Endothelial function in normal and pre-eclamptic pregnancy: a hypothesis.
Eur J Obstet Gynecol Reprod Biol
; 43(2): 113-22, 1992 Jan 31.
Article
en En
| MEDLINE
| ID: mdl-1563558
ABSTRACT
Pre-eclampsia is the most common medical complication of pregnancy. Immunologic maladaptation has been suggested to play a role in the etiology of pre-eclampsia. The putative misalliance of fetal trophoblast with maternal tissue in the uteroplacental vascular bed may give rise to an increase in oxygen free radicals. Oxygen free radicals and lipid peroxides might form the link between the hypothetical immunologic maladaptation and the endothelial cell damage known to occur in pre-eclampsia. Recent studies have demonstrated the existence of increased oxygen free radical production in pre-eclampsia. Oxygen free radicals and lipid peroxides decrease vascular prostacyclin and EDRF release and increase thromboxane A2 and endothelin release. The hypothesis is put forward that in pre-eclampsia a proposed immunologic maladaptation causes an increase in oxygen free radicals by decidual lymphoid cells. A decrease in vasodilatory autocoids, prostacyclin and EDRF may result from the endothelial cell damage induced by oxygen free radicals. Uteroplacental prostacyclin production might be essential as escape mechanism. The adequacy as escape mechanism seems to determine the final clinical outcome.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Preeclampsia
/
Embarazo
/
Endotelio
Límite:
Female
/
Humans
Idioma:
En
Revista:
Eur J Obstet Gynecol Reprod Biol
Año:
1992
Tipo del documento:
Article
País de afiliación:
Países Bajos