Hydrocortisone does not affect major platelet receptors in inflammation in vitro.

ABSTRACT

HYPOTHESIS: Platelet function is an important factor for the fate of intensive care patients. Several factors may influence this function. Recently, it was demonstrated that hydrocortisone has immunologic effects in septic shock and therefore may affect cell adhesion molecules. The aim of the present study was to examine effects of hydrocortisone on platelet receptor expression in healthy individuals and septic patients in vitro. METHODS: Citrated blood samples were drawn from 10 healthy volunteers and 10 septic patients. Samples were adjusted with hydrocortisone to final concentrations of 4.5 microg mL(-1), 9.0 microg mL(-1) (sepsis-equivalent bolus) and 90 microg mL(-1), respectively. A control group received no additional hydrocortisone. Expression of CD62P, CD41, PAC-1 and CD42b on the surface of resting or agonist-stimulated platelets was determined by whole blood flow cytometry using fluorescence-labeled monoclonal antibodies. RESULTS: Hydrocortisone had no significant influence on the expression of CD62P, CD41 and PAC-1. After administration of 90 microg mL(-1) hydrocortisone the expression of CD42b was decreased compared to controls after activation. Differences between volunteers and sepsis patients were found for all receptors after activation. CONCLUSIONS: Hydrocortisone mediates immunmodulating effects in therapy of patients suffering of septic shock without involvement of specific platelet receptors in vitro.