Related Experiment Video
Updated: Aug 10, 2026
In utero Measurement of Heart Rate in Mouse by Noninvasive M-mode Echocardiography
Published on: November 22, 2013
Effect of vinpocetine on embryonic heart rate in vitro
Helen Elizabeth Ritchie1, Jaimie W Polson1, Andrea Xia1
1School of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, NSW, Australia.
Insights
Vinpocetine may cause fetal harm by affecting heart rate, but effective doses are unlikely in humans. Further research is needed if vinpocetine is linked to adult cardiac arrhythmias.
Area of Science:
- Pharmacology
- Developmental Toxicology
- Cardiovascular Science
Background:
- Vinpocetine, a supplement for memory and weight loss, inhibits the Ikr current, crucial for cardiac repolarization.
- Ikr inhibition can lead to dangerous arrhythmias like torsade de pointes and sudden death.
- Ikr blockers have shown teratogenic effects, including birth defects and embryonic mortality in animal studies.
Purpose of the Study:
- To investigate the effects of vinpocetine and its metabolite, apovincaminic acid, on embryonic heart rate.
- To clarify the mechanisms behind vinpocetine's potential fetal toxicity.
Main Methods:
- Rat embryo culture was utilized to assess the impact of vinpocetine and apovincaminic acid.
- Embryonic heart rate was monitored in response to varying concentrations of the compounds.
Main Results:
- Both vinpocetine and apovincaminic acid induced concentration-dependent embryonic bradycardia.
- Vinpocetine was more potent in causing bradycardia, with effects observed at 100 nM.
- Embryonic arrhythmias occurred at higher concentrations, and vinpocetine was more potent.
Conclusions:
- The study suggests that FDA warnings about vinpocetine may cause unnecessary anxiety, as effective concentrations are unlikely in humans.
- Re-evaluation of teratogenicity risk is warranted if a link between vinpocetine and adult cardiac arrhythmias is established.
Abstract:
Vinpocetine is a readily available nutritional supplement claimed to improve memory and weight loss. However, it blocks the Ikr current essential for cardiac action potential repolarisation and Ikr inhibition can cause "torsade de pointes" arrhythmias and sudden death. Moreover, Ikr blockers have exhibited teratogenic effects in reproductive toxicology studies, leading to increased birth defects and embryonic mortality. The FDA advises against vinpocetine use in pregnant and prospective mothers based on animal studies showing dose-dependent fetal mortality in rats and rabbits, and cardiovascular malformations in surviving fetuses. However, the mechanisms responsible for vinpocetine's fetal toxicity remain unclear. The present study used rat embryo culture to evaluate vinpocetine and its major metabolite, apovincaminic acid, on embryonic heart rate, a possible causative factor behind its adverse effects. Both compounds induced embryonic bradycardia in a concentration-dependent manner, with vinpocetine proving more potent. The minimum vinpocentine concentration to induce bradycardia was 100 nM, a level unlikely to be reached in humans following typical doses. Embryonic arrhythmias were also observed at the highest concentrations. These results suggest that the FDA's cautionary statement may generate undue anxiety, although re-evaluation of teratogenicity risk associated with vinpocetine should be revisited if a link to cardiac arrhythmias in adults is established.
