Platelets and atherosclerosis.
Platelets and atherosclerosis.
复制标题
血小板和动脉粥样硬化。
DOI:
10.1016/0002-9343(81)90144-3
复制
发表时间:
1981
期刊:
影响因子:
--
通讯作者:
Nachman,RL
中科院分区:
文献类型:
--
作者:
Weksler,BB;Nachman,RL
In June 1989, the Department of Neurology of the Medical University of Lubeck organized an international symposium on Platelet-Vessel Wall Interaction. What was the purpose of this symposium? We felt that there was an ever-increasing gap between basic thrombosis research and its clinical applications. Traditional strategies for treating patients with thromboembolic complications had to be questioned critically. Clinical trials have demonstrated that aspirin in a high dosage of 1000 mg per day or more is able to prevent stroke in patients with transient ischemic attacks. The research on the mechanism of action of aspirin at the molecular level has led, however, to doubts about the antithrombotic effect of high-dosage aspirin, as it seems actually to further thrombogenicity.An explanation for this" aspirin dilemma" has yet to be formulated. Apart from aspirin, most drugs used clinically for preventing cardiovascular complications work as platelet aggregation inhibitors. This clinical strategy proceeds on the assumption that platelets play the predominant role in the development of atherosclerosis and its complications. As the latest results presented in this volume show, macrophages and vessel wall factors are now thought to play an important role in atherosclerosis and a new therapeutic approach should aim at influencing these pathways. Another important result of the Lubeck Symposium was that radiolabeling of platelets was established as an accepted laboratory method for evaluating the interaction of the platelets with the vessel wall (see the contributions by M. Goldman, L. Harker, and MK Dewanjee in this volume). There is thus an appropriate method for the in vivo quantification of platelet deposits in vessel segments. The injection of radiolabeled platelets allows the in vivo testing of different antithrombotic drugs.