Obstructive sleep apnoea syndrome (OSAS) is a disorder characterized
by repetitive episodes of complete (apnoea) or partial (hypopnoea) obstruction
of airflow during sleep. The severity of OSAS is defined by the apnoea hypopnoea
index (AHI) or number of obstructive episodes. An AHI greater than 30 is
considered severe, but it can reach values higher than 100 in some patients. Associated
to the OSA there is high incidence of cardiovascular and neuro-psychiatric
pathologies including systemic hypertension, stroke, cardiac arrhythmias and
atherosclerosis, diurnal somnolence, anxiety and depression. In the present study
we have used a model of intermittent hypoxia (IH) of moderately high intensity
(30 episodes/h) to evaluate arterial blood gases and plasma catecholamines as main
effectors in determining arterial blood pressure. Male rats were exposed to IH with
a regime of 80s, 20% O2 // 40s, 10%O2, 8 h/day, 8 or 15 days.
Lowering the breathing atmosphere to 10% O2 reduced arterial blood PO2 to
56.9mmHg (nadir HbO2 86, 3%). Plasma epinephrine (E) and norepinephrine (NE)
levels at the end of 8 and 15 days of IH showed a tendency to increase, being significant
the increase of norepinephrine (NE) levels in the group exposed to intermittent
hypoxia during 15 days. We conclude that IH causes an increase in sympathetic
activity and a concomitant increase in NE levels which in turn would generate an
increase in vascular tone and arterial blood pressure.
