Introduction: Hypoxia elicites a bradycardia within 100 seconds in the developing chick embryo1. This cardiovascular response resembles the carotid chemoreflex observed in fetal sheep. In this study we investigated the heart rate response in after administration of atropine, a muscarinic antogonist.

Methods: Fertile White Leghorn eggs were studied from d15 to d17(n=16)(total incubation time is 21 days). Atropine (50μg/0.1 ml) administration was performed through the allantoic venous catheter (a branch of the chorioallantoic vein, which resembles the umbilical vein). Chorioallantoic artery blood flow (CABF) and heart rate (HR) were measured before and after atropine in normoxia and during hypoxia (5% O2, during 5 min). Parasympathetic blockade was validated with acetylcholine injection(2μg/0.1 ml).

Results: Atropine failed to induce changes in baseline HR, HR variability or significant decrease in CABF (-52%) and HR (-43%) during hypoxia at d15-17.

Conclusion: Despite presence of parasympathic receptors and fibers d3 and d13 respectively, baseline HR and the bradycardic response to hypoxia is not affected by atropine. A possible explanation for this might be a delay between morphological and functional innervation. Alternatively bradycardia during hypoxia observed at this gestational age in the chick embryo, might result from direct depressive effects of hypoxia on the heart.