Linked Life Data

7408378

Source:http://linkedlifedata.com/resource/pubmed/id/7408378

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1980-11-24
pubmed:abstractText
The clinical syndrome known as persistent fetal circulation, or persistent pulmonary hypertension of the newborn, is characterized by maintenance of a high pulmonary vascular resistance after birth. The small pulmonary arteries of the fetus have a thick muscular medial layer; they are very reactive, being actively constricted by the low PO2 levels normally present during fetal life. The pulmonary vascular smooth muscle layer is hypertrophied in conditions that result in chronic fetal hypoxia, or a maintained increase in pulmonary arterial pressure. Normally, pulmonary vasodilation occurs rapidly after birth, partly related to physical expansion with gas, but mainly due to the increased PO2 associated with ventilation with air. Based on these developmental considerations, the factors responsible for an increased pulmonary vascular resistance after birth may be classified in three main groups: (A) Acute vasoconstriction due to postnatal hypoxia and aggravated by acidemia; (B) Prenatal increase in pulmonary vascular smooth muscle development; and (C) Decreased cross sectional area of the pulmonary vascular bed due to inadequate numbers of vessels. The various mechanisms that may promote these responses are presented.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0009-9228
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
585-90
pubmed:dateRevised
2005-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
High pulmonary vascular resistance after birth: I. Pathophysiologic considerations and etiologic classification.
pubmed:publicationType
Journal Article