The role of dysrhythmic heart function during cardiovascular teratogenesis in epinephrine-treated chick embryos.

Chick embryos were treated with a teratogenic dose (5 micrograms) of epinephrine hydrochloride at 4 days of development (stage 24). Heart rates were determined at 20, 40, and 60 minutes after treatment. The mean heart rate values for epinephrine-treated embryos were significantly less than values obtained for untreated and saline-treated control embryos. The decrements in mean heart rate could be explained by severe cardiac dysrhythmias that occurred in approximately 40% of epinephrine-treated embryos. The remaining 60% of embryos exhibited heartbeat patterns similar to controls. This finding enabled us to separate epinephrine-treated embryos into two physiologically distinct groups: dysrhythmia-positive and dysrhythmia-negative. Dysrhythmias were characterized by periods of bradycardia alternating with periods of asystole and were confirmed by electrocardiography. EKG data suggest that epinephrine induces cardiac conduction disturbances in some chick embryos. An additional experiment was conducted to identify the frequencies at which abnormally obliterated aortic arches, abnormally persistent aortic arches, ventricular septal defects, and embryonic death occurred in dysrhythmia-positive and negative embryos. Abnormally obliterated vessels and embryonic death occurred with significantly greater frequencies in dysrhythmia-positive embryos. Abnormally persistent vessels and ventricular septal defects occurred with significantly greater frequencies in dysrhythmia-negative embryos. We conclude that the production of specific malformations and decreased probability for survival in epinephrine-treated embryos are related to dysrhythmogenesis and bradycardia.