Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1992-3-30
pubmed:abstractText
The aim of this study was to determine whether an elevation of pulmonary venous pressure (PVP) and atrial natriuretic peptide (ANP) affects pulmonary vascular resistance (PVR) and pulmonary vascular incremental resistance (iPVR). We vascularly isolated the left lower lobe of the lung and perfused it with blood using a pulsatile pump. Blood flow (PBF) to the isolated lobe was decreased in 6 to 7 steps from about 8 to 1 ml/(kg.min). PVR was calculated from measurements of PBF and the pressure difference between pulmonary arterial pressure and PVP at four different levels of fixed PVP. iPVR was estimated from a slope of the pressure-flow relationships between effective pulmonary driving pressure and PBF at four different levels of fixed PVP. iPVR was 2.2 +/- 0.2, 2.2 +/- 0.1, 2.4 +/- 0.1, and 2.6 +/- 0.2 mmHg.min.kg/ml, when PVP was 0, 5, 10, and 15 mmHg, respectively. To test whether or not the response of the pulmonary vascular bed to the elevated PVP is modulated by ANP, iPVR was estimated before and after an administration of ANP in the perfusion circuit. Increased iPVR from 2.1 +/- 0.2 to 2.5 +/- 0.2 mmHg.min.kg/ml in response to the elevation of PVP from 0 to 15 mmHg decreased to the control level after the administration of ANP. ANP, however, did not change the control iPVR. PVR decreased with increasing PVP. ANP decreased PVR when PVP was 0 mmHg, but did not change it when PVP was 15 mmHg. These results suggest that ANP decreases PVR and restores the decreased pulmonary vascular compliance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0021-521X
pubmed:author
pubmed:issnType
Print
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
605-16
pubmed:dateRevised
2007-3-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Atrial natriuretic peptide attenuates an increase in pulmonary vascular incremental resistance due to high pulmonary venous pressure.
pubmed:affiliation
Department of Physiology, Kagawa Medical School, Japan.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't