Seuter F, Perzborn E, Fiedler V B
Institute of Pharmacology, BAYER AG, Wuppertal, FRG.
Adv Prostaglandin Thromboxane Leukot Res. 1991;21A:355-8.
The model of AA-induced sudden death employed in these investigations seems to be appropriate for studying the efficacy of TXA2-antagonists. The actions of TXA2 on platelets, respiratory and vascular tissue are considered as key events resulting in the death of the animals. The results obtained in this study, using BAY U 3405 as a selective TXA2 receptor antagonist, clearly show that TXA2 mediated processes are effectively abolished by this type of drug. Since TXA2 is implicated in the pathophysiology of many diseases, potent TXA2 antagonists appear to be useful for treatment of these disorders. BAY U 3405 seems to fulfil these requirements. The threshold dose is 1 to 3 mg/kg p.o. In addition, there is a rapid onset and long duration of action at 10 mg/kg p.o. under the experimental conditions used.
这些研究中所采用的AA诱导猝死模型似乎适用于研究血栓素A2（TXA2）拮抗剂的疗效。TXA2对血小板、呼吸和血管组织的作用被认为是导致动物死亡的关键事件。本研究使用BAY U 3405作为选择性TXA2受体拮抗剂所获得的结果清楚地表明，这类药物能有效消除TXA2介导的过程。由于TXA2与许多疾病的病理生理学有关，强效TXA2拮抗剂似乎可用于治疗这些疾病。BAY U 3405似乎满足这些要求。口服的阈剂量为1至3毫克/千克。此外，在所采用的实验条件下，口服10毫克/千克时起效迅速且作用持续时间长。
