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Modest maternal caffeine exposure affects developing embryonic cardiovascular function and growth.

Nobuo Momoi¹, Joseph P Tinney, Li J Liu

¹Cardiovascular Development Research Program, Children's Hospital of Pittsburgh of UPMC, and Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA. kimimasa.tobita@chp.edu

American Journal of Physiology. Heart and Circulatory Physiology

|March 25, 2008

Summary

Modest maternal caffeine intake impacts embryonic cardiovascular function and growth, potentially through adenosine A(2A) receptor blockade, without affecting maternal health. This research highlights risks associated with caffeine during pregnancy.

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Fetal Mouse Cardiovascular Imaging Using a High-frequency Ultrasound (30/45MHZ) System

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Published on: May 5, 2018

Area of Science:

Reproductive biology
Developmental toxicology
Cardiovascular physiology

Background:

Maternal caffeine consumption is linked to adverse pregnancy outcomes like growth restriction.
The precise mechanisms by which caffeine affects embryonic development, particularly cardiovascular function, remain unclear.

Purpose of the Study:

To investigate the effects of modest maternal caffeine exposure on embryonic cardiovascular function and growth.
To determine if maternal hemodynamics are altered by caffeine exposure.
To explore the potential role of adenosine A(2A) receptors in mediating caffeine's embryonic effects.

Main Methods:

Pregnant CD-1 mice received daily subcutaneous caffeine (10 mg/kg) from embryonic days (EDs) 9.5 to 18.5.
High-resolution echocardiography was used to assess maternal and embryonic cardiovascular function at multiple embryonic stages.
Embryonic growth parameters (crown-rump length, body weight) and hemodynamic parameters were measured.

Main Results:

Maternal caffeine exposure did not affect maternal weight gain, hemodynamics, or embryo resorption.
Embryos from caffeine-exposed mothers showed reduced crown-rump length and body weight by ED 18.5.
Transient decreases in embryonic blood flow (carotid artery, dorsal aorta, umbilical artery) were observed at ED 11.5 during peak maternal caffeine levels.
Adenosine A(2A) receptor inhibition mimicked the embryonic hemodynamic effects, and gene expression of this receptor was decreased in exposed embryos and maternal uterus.

Conclusions:

Modest maternal caffeine intake adversely affects embryonic cardiovascular function and growth.
These effects may be mediated by the blockade of adenosine A(2A) receptors.
Caffeine's impact on embryonic development warrants further investigation, especially concerning cardiovascular parameters.