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Objective: Hypertensive disorders of pregnancy (HDP) affect foetal outcome. Labetalol is frequently used to lower maternal blood pressure and prolong pregnancy. Conflicting evidence exists for specific neonatal side effects described after maternal labetalol treatment. Our aim was to investigate neonatal effects of foetal exposure to labetalol on cerebral oxygenation and extraction., Methods: In a prospective observational study, clinical characteristics, vital parameters and cerebral oxygen delivery and extraction were collected during the first 24 h of life in labetalol-exposed preterm neonates and compared with two control groups., Results: Twenty-two infants with a mean gestational age of 28.9 weeks, born from labetalol-treated mothers with HDP were included and matched with 22 infants with non-labetalol-treated mothers with HDP and 22 infants without maternal HDP. No significant differences between groups were found neither in heart rate, blood pressure and inotropic support, nor in mean regional cerebral oxygen saturation and fractional tissue oxygen extraction., Conclusion: Foetal labetalol exposure associated effects on preterm heart rate, blood pressure, cerebral oxygenation and extraction are not demonstrated. Maternal disease severity seems to play a more important role in neonatal cerebral haemodynamics. Maternal labetalol treatment has no clinically important short term side effects in the preterm neonate.

Labetalol is a drug used in the treatment of hypertensive disorders of pregnancy (HDP). In a previous study we investigated the influence of the maternal use of labetalol on the cerebral autoregulation (CA) mechanism of neonates. In that study, we found that labetalol induces impaired CA during the first day of life, with CA returning to a normal status by the third day after birth. This effect was hypothesized to be caused by labetalol-induced vasodilation. However, no strong evidence for this claim was found. In this study we aim to find stronger evidence for the vasodilation effect caused by labetalol, by investigating its effect on the neurogenic mechanism (NM) involved in CA. The status of the NM was assessed by means of transfer function analysis between the low frequency content of the autonomic control activity (LFA), obtained by processing of the heart rate (HR), and the regional cerebral oxygen saturation (rScO₂). We found that neonates from mothers treated with labetalol presented a lower LFA and an impaired NM response during the first day of life, with values returning to normal by the end of the third day. These results reflect a vasodilation effect caused by labetalol, and indicate that the impaired CA observed in the previous study is caused by vasodilation.

Hypertensive disorders of pregnancy (HDP) are normally treated to avoid maternal complications. In this study we aimed to investigate if there was an effect of maternal HDP treatment on the cerebral autoregulation of the neonates by analysing measurements of mean arterial blood pressure (MABP) and rScO2 by means of correlation, coherence, and transfer function analysis. We found that these infants presented higher values of transfer function gain, which indicates impaired cerebral autoregulation, with a decreasing trend towards normality. We hypothesised that this trend was due to a vasodilation effect of the maternal use of labetalol due to accumulation, which disappeared by the third day after birth. Therefore, we investigated the values of pulse pressure in order to find evidence for a vasodilatory effect. We found that lower values of pulse pressure were present in these infants when compared with a control population, which, together with increased transfer function gain values, suggests an effect of the drug on the cerebral autoregulation.