Linear regression results for the effect of sleep, inflammation, and hypoxia markers on heat pain at baseline and under remifentanil.

Sleep continuity and breathing polysomnographic (PSG) descriptors like the wake after sleep onset (WASO) time, number of sleep stage shifts, and the lowest recorded SaO2 during sleep (nadir SaO2), as well as basic inflammation and hypoxia markers were employed as predictors of heat pain-related variables (threshold and tolerance) in the model. At baseline, betas (standard errors, SE) for the various predictors in the regression equation reflect the change in the heat pain threshold and tolerance for every one unit of change in the PSG and inflammatory markers. Under remifentanil, betas reflect the change in the analgesic sensitivity to remifentanil for the heat pain threshold and tolerance. For example, for every 1-pg/ml-increase in the serum IL-1β the heat pain tolerance will additionally increase by 0.3899°C for every 1-µg/ml-increase in the target Ce of remifentanil. Betas for the PSG predictors were adjusted for the inflammatory and hypoxia markers. Alpha level was set at 0.05.