Linked Life Data

3436382

Source:http://linkedlifedata.com/resource/pubmed/id/3436382

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-4-5
pubmed:abstractText
The effects of ablation of the anteroventral portion of the third cerebral ventricle (AV3V) on cardiac output and distribution of regional blood flows were determined in conscious rats using 15 micron radiolabelled microspheres before, and 2 min and 15 min after hemorrhage (n = 11 for each group). Prior to hemorrhage, cerebral blood flow was significantly greater (216 +/- 30 ml/min/100 g), and cerebral vascular resistance was lower (0.60 +/- 0.09 mm Hg/ml/min/100 g) in rats with AV3V lesions than in control-operated animals (132 +/- 16 ml/min/100 g; 0.92 +/- 0.1 mm Hg/ml/min/100 g, respectively), while mean arterial blood pressure, cardiac output, and regional blood flow to other organs were similar. Less blood was withdrawn from animals with AV3V lesions (4.4 +/- 0.6 ml) than from control-operated rats (6.0 +/- 0.5 ml) to reduce blood pressure to approximately 65 mm Hg. Hemorrhage decreased cerebral vascular resistance in control-operated animals (0.52 +/- 0.07 mm Hg/ml/min/100 g), but not in rats with AV3V lesions (0.48 +/- 0.1 mm Hg/ml/min/100 g). Cardiac output and regional blood flow to other organs were similar between rats with AV3V lesions and control-operated animals following hemorrhage. These data demonstrate that electrolytic ablation of the AV3V region results in a selective increase in cerebral blood flow and decreased cerebral vascular resistance, but does not alter the reflex changes in regional blood flow evoked by hemorrhage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
0014-4819
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
107-12
pubmed:dateRevised
2009-11-11
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Redistribution of cardiac output after hypothalamic lesions and hemorrhage.
pubmed:affiliation
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't