The provided text contains only the editorial board and masthead information for the journal Thrombosis and Haemostasis, with no clinical study data available.
Do antithrombotic agents (vapiprost, r-hirudin, aspirin, ticlopidine) prevent electrically-induced coronary thrombosis in an anaesthetised dog model?
In a canine model of coronary thrombosis, TxA2 and thrombin play a major role, with vapiprost and r-hirudin showing superior efficacy over aspirin and ticlopidine in maintaining blood flow.
Vapiprost (GR32191, a TxA2 antagonist), r-hirudin, aspirin, ticlopidine and aspirin plus ticlopidine were examined for their ability to prevent electrically-induced thrombosis in an artificially stenosed coronary artery in the anaesthetised dog. Drugs or vehicle were administered prior to a 2 h period of electrical damage which was followed by a further 2 h observation period. In all vehicle-treated animals, blood flow markedly declined with onset of the damaging current; 80% completely occluded. All treatments reduced the incidence of complete occlusion to a similar extent. Vapiprost and r-hirudin also largely prevented the decline in blood flow both during and following the damage period whilst aspirin and ticlopidine, either alone or in combination were much less effective. With r-hirudin treatment, marked cyclic changes in flow occurred throughout the experiment; these were abolished by administration of vapiprost. In this dog model, TxA2 and thrombin appear to work in concert to produce coronary thrombosis, ADP being of minor importance. The superior effect of vapiprost over aspirin suggests a beneficial role for endogenous prostacyclin.
White et al. (1994) studied Intra-Coronary Thrombosis. The provided text contains only the editorial board and masthead information for the journal Thrombosis and Haemostasis, with no clinical study data available.