It is a known fact that there is a relationship between some ventilatory disorders and the incidence of ventricular arrhythmias. The aim of our study was to show this relation in the circadian dependence in in-vivo rat models. The electrical stability of the heart was measured by ventricular arrhythmia threshold (VAT) at 3h intervals during a 24h period. The experiments were performed in the Wistar rats (pentobarbital anaesthesia 40mg/l kg i.p., open chest experiments, adaptation to the light regime 12:12 hours, with the dark phase from 18.00h to 06.00h). The normal artificial ventilation was used in the control group (n = 17), hypoventilation (n = 10) and hyperventilation (n = 7) in the second and third ones. The fourth group (n = 4) was subjected to 20 min. hypoventilation and subsequent 20 min. reoxygenation. The significant circadian rhythm was detected under normal ventilatory conditions. Hypoventilation significantly decreased (alpha = 0.001) the VAT and changed the 24h rhythm to the moderate biphasic compared to the control group. The biphasic character was evident only after 10 min. of hypoventilation. Hyperventilation non-significantly increased the VAT, but did not change the rhythm. Reoxygenation, after 20 minutes of hypoventilation, expressively changed the VAT circadian rhythm, inversely compared to the control group. The biphasic character was kept only after 5 min. of reoxygenation. It is concluded that myocardial vulnerability to the ventricular arrhythmias is influenced by ventilatory disorders in the circadian dependence.