PMID- 23636813
OWN - NLM
STAT- MEDLINE
DCOM- 20131021
LR  - 20211021
IS  - 1529-7268 (Electronic)
IS  - 0006-3363 (Print)
IS  - 0006-3363 (Linking)
VI  - 88
IP  - 6
DP  - 2013 Jun
TI  - Analysis of maternal and fetal cardiovascular systems during hyperglycemic 
      pregnancy in the nonobese diabetic mouse.
PG  - 151
LID - 10.1095/biolreprod.112.105759 [doi]
AB  - Preconception or gestationally induced diabetes increases morbidities and 
      elevates long-term cardiovascular disease risks in women and their children. 
      Spontaneously hyperglycemic (d)-NOD/ShiLtJ female mice, a type 1 diabetes model, 
      develop bradycardia and hypotension after midpregnancy compared with 
      normoglycemic, age- and gestational day (GD)-matched control (c-NOD) females. We 
      hypothesized that onset of the placental circulation at GD 9-10 and rapid fetal 
      growth from GD 14 correlate with aberrant hemodynamic outcomes in d-NOD females. 
      To develop further gestational time-course correlations between maternal cardiac 
      and renal parameters, high-frequency ultrasonography was applied to d- and c-NOD 
      mice (virgin and at GD 8-16). Cardiac output and left ventricular (LV) mass 
      increased in c-NOD but not in d-NOD mice. Ultrasound and postmortem 
      histopathology showed overall greater LV dilation in d-NOD than in c-NOD mice at 
      mid to late gestation. These changes suggest blunted remodeling and altered 
      functional adaptation of d-NOD hearts. Umbilical cord ultrasounds revealed lower 
      fetal heart rates from GD 12 and lower umbilical flow velocities at GD 14 and GD 
      16 in d-NOD versus c-NOD pregnancies. From GD 14 to GD 16, d-NOD fetal losses 
      exceeded c-NOD fetal losses. Similar aberrant responses in pregnancies of women 
      with diabetes may elevate postpartum maternal and child cardiovascular risk, 
      particularly if mothers lack adequate prenatal care or have poor glycemic control 
      during gestation.
FAU - Aasa, Kristiina L
AU  - Aasa KL
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston, 
      Ontario, Canada.
FAU - Kwong, Kenneth K
AU  - Kwong KK
FAU - Adams, Michael A
AU  - Adams MA
FAU - Croy, B Anne
AU  - Croy BA
LA  - eng
GR  - 77519-2/CAPMC/CIHR/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130620
PL  - United States
TA  - Biol Reprod
JT  - Biology of reproduction
JID - 0207224
SB  - IM
MH  - Animals
MH  - Blood Pressure/physiology
MH  - Cardiac Output/*physiology
MH  - Diabetes Mellitus, Type 1/*physiopathology
MH  - Diabetes, Gestational/*physiopathology
MH  - Echocardiography
MH  - Female
MH  - Fetal Blood/physiology
MH  - Fetal Development/physiology
MH  - Heart/*physiopathology
MH  - Kidney/physiopathology
MH  - Mice
MH  - Mice, Inbred NOD
MH  - Pregnancy
MH  - Risk Factors
MH  - Ventricular Remodeling/*physiology
PMC - PMC3699463
MID - CAMS2944
OID - NLM: CAMS2944
OTO - NOTNLM
OT  - NOD mouse
OT  - cardiac adaptations
OT  - cardiovascular
OT  - cardiovascular system
OT  - developmental origins of health and disease
OT  - diabetes
OT  - pregnancy
EDAT- 2013/05/03 06:00
MHDA- 2013/10/22 06:00
PMCR- 2013/07/02
CRDT- 2013/05/03 06:00
PHST- 2013/05/03 06:00 [entrez]
PHST- 2013/05/03 06:00 [pubmed]
PHST- 2013/10/22 06:00 [medline]
PHST- 2013/07/02 00:00 [pmc-release]
AID - biolreprod.112.105759 [pii]
AID - 10.1095/biolreprod.112.105759 [doi]
PST - epublish
SO  - Biol Reprod. 2013 Jun 20;88(6):151. doi: 10.1095/biolreprod.112.105759. Print 
      2013 Jun.