Cortisol Production Rate is Related to Mean Arterial Blood Pressure in Neonates. † 811

Abstract

There are few data on clinical factors that influence cortisol production rate (FPR) in neonates. This study aimed to provide such information. Blood samples for plasma cortisol (F) were taken via indwelling arterial lines at 15 min intervals for 6 hours in 42 clinically stable neonates (median ga 32 wks, range 25-41; median bw 1.95kg, range 0.64-3.88) studied in the first 9 postnatal days. None of the infants received vasopressor agents during the study and none received postnatal glucocorticoids prior to the study. We estimated FPR using deconvolution analysis. We prospectively collected data on antenatal steroid exposure, body surface area, gestational age, birth weight, the presence or absence of clinical interventions during the study, whether the neonate was intubated or extubated at time of study, mean arterial blood pressure (MABP), sex, SNAP score, and postnatal study day. MABP was recorded at 15 min intervals during the study and the values averaged to provide a single value for each neonate. The relationship between FPR and the above mentioned clinical factors was examined using univariate linear regression analysis (ULRA) and stepwise multiple linear regression analysis (SMLRA). Using ULRA, FPR correlated positively with postnatal study day (P = 0.0005, r= 0.51), MABP (P = 0.0006, r = 0.51) and being intubated (P = 0.011, r = 0.39). FPR did not significantly correlate with any other clinical factor. On SMLRA, these 3 clinical factors remained significantly correlated with FPR,(MABP, P = 0.0005; study day, P = 0.0085; intubated, P = 0.018). These 3 factors combined accounted for 51% of the variation in FPR (r2 = 0.51). We conclude that, assuming similar corticosteroid-binding globulin levels, FPR is related to MABP in neonates and to our knowledge this is the first time this relationship has been described. Our data support the concept that the low plasma F levels seen in association with hypotension in some premature neonates are consistent with cortisol insufficiency. We propose that this may be explained by decreased FPR in these neonates.