Erythrocytosis Ends Pregnancy

Abortion in Mice with Excessive Erythrocytosis Is Due to Impaired
Arteriogenesis of the Uterine Arcade.
Biol Reprod 2008 Feb 6.
Gassmann M, Manini A, Stallmach T, Saam B, Kuhn G, Grenacher B,
Bogdanova AY, Vogel J

We postulate that repeated pregnancy loss, intrauterine growth
restriction and preeclampsia are caused by impaired elevation of
uterine blood flow due to disturbed arteriogenesis of the uterine
arcade. This hypothesis is based on the observation that pregnant
human erythropoietin overexpressing (plasma levels elevated 12-fold)
mice (termed tg6) suffering from excessive erythrocytosis generally
abort at mid-gestation unless their hematocrit of 0.85 is drastically
lowered. Transgenic mice show placental malformations that parallel
those observed in pregnant women suffering from impaired uterine
perfusion. Shear stress, a key factor inducing arteriogenesis, was 5-
fold lower in tg6 mice compared to wild type (wt) littermates.
Consequently, uterine artery growth was reduced and dramatically less
viable pups (1.63 +/- 2.20 vs. 8.10 +/- 0.74 in wt) of lower weight
(1.29 +/- 0.07g vs. 1.62 +/- 0.12g in wt) were delivered in first
pregnancies. Only in subsequent pregnancies did tg6 deliver
approximately the expected number of pups. Birth weights of tg6
offspring however, remained reduced. As the spleen is a major site of
extramedullary erythropoiesis in tg6 animals, splenectomy reduced the
hematocrit to 0.6-0.7. In turn, shear stress increased to normal
values and splenectomized primiparous tg6 showed normal uterine artery
growth and delivery of pups similar in number and weight compared to
wt. We conclude that poor arteriogenesis is a previously unappreciated
cause for clinically important pregnancy complications.
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Biology of reproduction [Biol Reprod]

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