목적: Obstructive sleep apnea(OSA) is a common condition characterized by chronic intermittent hypoxia(CIH) and frequent arousals from sleep. Recent evidence suggests that OSA is directly linked to high cardiovascular mortality and morbidity. The aim was to establish OSA mouse model using chronic intermittent hypoxia and to identify features of cardiovascular phenotype. 방법:C57BL/6J mice were used. Normoxic control mice were placed in neighboring chambers under room air. Chronic intermittent hypoxia and normoxic were administered during the light phase for 12 hours to coincide with the mouse sleep cycle and the duration of exposure was until 8 weeks. Heart, lungs, blood were obtained for realtime PCR and ELISA. Heart function was measured using cine-MRI. Histology of heart muscle and lung vessels were checked. 결과:For CIH, FiO2 decreased from 21 to 5 % over a 120 s period. This regimen induced oxyhemoglobin desaturations from 90% to 70% sensored from mouse foot. The left ventricle shortening fraction was higher in control group, but right ventricle shortening fraction was significantly lower in CIH group. Systolic blood pressure was elevated after 4 weeks of CIH. The pathologic cardiac hypertrophic markers, such as Beta-MHC and BNP mRNA were significantly elevated in CIH group. However, oxidative stress markers such as p22phox, NOX2, NOX4, HIF-1a in between CIH and normoxic group were not different in the heart tissue. From lung tissues, interestingly, p22phox, NOX2, HIF-1 were significantly elevated in CIH group. The formation of fibrosis and accumulation of inflammatory cells around pulmonary vessels was identified on histologic examination. 결론:We identified pathologic change of cardiovascular phenotype and established OSA mouse model using chronic intermittent hypoxia. This OSA mouse model could be utilized to investigate OSA-related complications and to discover possible biomarker for OSA.