M. A. Barradas

The effect of ethanol on platelet function and vascular prostanoids

The present review will discuss the effects of ethanol on platelet function and vascular prostanoids. Whenever possible we have considered human studies because there are marked species differences in platelet function and vascular prostanoid release even in the absence of ethanol. Because of the specialised nature of some parts of the text, we have included brief introductions to help readers who are not familiar with this field.

N-formyl-methionine-leucine-phenylalanine (fMLP), a Bacterial Chemotactic Peptide, Stimulates Platelet Shape Change in Human Whole Blood

In order to investigate platelet-leucocyte interactions, the effect of N-formyl-methionine-leucine-phenylalonine (fMLP) a bacterial peptide, on platelet shape change (PSC) was studied. fMLP stimulated PSC in human platelets in a dose dependent manner in whole blood but did not cause PSC in platelet rich plasma. Furthermore, PSC induced by fMLP was inhibited by a PAF-antagonist indicating that PAF (a leucocyte release substance) is central to this effect. The present data suggests that PSC in whole blood constitutes a convenient method for the assessment of platelet-leucocyte interactions in health and disease.

The effect of tiaprofenic acid and indomethacin administration of human platelet function

The present study compares the effects of two non-steroidal anti-inflammatory drugs (NSAIDs) on platelet function. Tiaprofenic acid (300 mg twice daily) and indomethacin (25 mg thrice daily) were administered to healthy volunteers for 6 days. Platelet aggregation and thromboxane A2 (TXA2) release (assessed as TXB2, the stable, spontaneous breakdown product of TXA2) were assessed before the adminstration of NSAIDs; on day 6 (2–3 h after the last dose of NSAID); and on days 7 and 8 (24 h and 48 h after the last dose of NSAID). Both tiaprofenic acid and indomethacin significantly inhibited platelet aggregation and TXA2 release. The extent and duration of inhibition was similar for both drugs, and the inhibition tended to reverse within 24–48 h of cessation of medication. The time required for reversal of the inhbitiory effect of NSAIDs on platelets may be of relevance in patients who are bleeding (e.g. from gastric erosions caused by NSAIDs). Tiaprofenic acid in the present study and in previous work has not been shown to be a selective inhibitor of prostanoid synthesis, as was originally claimed.