broilers cannot be attributed to the source or dosage of LPS, or to differences in the baseline pulmonary arterial pressure or micro-particle selection before injecting LPS. These findings are consistent with the hypothesis that innate rather than acquired variability may influence the profile of chemical mediators released during the inflammatory cascade.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0032-5791
pubmed:author
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
432-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Pulmonary hypertensive responses of broilers to bacterial lipopolysaccharide (LPS): evaluation of LPS source and dose, and impact of pre-existing pulmonary hypertension and cellulose micro-particle selection.
pubmed:affiliation
Department of Poultry Science, University of Arkansas, Fayetteville, Arkansas 72701, USA. mchapman@uark.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't