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Blood oxygen partial pressure affects plasma prolactin concentration in humans
Authors:Strüder H K  Hollmann W  Weicker H  Schiffer T  Weber K
Affiliation:Institute of Sports Games, German Sport University, Cologne.
Abstract:Responses of plasma prolactin (PRL) concentration to acute and repeated changes in blood oxygen partial pressure (PO2a) at rest were investigated in two studies (A; B), with special reference to possible effects mediated via serotonin (5-HT) synthesis. In A, nine male subjects inhaled for 105 min gas containing different oxygen fractions for 6 days. Gas concentrations consisted of 14% (A14), 21 % (A21), 40% (A40), 60% (A60) and 80% (A80) O2 mixed with N2 as well as 100% O2 (A100). Venous and capillary blood samples were drawn before and every 15 min during gas inhalation for analysis of plasma PRL and PO2a. In B, two groups of subjects (B I; B II) were exposed to 30 min day(-1) of gas inhalation over 14 consecutive days. Gas concentration consisted for B I of 14% O2/86% N2 and for B II of 100% O2. During pre- and post-examination a baseline blood sample was drawn, followed by a neuroendocrine test of serotonergic function using a partial 5-HT1A receptor agonist (60 mg of buspirone hydrochloride). In A, each increase of inhaled oxygen fraction also resulted in higher blood POb2a. In A14, A21 and A40, plasma PRL concentrations did not change from basal level. Increases in plasma PRL concentration were found in A60 after 30 min as well as in A80 and A100 after 15 min. A higher blood PO2a induced a higher plasma PRL secretion but also an earlier decline from peak plasma PRL value despite continued inhalation of the respective oxygen concentration. During post-examination in B, basal plasma PRL concentrations were increased in B I and decreased in B II. Plasma PRL response to stimulation challenge was not affected by treatments. Thus, chronic adaptations of basal plasma PRL concentrations to decreased/increased blood PO2a were not related to up/down-regulation, respectively, of central serotonergic receptor function.
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