Compensatory excretion of prostacyclin and thromboxane metabolites in obstructive sleep apnea syndrome

Since obstructive sleep apnea syndrome (OSAS) is often linked with systemic hypertension, we sought to clarify the characteristics of prostanoid metabolism in OSAS, In 7 OSAS patients (apneahypopnea index, 51.0 +/- 23.4) and 7 non-snorers as control, nocturnal urine was sampled and analyzed for stable metabolites of prostacyclin (PGI(2)) and thromboxane A(2) (TxA(2)), [6-keto-PGF(1 alpha) and thromboxane B-2(TxB(2))]. The ratio of 6-keto-PGF(1 alpha), to TxB(2) was significantly higher in OSAS (2.97 +/- 1.52) than in control (1.38 +/- 0.38), Successful treatment with nasal continuous positive airway pressure (8.3 +/- 1.5 cmH(2)O) for 3 days caused a significant decrease in mean blood pressure in OSAS, Moreover, the 6-keto-PGF(1 alpha), to TxB(2) ratio also significantly decreased to 1.74 +/- 0.58, a level which may not significantly different from control, These results suggest that the production ratio of PGI(2) to TxA(2) is shifted toward vasodilatation in untreated OSAS, We conclude that the production of prostanoids plays a role in compensating for the systemic hypertension in OSAS.