| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Research Abstract |
Although the overnight increase in urinary uric acid/ creatinine ratio (AUA/Cr) is considered by some to be a marker of arterial oxygen desaturation in obstructive sleep apnea syndrome (OSAS), this index does not necessarily parallel the level of arterial desaturation. We examined the validity of △UA/Cr as a marker of tissue hypoxia, not of arterial desaturation, during sleep by measuring the plasma level of adenosine, an intermediary in the process of ATP degradation to uric acid. Additionally, we hypothesized that inter-subject variability in the heart rate response to apnea is a determinant of tissue hypoxia. Methods and Results: We classified 18 patients with OSAS who had apnea-associated moderate to severe arterial desaturation into the two groups; the △UA/Cr-positive group who were considered to have tissue hypoxia and the △UA/Cr-normal group who were not. Venous levels of adenosine were measured before, during and after sleep. Although there were no significant differences between the two groups in either arterial desaturation parameters or apnea index, the plasma level of adenosine during sleep was significantly higher in the ΔUA/Cr-positive group than the normal group (15.2【minus-plus】1.9 SE nM vs. 9.8【minus-plus】1.7 nM, p <0.05]. Successful treatment with nasal CPAP significantly decreased both indices only in the ΔUA/Cr-positive group, but did not in the normal group. The magnitude of heart rate increase after the termination of apnea was significantly smaller in the △UA/Cr-positive group. Conclusions: The ΔUA/Cr can be a marker of tissue hypoxia, which may not be predicted by arterial desaturation indices in sleep apnea syndrome. The poor heart rate response to apnea is a determinant of tissue hypoxia.
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