Modest maternal caffeine exposure affects murine embryonic cardiovascular function. (A) Representative in vivo high-frequency echocardiogram images and pulsed-Doppler waveforms from CD-1 mouse embryos. 1. B-mode image of an embryonic day (ED) 10.5 embryo. Arrowheads indicate velocity sampling locations; 2. dorsal aortic pulsed-Doppler velocity waveforms at ED 12.5. The scale on the right denotes Doppler velocity (cm/s); 3. internal carotid arterial pulsed-Doppler velocity waveforms at ED 12.5; 4. Umbilical arterial pulsed-Doppler velocity waveforms at ED 11.5; 5. M-mode image of an ED 11.5 embryonic LV planimetered to determine end-diastolic and end-systolic dimensions. This was adapted with permission (Momoi et al. 2007). (B) Representative changes in maternal and embryo hemodynamics 30 min after maternal treatment with caffeine (10 mg/kg), adenosine A1 selective antagonist 8-cyclopentyl-1,3-dimethylxanthine (CPT) (4.8 mg/kg), or adenosine A2A selective antagonist MSX-3 (3.0 mg/kg). Maternal HR, cardiac output (CO), and systolic blood pressure (BP) did not change from baseline in response to any treatment (top). MSX-3 mirrored the caffeine effects on embryonic hemodynamics (bottom), and no additive effects occurred by concurrent treatment of caffeine and MSX-3, suggesting that the negative CV effects of caffeine on embryonic hemodynamics occur via the adenosine A2A receptor. The values are mean ± SD and represent changes from baseline. *p < 0.05 vs. the control (ANOVA). This was adapted with permission [245].
|
