Abstract
Obstructive sleep apnea syndrome (OSAS) is associated with many cardiovascular disorders such as heart failure, hypertension, atherosclerosis, and arrhythmia and so on. Of the many associated factors, chronic intermittent hypoxia (CIH) in particular is the primary player in OSAS. To assess the effects of CIH on cardiac function secondary to OSAS, we established a model to study the effects of CIH on Wistar rats. Specifically, we examined the possible underlying cellular mechanisms of hypoxic tissue damage and the possible protective role of adiponectin against hypoxic insults. In the first treatment group, rats were exposed to CIH conditions (nadir O2, 5–6%) for 8 hours/day, for 5 weeks. Subsequent CIH-induced cardiac dysfunction was measured by echocardiograph. Compared with the normal control (NC) group, rats in the CIH-exposed group experienced elevated levels of left ventricular end-systolic dimension and left ventricular end-systolic volume and depressed levels of left ventricular ejection fraction and left ventricular fractional shortening (p<0.05). However, when adiponectin (Ad) was added in CIH + Ad group, we saw a rescue in the elevations of the aforementioned left ventricular function (p<0.05). To assess critical cardiac injury, we detected myocardial apoptosis by Terminal deoxynucleotidyl transfer-mediated dUTP nick end-labeling (TUNEL) analysis. It was showed that the apoptosis percentage in CIH group (2.948%) was significantly higher than that in NC group (0.4167%) and CIH + Ad group (1.219%) (p<0.05). Protein expressions of cleaved caspase-3, cleaved caspase-9, and cleaved-caspase-12 validated our TUNEL results (p<0.05). Mechanistically, our results demonstrated that the proteins expressed with endoplasmic reticulum stress and the expression of reactive oxygen species (ROS) were significantly elevated under CIH conditions, whereas Ad supplementation partially decreased them. Overall, our results suggested that Ad augmentation could improve CIH-induced left ventricular dysfunction and associated myocardial apoptosis by inhibition of ROS-dependent ER stress.
Highlights
Obstructive sleep apnea syndrome (OSAS) is a common disease characterized by repetitive episodes of complete or partial upper airway occlusion during sleep, leading to intermittent hypoxemia, frequent arousals, daytime fatigue and negative intrathoracic pressure
Echocardiographic Data Compared with the normal control (NC) group, the echocardiograph, on day 35 of the experiment, showed that in the chronic intermittent hypoxia (CIH) group there was a significant elevation in both LVDs (4.19760.6035 mm vs 3.27660.6192 mm, p,0.05) and LVESV (77.86621.18 ml vs 47.60624.32 ml, p,0.05) along with the expected decrease in both LVEF (67.9766.687% vs 80.7567.624%, p,0.01) and LVFS (39.2665.905% vs 51.4268.047%, p,0.01) (Table 1)
Compared with the CIH group alone, the left ventricular function parameters mentioned above had improved compared to CIH + Ad group (p,0.05)
Summary
Obstructive sleep apnea syndrome (OSAS) is a common disease characterized by repetitive episodes of complete or partial upper airway occlusion during sleep, leading to intermittent hypoxemia, frequent arousals, daytime fatigue and negative intrathoracic pressure. Pischon et al’s landmark study showed that high plasma Ad levels correlated to a lower incidence of coronary heart disease in healthy participants [13]. Other studies have shown that plasma Ad level decreased in obese people [14,15] and patients with diabetes mellitus [15], hypertension [16], insulinresistance [17] and coronary artery disease [18,19]. It has been observed that the plasma Ad level was decreased in OSAS patients compared to healthy controls [22,23]. We believe the decrease in plasma/serum Ad levels within chronically hypoxic OSAS patients is a direct result of cell oxidative stress
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