Linked Life Data

2148435

Source:http://linkedlifedata.com/resource/pubmed/id/2148435

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23 Suppl
pubmed:dateCreated
1991-2-14
pubmed:abstractText
The failing heart is unable to provide some organs, notably the brain and the myocardium, with the amount of blood flow they require. To this myocardial inadequacy and resulting "circulatory insufficient" the body reacts by setting in action compensatory mechanisms which are "intracardiac" first (Starling's heterometric regulation, ventricular hypertrophy), then neurohormonal, with the activation of vasoconstrictor systems (noradrenergic system, renin-angiotensin-aldosterone system, arginine-vasopressin system) counterbalanced by the activation of vasodilator systems (vasodilator prostaglandins, atrial natriuretic factor and kinins). However, the vasoconstrictor systems outweigh the vasodilator systems. They create an excessive arterial and venous vasoconstriction, together with water-and-salt retention, which leads to an increase of left ventricular work during both systole and diastole and to a gradual worsening of the heart failure. The present-day treatment of heart failure aims at reducing the water-and-salt retention and at restoring the balance between the vasoconstrictor and vasodilator systems.
pubmed:language
fre
pubmed:journal
pubmed:citationSubset
F
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0035-2640
pubmed:author
pubmed:issnType
Print
pubmed:day
11
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7-12
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
[General physiopathology of chronic left ventricular insufficiency].
pubmed:affiliation
Service de cardiologie, hôpital Saint-Jacques, Clermont-Ferrand.
pubmed:publicationType
Journal Article, English Abstract