Impact of obstructive sleep apnea and intermittent hypoxia on blood rheology - a translational study.

Rationale Hemorheological alterations are reported in obstructive sleep apnea (OSA) and reversed with continuous positive airway pressure (CPAP), observations potentially explained by intermittent hypoxia (IH)-induced oxidative stress. Objective To investigate whether IH causes hemorheological alterations viaoxidative stress. Methods Wistar rats were exposed to normoxia (n=7) or IH (n=8) for 14 days. Twenty-three moderate-to-severe OSA patients were assessed at three time points: baseline, after randomisation to either 2 weeks of nocturnal oxygen (n=13) or no treatment (n=10), and after 1-month of CPAP treatment (n=17). Further, an OSA-free control group (n=13) was assessed at baseline and after time-matched follow-up. Measurements We measured hemorheological parameters [hematocrit, blood viscosity, plasma viscosity (rats only), erythrocyte aggregation and deformability (humans only)] and redox balance (SOD, GPX, protein oxidation [AOPP] and lipid peroxidation [MDA]). We also tested erythrocytes hemorheological sensitivity to reactive oxygen species (ROS) in our human participants using the oxidant t-butyl hydroperoxide (TBHP). Results In rats, IH increased blood viscosity by increasing hematocrit without altering erythrocytes hemorheological properties. IH also reduced SOD activity and increased AOPP. In humans, baseline hemorheological properties were similar between patients and controls, and properties were unaltered following oxygen and CPAP, except erythrocyte deformability was reduced following oxygen therapy. Redox balance was comparable between patients and controls. At baseline, TBHP induced a greater reduction of erythrocyte deformability in patients while CPAP reduced TBHP-induced increase in aggregation strength. Conclusion IH and OSA per se do not cause hemorheological alterations despite the presence of oxidative stress or higher sensitivity to ROS, respectively.