**Effect of Glyceryl Trinitrate onStaphylococcus aureusGrowth and Leukocyte Activation during Simulated Extracorporeal Circulation**

Melki, Vilyam
Tano, Eva
Douhan Hakansson, Lena
Tran, Phan-Kiet
Knutson, Folke
Malinski, Tadeusz
Borowiec, Jan

¹Department of Surgical Sciences, Uppsala University, Uppsala, Sweden
²Department of Medical Sciences, Uppsala University, Uppsala, Sweden
³Department of Clinical Immunology and Transfusion Medicine, Uppsala University, Uppsala, Sweden
⁴Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio, United States

Address for correspondence Vilyam Melki, MD, Department of Cardiothoracic Surgery, Uppsala University Hospital, SE-781 85 Uppsala, Sweden, [email protected]

received August, 16, 2013

accepted after revision October, 27, 2013

published online December, 16, 2013

Conflict of Interest None.

Acknowledgments

This study was supported by Swedish Heart-Lung Foundation (V.M.), and Sellanders' Family Fund and the Heart Lung Fund, Uppsala University Hospital (J.B.).

Note

This study was approved by the appropriate ethics committee and performed in accordance with the ethical standards laid down in the 1964 Declaration of Helsinki and its later amendments.

The Thoracic and Cardiovascular Surgeon 62(5):p 402-408, August 2014. | DOI: 10.1055/s-0033-1363296

Abstract

Background

Previously, nitric oxide has been shown to possess antimicrobial effects. In this study, we aim to test the effect of glyceryl trinitrate (GTN) on Staphylococcus aureus growth during simulated extracorporeal circulation (SECC) and also to examine the effect of S. aureus, alone and in combination with GTN, on activation markers of the innate immune system during SECC.

Methods

In an in vitro system of SECC, we measured GTN-induced changes in markers of leukocyte activation in whole blood caused by S. aureus infestation, as well as the effect of GTN on S. aureus growth.

Results

GTN had no effect on S. aureus growth after 240 minutes SECC. Staphylococcus aureus reduced the expression of granulocyte Fcγ-receptor CD32 but stimulated the expression of monocyte CD32. Staphylococcus aureus stimulated expression of some leukocyte adhesion key proteins, activation marker CD66b, lipopolysaccharide-receptor CD14, and C3b-receptor CD35. Staphylococcus aureus and GTN addition induced significant increases in monocyte CD63 (lysosomal granule protein) levels.

Conclusion

GTN does not affect S. aureus growth during SECC and has no effect on SECC-induced leukocyte activation.