Linked Life Data

19109376

Source:http://linkedlifedata.com/resource/pubmed/id/19109376

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2009-2-27
pubmed:abstractText
We studied the impact of endotoxemia on cerebral blood flow (CBF), cerebral vascular resistance (CVR), and cerebral oxygen transport (O(2) transport) in fetal sheep. We hypothesized that endotoxemia impairs CBF regulation and O(2) transport, exposing the brain to hypoxic-ischemic injury. Responses to lipopolysaccharide (LPS; 1 microg/kg iv on 3 consecutive days, n = 9) or normal saline (n = 5) were studied. Of LPS-treated fetuses, five survived and four died; in surviving fetuses, transient cerebral vasoconstriction at 0.5 h (DeltaCVR approximately +50%) was followed by vasodilatation maximal at 5-6 h (DeltaCVR approximately -50%) when CBF had increased (approximately +60%) despite reduced ABP (approximately -20%). Decreased CVR and increased CBF persisted 24 h post-LPS and the two subsequent LPS infusions. Cerebral O(2) transport was sustained, although arterial O(2) saturation was reduced (P < 0.05). Histological evidence of neuronal injury was found in all surviving LPS-treated fetuses; one experienced grade IV intracranial hemorrhage. Bradykinin-induced cerebral vasodilatation (DeltaCVR approximately -20%, P < 0.05) was abolished after LPS. Fetuses that died post-LPS (n = 4) differed from survivors in three respects: CVR did not fall, CBF did not rise, and O(2) transport fell progressively. In conclusion, endotoxin disrupts the cerebral circulation in two phases: 1) acute vasoconstriction (1 h) and 2) prolonged vasodilatation despite impaired endothelial dilatation (24 h). In surviving fetuses, LPS causes brain injury despite cerebral O(2) transport being maintained by elevated cerebral perfusion; thus sustained O(2) transport does not prevent brain injury in endotoxemia. In contrast, cerebral hypoperfusion and reduced O(2) transport occur in fetuses destined to die, emphasizing the importance of sustaining O(2) transport for survival.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0363-6119
pubmed:author
pubmed:issnType
Print
pubmed:volume
296
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R640-50
pubmed:meshHeading
pubmed-meshheading:19109376-Animals, pubmed-meshheading:19109376-Blood Pressure, pubmed-meshheading:19109376-Cerebrospinal Fluid, pubmed-meshheading:19109376-Cerebrovascular Circulation, pubmed-meshheading:19109376-Cytokines, pubmed-meshheading:19109376-Data Interpretation, Statistical, pubmed-meshheading:19109376-Endothelial Cells, pubmed-meshheading:19109376-Endotoxins, pubmed-meshheading:19109376-Female, pubmed-meshheading:19109376-Fetal Death, pubmed-meshheading:19109376-Fetus, pubmed-meshheading:19109376-Lipopolysaccharides, pubmed-meshheading:19109376-Nitrates, pubmed-meshheading:19109376-Nitrites, pubmed-meshheading:19109376-Oxygen Consumption, pubmed-meshheading:19109376-Pregnancy, pubmed-meshheading:19109376-Sheep, pubmed-meshheading:19109376-Tumor Necrosis Factor-alpha, pubmed-meshheading:19109376-Vasodilation
pubmed:year
2009
pubmed:articleTitle
Endotoxin has acute and chronic effects on the cerebral circulation of fetal sheep.
pubmed:affiliation
Ritchie Centre for Baby Health Research, Monash Institute of Medical Research, Monash Medical Centre, Clayton, Melbourne, Victoria, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't