BACKGROUND: Patients with obstructive sleep apnea syndrome are known to have high long-term mortality compared to healthy subjects because of their cardiovascular dysfunction. The observation of hemodynamic changes by obstructive apneas is helpful to understand when attempting to understand the pathophysiological mechanism of the development of cardiovascular dysfunction in those patients. Therefore, we studied the changes of in cardiovascular function with the an animal model and tried to obtain the basic data for an ideal experimental model (this phrase is unclear), which is required a requirement for the a more advanced study. METHODS: In 16 Sixteen anesthetized dogs with alpha-chloralose, experimental subjects (delete) were divided into two groups : 8 dogs of room air breathing group and 8 dogs of oxygen breathing group. We measured PaO2, PaCO2, heart rate, cardiac output, mean femoral artery pressure, and mean pulmonary artery pressure at specified times during the apnea-breathing cycle : before endotracheal tube occlusion (baseline), 25 seconds after endotracheal tube occlusion (apneic period), 10 seconds (early phase of postapneic period, EPA) and 25 seconds (late phase of postapneic period, LPA) after spontaneous breathing. RESULTS: In room air breathing group, the heart rate significantly decreased significantly decreased at during the apneic period compared to that at baseline (P<0.01) and increased at EPA and LPA compared to that during the apneic period (P<0.01). But, the heart rate showed no significant changes during apneic and postapneic periods in the oxygen breathing group. Cardiac output tended to decrease at during apneic period compared to that at baseline, but did not show statistical significance was statistically significant. Cardiac output significantly decreased at LPA compared to at baseline (P<0.01). Mean femoral artery pressure was significantly decreased at during apneic period compared to that at baseline (P<0.05). CONCLUSION: Through this experiment, we were partially able to understand the changes of cardiovascular function indirectly, but it is suggested that the (delete) new experimental animal model displaying physiological mechanism close to sleep in nature might natural sleep should be established (,)and the advanced study of in the changes of cardiovascular function and its cause their causes should be continued.