Angiotensin mediated interaction of fetal kidney and placenta in the control of fetal arterial pressure and its role in hydrops fetalis
Identifieur interne : 00C402 ( Main/Merge ); précédent : 00C401; suivant : 00C403Angiotensin mediated interaction of fetal kidney and placenta in the control of fetal arterial pressure and its role in hydrops fetalis
Auteurs : J. J. Faber [États-Unis] ; D. F. Anderson [États-Unis]Source :
- Placenta : (Eastbourne) [ 0143-4004 ] ; 1997.
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Abstract
Fetal cardiovascular control is effected by an interaction of the fetal somatic and placental circulations. Three primary regulatory mechanisms are involved: transplacental transfer of extracellular fluid, driven by a difference in hydrostatic and oncotic pressures; modulation of fetal placental and somatic vascular resistances by means of blood pressure controlled production of angiotensin; and somatic autoregulation of flow. A systems analysis incorporates these and other fetal cardiovascular functions and this analysis was modelled for computer simulation. Given physiologically plausible values for known cardiovascular parameters in the fetal sheep, the model reproduced in detail a variety of experimental protocols with known outcomes; these included the normal fetus, the fetus after bilateral nephrectomy, the nephrectomized fetus infused with angiotensin, the intact fetus infused with NaCl solutions, the fetus with lymphatic obstruction and the severely anaemic fetus. The systems analysis demonstrated that fetal cardiac failure constituted the strongest stimulus for the formation of fetal oedema of any tested pathological intervention.
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Pascal:97-0330119Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Angiotensin mediated interaction of fetal kidney and placenta in the control of fetal arterial pressure and its role in hydrops fetalis</title><author><name sortKey="Faber, J J" sort="Faber, J J" uniqKey="Faber J" first="J. J." last="Faber">J. J. Faber</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Physiology and Pharmacology, School of Medicine, L334, Oregon Health Sciences University</s1><s2>Portland, OR 97201-3098</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Oregon</region></placeName></affiliation></author><author><name sortKey="Anderson, D F" sort="Anderson, D F" uniqKey="Anderson D" first="D. F." last="Anderson">D. F. Anderson</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Physiology and Pharmacology, School of Medicine, L334, Oregon Health Sciences University</s1><s2>Portland, OR 97201-3098</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Oregon</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">97-0330119</idno><date when="1997">1997</date><idno type="stanalyst">PASCAL 97-0330119 INIST</idno><idno type="RBID">Pascal:97-0330119</idno><idno type="wicri:Area/PascalFrancis/Corpus">000B45</idno><idno type="wicri:Area/PascalFrancis/Curation">000F63</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000B48</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000B48</idno><idno type="wicri:doubleKey">0143-4004:1997:Faber J:angiotensin:mediated:interaction</idno><idno type="wicri:Area/Main/Merge">00C402</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Angiotensin mediated interaction of fetal kidney and placenta in the control of fetal arterial pressure and its role in hydrops fetalis</title><author><name sortKey="Faber, J J" sort="Faber, J J" uniqKey="Faber J" first="J. J." last="Faber">J. J. Faber</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Physiology and Pharmacology, School of Medicine, L334, Oregon Health Sciences University</s1><s2>Portland, OR 97201-3098</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Oregon</region></placeName></affiliation></author><author><name sortKey="Anderson, D F" sort="Anderson, D F" uniqKey="Anderson D" first="D. F." last="Anderson">D. F. Anderson</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Physiology and Pharmacology, School of Medicine, L334, Oregon Health Sciences University</s1><s2>Portland, OR 97201-3098</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Oregon</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Placenta : (Eastbourne)</title><title level="j" type="abbreviated">Placenta : (Eastbourne)</title><idno type="ISSN">0143-4004</idno><imprint><date when="1997">1997</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Placenta : (Eastbourne)</title><title level="j" type="abbreviated">Placenta : (Eastbourne)</title><idno type="ISSN">0143-4004</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anemia</term><term>Angiotensin</term><term>Animal model</term><term>Cardiovascular control</term><term>Cardiovascular disease</term><term>Computer aided analysis</term><term>Fetal diseases</term><term>Fetus</term><term>Hemodynamics</term><term>Hydrops fetalis</term><term>Kidney</term><term>Lymphedema</term><term>Nephrectomy</term><term>Placenta</term><term>Sheep</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Foetus</term><term>Angiotensine</term><term>Contrôle cardiovasculaire</term><term>Rein</term><term>Placenta</term><term>Hémodynamique</term><term>Analyse assistée</term><term>Néphrectomie</term><term>Foetus pathologie</term><term>Lymphoedème</term><term>Anasarque foetoplacentaire</term><term>Anémie</term><term>Appareil circulatoire pathologie</term><term>Mouton</term><term>Modèle animal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fetal cardiovascular control is effected by an interaction of the fetal somatic and placental circulations. Three primary regulatory mechanisms are involved: transplacental transfer of extracellular fluid, driven by a difference in hydrostatic and oncotic pressures; modulation of fetal placental and somatic vascular resistances by means of blood pressure controlled production of angiotensin; and somatic autoregulation of flow. A systems analysis incorporates these and other fetal cardiovascular functions and this analysis was modelled for computer simulation. Given physiologically plausible values for known cardiovascular parameters in the fetal sheep, the model reproduced in detail a variety of experimental protocols with known outcomes; these included the normal fetus, the fetus after bilateral nephrectomy, the nephrectomized fetus infused with angiotensin, the intact fetus infused with NaCl solutions, the fetus with lymphatic obstruction and the severely anaemic fetus. The systems analysis demonstrated that fetal cardiac failure constituted the strongest stimulus for the formation of fetal oedema of any tested pathological intervention.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Oregon</li></region></list><tree><country name="États-Unis"><region name="Oregon"><name sortKey="Faber, J J" sort="Faber, J J" uniqKey="Faber J" first="J. J." last="Faber">J. J. Faber</name></region><name sortKey="Anderson, D F" sort="Anderson, D F" uniqKey="Anderson D" first="D. F." last="Anderson">D. F. Anderson</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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