The elevated plasma orexin level reflects central manifestations of apnea-hypopnea

In the present study, we found that plasma orexin-A levels correlated with the clinical severity of OSAHS, AHI (r = 0.52), and arousal index (r = 0.51). In addition, plasma orexin-A levels decreased in patients who received nCPAP therapy. These results suggest that plasma orexin-A could be used as a biological marker of the severity of OSAHS.

It has been reported that orexin-A is present in the cerebrospinal fluid (CSF) and peripheral blood of healthy individuals and some narcoleptic patients buy Kamagra Australia. The origin of plasma orexin-A has not yet been determined. Orexin-A neurons are restricted to the lateral and posterior hypothalamus, and medulla, and orexin-A has been shown to rapidly cross the blood-brain barrier by simple diffusion. Therefore, circulating orexin-A could originate from the hypothalamus via blood-brain barrier, in which case plasma orexin-A levels at least partially reflect the production of orexin-A in the hypothalamus. However, a consensus regarding the exact functions of the brain orexin system has not yet emerged, although it is reasonable to assume that an elevated plasma orexin level reflects central manifestations of apnea-hypopnea-related arousals.

Alternatively, plasma orexin-A might stem from cells that express orexin-like immunoreactivity, together with functional orexin receptors in human gut cells. There are peripheral manifestations of arousal, particularly arousal from obstructive respiratory events (ie, changes in BP and heart rate, sympathetic activation, intrathoracic pressure swings, and elevated muscle activity) that could conceivably activate peripheral cells containing orexin or orexin-like immunoreactivity.

Higuchi et al measured plasma orexin-A, using the same radioimmunoassay method that we have used, in Japanese patients with narcolepsy, and they found that plasma orexin-A levels in patients with narcolepsy (range, 11 to 25 pg/mL; mean, 20.8 ± 4.3 pg/mL) were lower than those in control subjects (range, 20 to 33 pg/mL; mean, 26.7 ± 3.2 pg/mL). Compared with those measurements, the orexin-A levels were higher in the present study, partly because obesity may influence the plasma levels of orexin-A. The plasma levels of orexin-A were higher in patients with OSAHS than in an age-matched, BMI-matched, and gender-matched group of control subjects, suggesting that the production of orexin-A is augmented in patients with OSAHS.

Responses are currently closed, but you can trackback from your own site.

Comments are closed.