PMID- 3738814
OWN - NLM
STAT- MEDLINE
DCOM- 19860916
LR  - 20131121
IS  - 0040-3709 (Print)
IS  - 0040-3709 (Linking)
VI  - 33
IP  - 1
DP  - 1986 Feb
TI  - Abnormal heart and great vessel development following acute ethanol exposure in 
      mice.
PG  - 93-104
AB  - Two maternal intraperitoneal doses of ethanol (2.9 g/kg) administered on 
      gestational day (GD) 8, 12 hours (8 d, 12 h) and 8 d, 16 h result in abnormal 
      heart and great vessel development in C57B1/6J mice. Heparinized hearts from GD 9 
      to 18 conceptuses were dissected to expose the forming or already completed 
      ventricular septum and great vessels and then routinely processed for scanning 
      electron microscopy. As early as GD 9 (12 hours post-treatment), size deficiency 
      and abnormal external contour of the cardiac tube were notable. By GD 12, 
      deficiencies in the size of the conal and atrioventricular (A-V) endocardial 
      cushions, as well as abnormal positioning of the A-V canal, were demonstrable. On 
      GD 13, when the ventricular septum should be complete, a range of deficiencies in 
      the conal tissue was observed. Deficiencies observed were a lack of closure of 
      the ventricular septum in the region of the membranous septum, and lack of 
      septation of the conal portion of the developing heart. These deficiencies 
      persist and have been documented through GD 18. Other abnormalities noted on GD 
      18 include double-outlet right ventricle, as well as distal defects of the great 
      vessels including interrupted aortic arch, right aortic arch, and a vascular 
      ring. While these defects are comparable to those seen in the fetal alcohol 
      syndrome, they also overlap considerably with cardiac defects that are 
      characteristic of those in the DiGeorge Syndrome as well as in the CHARGE 
      Association. Recent work by others as well as the fact that acute ethanol 
      exposure in this animal model corresponds to a time of neural crest cell 
      migration has led to the speculation that this cell population is involved in the 
      cardiovascular pathogenesis described.
FAU - Daft, P A
AU  - Daft PA
FAU - Johnston, M C
AU  - Johnston MC
FAU - Sulik, K K
AU  - Sulik KK
LA  - eng
GR  - DE-02668/DE/NIDCR NIH HHS/United States
GR  - DE-05248/DE/NIDCR NIH HHS/United States
GR  - RR-05333/RR/NCRR NIH HHS/United States
GR  - etc.
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Teratology
JT  - Teratology
JID - 0153257
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Abnormalities, Drug-Induced/*pathology
MH  - Abnormalities, Multiple/chemically induced/pathology
MH  - Animals
MH  - *Cardiovascular Abnormalities
MH  - Cardiovascular System/drug effects/ultrastructure
MH  - Embryo Loss/chemically induced
MH  - Embryonic and Fetal Development/drug effects
MH  - Ethanol/*toxicity
MH  - Female
MH  - Gestational Age
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Microscopy, Electron, Scanning
MH  - Pregnancy
EDAT- 1986/02/01 00:00
MHDA- 1986/02/01 00:01
CRDT- 1986/02/01 00:00
PHST- 1986/02/01 00:00 [pubmed]
PHST- 1986/02/01 00:01 [medline]
PHST- 1986/02/01 00:00 [entrez]
AID - 10.1002/tera.1420330112 [doi]
PST - ppublish
SO  - Teratology. 1986 Feb;33(1):93-104. doi: 10.1002/tera.1420330112.