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This Article Full Text Full Text (PDF) All Versions of this Article: 294/5/H2248    most recent 91469.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Momoi, N. Articles by Tobita, K. Search for Related Content PubMed PubMed Citation Articles by Momoi, N. Articles by Tobita, K.

Modest maternal caffeine exposure affects developing embryonic cardiovascular function and growth

Cardiovascular Development Research Program, Children's Hospital of Pittsburgh of University of Pittsburgh Medical Center, Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania

Submitted 14 December 2007 ; accepted in final form 13 March 2008

Caffeine consumption during pregnancy is reported to increase the risk of in utero growth restriction and spontaneous abortion. In the present study, we tested the hypothesis that modest maternal caffeine exposure affects in utero developing embryonic cardiovascular (CV) function and growth without altering maternal hemodynamics. Caffeine (10 mg·kg^–1·day^–1 subcutaneous) was administered daily to pregnant CD-1 mice from embryonic days (EDs) 9.5 to 18.5 of a 21-day gestation. We assessed maternal and embryonic CV function at baseline and at peak maternal serum caffeine concentration using high-resolution echocardiography on EDs 9.5, 11.5, 13.5, and 18.5. Maternal caffeine exposure did not influence maternal body weight gain, maternal CV function, or embryo resorption. However, crown-rump length and body weight were reduced in maternal caffeine treated embryos by ED 18.5 (P < 0.05). At peak maternal serum caffeine concentration, embryonic carotid artery, dorsal aorta, and umbilical artery flows transiently decreased from baseline at ED 11.5 (P < 0.05). By ED 13.5, embryonic aortic and umbilical artery flows were insensitive to the peak maternal caffeine concentration; however, the carotid artery flow remained affected. By ED 18.5, baseline embryonic carotid artery flow increased and descending aortic flow decreased versus non-caffeine-exposed embryos. Maternal treatment with the adenosine A_2A receptor inhibitor reproduced the embryonic hemodynamic effects of maternal caffeine exposure. Adenosine A_2A receptor gene expression levels of ED 11.5 embryo and ED 18.5 uterus were decreased. Results suggest that modest maternal caffeine exposure has adverse effects on developing embryonic CV function and growth, possibly mediated via adenosine A_2A receptor blockade.

adenosine A_2A receptor; cardiovascular development; carotid artery; pregnancy