Postoperative elevated cortisol excretion is not associated with suppression of 6-sulfatoxymelatonin excretion.

This study tests the hypothesis that elevated postoperative excretion of cortisol is associated with suppression of the nocturnal excretion of 6-sulfatoxymelatonin, the chief metabolite of the circadian hormone, melatonin. Postoperative patients demonstrate circadian rhythm disturbances and suppression of nocturnal melatonin plasma concentration. Since the nocturnal surge in melatonin concentration in normal volunteers is time-locked to the circadian nadir of cortisol concentration, perhaps the attenuation of the nocturnal melatonin surge in postoperative patients results from prolonged elevation in the plasma cortisol concentration. In this observational study performed in 21 patients having unilateral hip or knee arthroplasty, urine was collected every 4 h for the first 48 h after surgery for measurement of urinary 6-sulfatoxymelatonin (EIA) and free cortisol (RIA) excretion. The total (P < 0.05) and peak (P < 0.02) nocturnal 6-sulfatoxymelatonin excretions were lower on the first than the second postoperative night. The nocturnal cortisol nadir preceded the 6-sulfatoxymelatonin surge in 20% of the subjects on night 1 and in 75% of the subjects on night 2. The lack of a consistent relationship between the magnitude or timing of cortisol excretion and 6-sulfatoxymelatonin excretion suggests that cortisol does not mediate postoperative 6-sulfatoxymelatonin suppression.

Low-dose remifentanil infusion does not impair natural killer cell function in healthy volunteers.

BACKGROUND: Mu opioid agonists suppress natural killer (NK) cell activity in animal models. Studies in human volunteers, however, have yielded conflicting results, with morphine suppressing and fentanyl increasing NK cell activity. This study evaluated the effect of a constant 8-h infusion of remifentanil on NK cell number and function in human volunteers. METHODS: After IRB approval and informed consent was obtained, 10 healthy volunteers underwent an 11 pm to 7 am infusion of saline, and at least 1 week later an infusion of 0.02-0.04 microg x kg(-1) min(-1) remifentanil. Blood was collected at 7 am for measurement of NK cell cytotoxicity using a (51)Cr release assay and measurement of NK cell number using fluorescent flow cytometry. RESULTS: Median and range of the total NK cell cytotoxicity (KU ml(-1)) was 745.0 (498.3-1483.6) on the control morning and 818.6 (238.5-1454.5) on the morning following the remifentanil infusion. Neither the number of NK cells ml(-1) (2.5 x 10(5) (1.4 x 10(5)-4.2 x 10(5)) vs 2.7 x 10(5) (1.1 x 10(5)-4.4 x 10(5))) nor the cytotoxicity per 1000 NK cells (KU 1000 NK cells(-1)) (3.0 (1.8-5.2) vs 2.9 (0.9-6.7)) changed between the control and remifentanil conditions. CONCLUSIONS: An 8-h infusion of remifentanil did not affect NK cell activity in normal volunteers. This result differs from previous findings of morphine-induced NK cell activity suppression and fentanyl-induced NK cell activity enhancement in normal volunteers.