[Animal experiment models of hypertension in pregnancy--an alternative to clinical studies?].
Because of ethical constraints upon research during human pregnancy and of the heterogeneity of preeclampsia a number of experimental animal models were used to study pathophysiology of preeclampsia. We reduced the uteroplacental flow by aortic clip technique in 72 SHR-rats in 4 groups (G 1 not gravid--no clip, G 2 not gravid--aortic clip, G 3 gravid--no clip, G 4 gravid--aortic clip). While gravidity normalised blood pressure in SHR (G 3), reduction of the uteroplacental flow significantly increased maternal blood pressure (G1 240/180 mmHG, G2 238/183 mmHg, G3 148/99 mmHG, G4 200/145 mmHg) and leads to significant higher hematocrit, significant lower plasma renin activity and aldosterone plasma concentration, as it is found in human superimposed preeclampsia. SDS-page electrophoresis proved a significant increase of urinary high density proteins.


CONCLUSIONS
In comparison to chronical inhibition of NO-synthesis or chronical application of ultra-low-doses-endotoxin, reduction of uterine flow by aortic compression is a reliable animal model and leads in SHR to a superimposed preeclampsia-like syndrome with many similarities to human clinical findings. Animal models for preeclampsia are no alternative to clinical studies, but they are furthering our understanding of pathophysiology in many fields.
Seufert
R
R
Universitätsfrauenklinik Mainz. Seufert@mail.uni-mainz.de
Hropot
M
M
Casper
F
F
Leiser
R
R
D000450:Aldosterone / Q000097:blood; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D006400:Hematocrit; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D007231:Infant, Newborn; D010920:Placenta / Q000098:blood supply; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D051381:Rats; D011918:Rats, Inbred SHR; D012039:Regional Blood Flow / Q000502:physiology; D012083:Renin / Q000097:blood; D014599:Uterus / Q000098:blood supply
D000450:Aldosterone; D012083:Renin