Linked Life Data

2338820

Source:http://linkedlifedata.com/resource/pubmed/id/2338820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1990-6-21
pubmed:abstractText
We studied the mesenteric and systemic vascular response to angiotensin II in normotensive and portal hypertensive (PHT) rabbits, because of the documented poor tolerance of hemorrhagic shock in PHT. Normally, the hemodynamic response to angiotensin II (AII) is characterized by selective and disproportionate splanchnic vasoconstriction. We postulated that the response to AII could be diminished in PHT. Chronic PHT was induced by partial portal vein ligation 3 weeks prior to graded angiotensin II infusion. Baseline hemodynamic measurements showed markedly elevated portal pressure (PPV) and superior mesenteric artery blood flow (QSMA) compared with those of normotensive animals (P less than 0.01). Superior mesenteric artery resistance (RSMA) was markedly reduced in PHT compared to that in controls (P less than 0.05). Angiotensin II infusion in normals resulted in a marked selective rise in RSMA compared with the rise in systemic resistance (RSYS) (P less than 0.01). AII infusion in PHT resulted in a rise in RSMA and RSYS, but the disproportionate in RSMA was attenuated. Furthermore, in both normal and PHT, AII caused a significant rise in PPV (P less than 0.01). We conclude that the findings indicate that the splanchnic vasoconstrictive response to AII is substantially impaired in PHT, and that AII will paradoxically cause a rise in PPV, possibly aggravating the tendency to hemorrhage in PHT.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-4804
pubmed:author
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
341-4
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Decreased mesenteric vascular response to angiotensin II in portal hypertension.
pubmed:affiliation
Johns Hopkins University, Department of Surgery, Baltimore, Maryland 21205.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.