Chronic intermittent hypoxia worsens brain damage and sensorimotor behavioral abnormalities after ischemic stroke:...

Sleep apnea (SA) is characterized by intermittent hypoxia (IH), which increases sympathetic activity and sleep fragmentation, thus increasing the risk of stroke. SA is a highly prevalent disease and can worsen prognosis in patients with stroke. However, the correlation of changes in the cardiac autonomic nervous system and sleep patterns under IH with sensorimotor behavior and cerebral infarction after stroke remains unclear. We hypothesized that dysregulated autonomic activity and unstable sleep patterns induced by IH and correlated with cerebral infarction and abnormal sensorimotor behavior after middle cerebral artery occlusion (MCAO).

Wistar-Kyoto rats (WKY) were divided into IH (hypoxia: 5 % O_2, 8 h/day) and RA group (room air) for 2 weeks and both groups were subjected to MCAO. After MCAO, the IH group was continuously exposed to IH for 1 week. The 24-h physiological signals, blood pressure, and sensorimotor behavior were recorded at baseline (Bas), the first and second weeks during IH (RA/IH1W and RA/IH2W, respectively), and poststroke.

Before MCAO, IH caused sympathetic activity during sleep and parasympathetic activity of active waking (AW) to increase. Moreover, IH reduced the accumulated time and duration of paradoxical sleep (PS) and increased the interruption during sleep. After MCAO, IH increased blood pressure, more severe brain damage, and poor sensorimotor performance. Moreover, IH reduced autonomic activity after MCAO and decreased sympathetic activity was associated with poor sensorimotor performance.

Autonomic activity and sleep patterns affected by IH were correlated with increased cerebral infarction and poor sensorimotor behavior after MCAO.