Studies on development of vascular function test for prediction of thrombotic states
Grant-in-Aid for Scientific Research (C)
|Research Institution||TOKUSHIMA UNIVERSITY|
ISOBE Jun-ich Tokushima University, Department of Medical Technology School of Medical Sciences, Professor, 医療技術短期大学部, 教授 (30035711)
MIZUNO Akira Tokushima University Hospital, Department of Clinical Laboratory, Assistant, 医学部・附属病院・検査部, 助手 (80219641)
|Project Fiscal Year
1995 – 1997
Completed(Fiscal Year 1997)
|Budget Amount *help
¥2,300,000 (Direct Cost : ¥2,300,000)
Fiscal Year 1997 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1996 : ¥700,000 (Direct Cost : ¥700,000)
Fiscal Year 1995 : ¥1,100,000 (Direct Cost : ¥1,100,000)
|Keywords||Einephrine-potentiated platelet aggregation / Antiplatelet therapy monitoring / Anti GPIIb / IIIa monoclonal antibody / Venous occlusion test / nitric oxide / Superoxide dismutase / 血小板エピネフリン凝集 / 抗血小板療法モニタリング / 抗ヒトGP(IIb) / (IIIa)モノクローナル抗体 / 静脈圧迫試験 / 一酸化窒素(NO) / スーパーオキサイド・ジスムターゼ(SOD) / 抗ヒトGPIIb / IIIaモノクローナル抗体 / 一酸化窒素 / 血栓-血管機能 / 血小板凝集 / 抗ヒトGP IIb / 血小板内カルシウム濃度 / 血管機能 / 血栓症|
In term of 1995-1997, we examined to some theme associated with an platelet aggregation -vascular function relationship.
(1) A trial of monitoring in antiplatelet therapy using epinephrine-potentiated platelet aggregation
Potentiating actions by the low concentration of epinephrine to ADP-, or collagen-induced platelet aggregation were investigated using 80 patinets with cerebrovascular infarction and 12 patients with other various diseases.
As the results, epinephrine highly potentiated to ADP-induced platelet aggregation in the patient group. Moreover, some cases were in hypersensitive against the epinephrine among the patients undergoing antiplatelet therapy.
It is suggested that the measurement of epinephrine-potentiated platelet aggregation contributes to the monitoring in antiplatelet therapy.
(2) Inhibitory effect of anti-human GpIIb/IIIa monoclonal antibody (MoAb) to platelet aggregations in vitro
In ADP-, collagen-, epinephrine-, thrombin-, or PAF-induced platelet aggregations, they
were highly inhibited by the MoAb in a dose dependent manner. The combination of MoAb and antifibrinogen antibody depressed intensively these aggregations by the additive effect. The inhibitory action of MoAb on these aggregations was also enhanced by the addition of fibronectin or its fragments. Antiaggregating action of MoAb was radical, consequently hemorrhagic episodes were uneasy in its clinical applications
(3) Changes of some thrombotic markers in patients with collagen diseases by vonous acclusion test (VOT)
In the relative changes of some markers before and after VOT,normal subjects were supperior to the patients in tPA levels and the patients were equal to normals in PAI-1 levels, incidentally there was no significant difference between normals and patients in thrombomodulin levels.
(4) Studies on the inhibition of platelet aggregation by nitric oxide (NO)
NO acts as a week antagonist to ADP-induced platelet aggregation, but it enhances the antiaggregating action by a selective PDE inhibitor (dipyridamole) through the elevation in platelet cGMP,and is to be synergistic with prostanoid in a rise of platelet cAMP.
(5) Effect of superoxide dismutase (SOD) on platelet aggregation
SOD enhanced the inhibitory action of platelet aggregation by PGI_2, besides demonstrating a long-lasting action of nitric oxide, through the inhibition of superoxide (・O_2^-). It has been suggested that SOD might contribute to the antithrombotic ability of vascular endothelium. Less
Research Output (19results)