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BJA Advance Access originally published online on August 26, 2005
British Journal of Anaesthesia 2005 95(4):495-499; doi:10.1093/bja/aei222
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved. For Permissions, please e-mail: journal.permissions@oupjournals.org


OBSTETRICS

Effects of pre-eclampsia on maternal plasma, cerebrospinal fluid, and umbilical cord urotensin II concentrations: a pilot study{dagger}

E. Cowley1, J. P. Thompson1, P. Sharpe1, J. Waugh2, N. Ali1 and D. G. Lambert1,*

1 University Department of Cardiovascular Sciences (Pharmacology and Therapeutics Group), Division of Anaesthesia, Critical Care and Pain Management and 2 Reproductive Science Section, Department of Cancer Studies and Molecular Medicine, University of Leicester, Leicester Royal Infirmary, Leicester LE1 5WW, UK

* Corresponding author. E-mail: DGL3{at}le.ac.uk

Background. Urotensin II (UII) is the most potent endogenous vasoconstrictor identified to date. Pre-eclampsia is associated with arteriolar vasospasm but the precise underlying mechanism is uncertain and we hypothesized that UII concentrations might also be elevated. In this study we measured UII concentrations in maternal plasma and cerebrospinal fluid (CSF), and umbilical vein plasma from pre-eclamptic (PET) and normotensive patients undergoing elective Caesarean section under spinal or combined spinal–epidural anaesthesia.

Methods. With LREC approval and informed consent we recruited two groups of 10 patients; control [mean (range) age, 29 (22–43) yr; BMI, 25 (20–32); gestation, 273 (267–281) days; mean arterial pressure (MAP) on day of delivery, 81 (75–96) mm Hg] and PET [age, 34 (22–40) yr; BMI, 25 (21–46); gestation, 253 (203–289) days; MAP on day of delivery, 106 (88–128) mm Hg]. Maternal blood and CSF samples and umbilical vein blood samples were taken. UII was extracted and concentrations measured using a radioimmunoassay.

Results. Two plasma and two CSF samples in the control and two CSF samples in the PET group were below the assay detection limits. There were no differences in maternal plasma or CSF or umbilical vein UII concentrations between the groups. However, there was a small (~40%) but significant increase in cord UII concentrations when compared with paired plasma in the PET group. There was a weak but significant negative correlation (r=–0.4, P=0.049) between cord UII concentrations and gestation in the PET group. In addition, we observed a significant positive correlation between plasma and CSF (r2=+0.57, P=0.0009, n=16), plasma and cord (r2=+0.43, P=0.0031, n=18) and CSF and cord (r2=+0.32, P=0.022, n=16) UII concentrations for the whole data set.

Conclusions. Collectively the data indicate that UII concentrations do not increase in PET compared with controls but, in PET patients, cord UII concentrations are elevated relative to paired plasma samples. Elevated umbilical vein UII concentrations may simply indicate reduced placental viability and possibly UII metabolism as a result of reduced blood flow or possibly that the placenta is producing UII.

{dagger} This work was presented at the Liverpool meeting of the Anaesthetic Research Society, July 8–9, 2004 (E. Cowley, J. Waugh, N. Ali, P. Sharpe, J. P. Thompson and D. G. Lambert. Urotensin II concentrations are not elevated in pre-eclampsia. Br J Anaesth 2004; 612P).


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