Hao Wu1, Qianwen Lv2, Huina Zhang3,4, Yanwen Qin3,4, Fang Fang3,4, Haili Sun1, Yongxiang Wei5. 1. Beijing An Zhen Hospital, Capital Medical University, #2 Anzhen Road, Chaoyang District, Beijing, 100029, People's Republic of China. 2. Beijing An Zhen Hospital, Capital Medical University, Beijing Institute of Heart, Lung and Blood Vessel Diseases, Beijing, China. 3. Beijing An Zhen Hospital, Capital Medical University, Beijing, China. 4. Key Laboratory of Upper Airway Dysfunction-related Cardiovascular Diseases, Beijing Institute of Heart Lung and Blood Vessel Disease, Sleep Centre, Beijing, China. 5. Beijing An Zhen Hospital, Capital Medical University, #2 Anzhen Road, Chaoyang District, Beijing, 100029, People's Republic of China. weiyongxiang1208@163.com.
Abstract
PURPOSE: We aimed to investigate the effect of obstructive sleep apnea (OSA) and apnea-hypopnea duration on endothelial, ventricular function, blood pressure, and inflammation in a rat model. METHODS: We established a novel rat model of OSA. Wistar rats were randomized to six groups according to 4-week different treatments: (1) OSA (apnea for 60 s in a 90-s window of breathing [60 s/90 s] with anesthesia), (2) OSA 30 s/90 s with anesthesia, (3) partial recovery (60 s/90 s for 2 weeks, followed by 15 s/90 s for 2 weeks with anesthesia), (4) complete recovery (60 s/90 s for 2 weeks with anesthesia, and then normal breathing for 2 weeks), (5) sham (normal breathing in the device with anesthesia), and (6) control group (normal breathing, normal cage, no anesthesia). We recorded blood pressure, endothelial function, left ventricular function, and inflammation at different time points. RESULTS: Vascular inflammation and endothelial dysfunction occurred in OSA models. More systemic inflammatory and endothelial dysfunction were observed in longer apnea-hypopnea duration group and they were reversed in both partial and complete recovery groups. Left ventricular weight/body weight ratio was significantly higher in the OSA (60s/90s) group than complete recovery, sham, and control groups, which remained unchanged in partial recovery group (p < 0.05). CONCLUSIONS: Longer apnea-hypopnea duration is related to more systemic inflammatory and endothelial dysfunction, and hypertension and cardiac remodeling. These can be reversed after a period of recovery, which indicates that time parameters for assessing OSA, such as apnea-hypopnea duration, should be considered instead of apnea-hypopnea index only.
PURPOSE: We aimed to investigate the effect of obstructive sleep apnea (OSA) and apnea-hypopnea duration on endothelial, ventricular function, blood pressure, and inflammation in a rat model. METHODS: We established a novel rat model of OSA. Wistar rats were randomized to six groups according to 4-week different treatments: (1) OSA (apnea for 60 s in a 90-s window of breathing [60 s/90 s] with anesthesia), (2) OSA 30 s/90 s with anesthesia, (3) partial recovery (60 s/90 s for 2 weeks, followed by 15 s/90 s for 2 weeks with anesthesia), (4) complete recovery (60 s/90 s for 2 weeks with anesthesia, and then normal breathing for 2 weeks), (5) sham (normal breathing in the device with anesthesia), and (6) control group (normal breathing, normal cage, no anesthesia). We recorded blood pressure, endothelial function, left ventricular function, and inflammation at different time points. RESULTS:Vascular inflammation and endothelial dysfunction occurred in OSA models. More systemic inflammatory and endothelial dysfunction were observed in longer apnea-hypopnea duration group and they were reversed in both partial and complete recovery groups. Left ventricular weight/body weight ratio was significantly higher in the OSA (60s/90s) group than complete recovery, sham, and control groups, which remained unchanged in partial recovery group (p < 0.05). CONCLUSIONS: Longer apnea-hypopnea duration is related to more systemic inflammatory and endothelial dysfunction, and hypertension and cardiac remodeling. These can be reversed after a period of recovery, which indicates that time parameters for assessing OSA, such as apnea-hypopnea duration, should be considered instead of apnea-hypopnea index only.
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