Platelets and artificial surfaces: the effects of drugs

Publisher Website
Google Scholar
Abstract
Contact of blood with a foreign surface activates platelets and leads to their consumption. This property is shared by most non-biological materials, including air, but can be reduced by an optimal balance of hydrophobicity and hydrophilicity, minimal capacity for hydrogen bonding, avoidance of crystallinity, maintenance of polymer backbone mobility, and other manipulations of the chemistry of the polymer. None the less, no totally non-thrombogenic artificial surface has been developed. Attention has therefore turned to suppression of platelet-surface interaction by drugs that alter platelet function. Agents that block cyclo-oxygenase inhibit surface-induced secretion and aggregation but have no effect on platelet adhesion. Drugs that increase platelet cyclic AMP levels have a dose-related effect, which at high concentrations can eliminate adhesion to surfaces. The most successful agent, prostacyclin, has achieved total protection of platelets during cardiopulmonary bypass, with preservation of normal platelet number and function. Associated vasodilatation is a notable side effect, and hypotension may prove to be a significant problem in clinical practice. The development of more selective analogues with minimal vasodepressor activity is to be encouraged.

This publication has 2 references indexed in Scilit: