Aortic and ventricular dilation and myocardial reduction in gestation day 17 ICR mouse fetuses of diabetic mothers.
BACKGROUND
Maternal diabetes mellitus is associated with increased fetal teratogenesis, including cardiovascular defects. Information regarding cardiovascular changes in late-gestation fetal mice, related to maternal hyperglycemia, is not present in the literature.


METHODS
Late-gestation fetal heart and great vessel morphology were analyzed in fetuses from control and diabetic mice. Female ICR mice were injected with streptozocin (200 mg/kg IP) prior to mating to induce diabetes (n = 8). Nonhyperglycemic females were used as controls (n = 8). At day 17 of gestation, females were euthanized and one fetus was arbitrarily selected per litter to analyze the heart and great vessels. Six additional fetuses from different litters, showing external malformations (spina bifida and/or exencephaly), were also evaluated from the diabetic group. Fetal thoraxes were processed using routine histopathologic techniques, and 7-mum transversal sections were stained with hematoxylin-eosin. Digital images of sections were made and analyzed using NIH Image J software to compare regional cardiac development. Student's t tests for means were performed to determine differences between groups (p < .05).


RESULTS
Maternal hyperglycemia caused a dilation of late-gestation fetal ventricular chambers, a reduction of total ventricular myocardial area, and an increase in transversal ascending thoracic aortic area. Three of six fetuses that displayed external malformations showed an overt cardiac defect, beyond the ventricular and myocardial changes.


CONCLUSIONS
Maternal hyperglycemia altered morphology of the late-gestation fetal mouse heart. Postnatal persistence or consequences of late-gestation heart chamber dilation and myocardial reduction are not yet known.
Gutierrez
J Claudio
JC
Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute & State University, Blacksburg, Virginia, USA. jcgutier@vt.edu
Hrubec
Terry C
TC
Prater
M Renee
MR
Smith
Bonnie J
BJ
Freeman
Larry E
LE
Holladay
Steven D
SD
D000818:Animals; D001013:Aorta, Thoracic / Q000196:embryology / Q000473:pathology*; D002312:Cardiomyopathy, Hypertrophic / Q000209:etiology / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D003922:Diabetes Mellitus, Type 1 / Q000150:complications*; D004108:Dilatation, Pathologic; D005260:Female; D005865:Gestational Age; D006330:Heart Defects, Congenital / Q000209:etiology* / Q000473:pathology; D006340:Heart Rate, Fetal; D006352:Heart Ventricles / Q000196:embryology / Q000473:pathology*; D006943:Hyperglycemia / Q000150:complications; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D011247:Pregnancy; D011254:Pregnancy in Diabetics