Table 1.

Hyperglycemia-Induced Yolk Sac Vasculopathy Is Developmental Stage-Dependent

Developmental stages at 7.5 days p.c.	Yolk sac vasculopathy
(20 mmol/L d-glucose) Primitive streak stages 50%	25 /25 (100%)
(20 mmol/L d-glucose) Neural plate stages 38%	22 /22 (100%)
(20 mmol/L d-glucose) Headfold stages 12%	03 /32 (9%)
(15 mmol/L l-glucose) (5 mmol/L d-glucose) Primitive streak stages Neural plate stages	06 /86 (7%)
(15 mmol/L d-Mannitol)(5 mmol/L d-glucose) Primitive streak stages Neural plate stages	02 /35 (6%)
Normoglycemic (5 mmol/L d-glucose) Control cultures	04 /189 (2%)

The incidence of yolk sac vasculopathy (arrest of the vasculature at the primary capillary plexus stage) was determined in stage-sorted day 7.5 p.c. conceptuses harvested from several mothers. As illustrated, conceptuses at the primitive streak and neural plate stages exhibited 100% yolk sac vasculopathy, whereas only 9% of conceptuses at headfold stages exhibited any yolk sac vasculopathy when cultured in hyperglycemic conditions (20 mmol/L d-glucose). Conceptuses cultured in rat sera supplemented with either 15 mmol/L αl-glucose or 15 mmol/L d-mannitol exhibited incidences of 7% and 6% vasculopathy, respectively. Day 7.5 p.c. conceptuses cultured in normoglycemic conditions (5 mmol/L d-glucose) exhibited a 2% incidence of vasculopathy.