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BJA Advance Access originally published online on April 2, 2008
British Journal of Anaesthesia 2008 100(5):612-621; doi:10.1093/bja/aen073
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2008. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Examination of the effect of procalcitonin on human leucocytes and the porcine isolated coronary artery

J. X. Wei1, A. Verity2, M. Garle2, R. Mahajan1,* and V. Wilson2

1 Department of Anaesthesia and Intensive Care Medicine
2 School of Biomedical Sciences and Centre for Integrated Systems Biology and Medicine, Queen's Medical Centre, University of Nottingham, Nottingham NG7 2 UH, UK

* Corresponding author. E-mail: ravi.mahajan{at}nottingham.ac.uk

Background: The aim of this study was to investigate the effects of procalcitonin on the lipopolysaccharide (LPS)-induced changes in human leucocytes and porcine isolated coronary artery.

Methods: Using flow cytometry, changes in forward scatter and intracellular calcium in human neutrophils and monocytes were determined after exposure to procalcitonin, calcitonin gene-related peptide (CGRP), LPS, and the known chemoattractants formylated methionine-leucine-phenylalanine (fMLP) and interleukin-8 (IL-8). In porcine isolated coronary artery, the effects of procalcitonin were evaluated using the contractile function change and the release of TNF{alpha}.

Results: In human neutrophils and monocytes, procalcitonin (100 nM), but not CGRP, increased forward scatter and the expression of surface markers (CD16 and CD14, respectively) in a similar manner to 10 µg ml–1 LPS. Procalcitonin, but not CGRP, also increased the proportion of cells exhibiting an increase in intracellular calcium ions similar to that produced by fMLP and IL-8. Acute exposure of the coronary artery to procalcitonin produced a small, endothelium-independent relaxation (approximately 15% of constrictor tone), but failed to modify subsequent relaxations to CGRP. After 16 h exposure, procalcitonin (100 nM) increased TNF{alpha} release from the coronary artery equivalent to 70% of that produced by LPS, but did not modify the inhibitory effect of LPS (100 µg ml–1) on contractile responses.

Conclusions: Procalcitonin has a proinflammatory effect on human leucocytes and porcine coronary artery, but it is not capable of modulating LPS-induced changes in vascular responsiveness in vitro.

Keywords: arteries, coronary; complications, endotoxaemia; cytokines, LPS; procalcitonin


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