Enzan K, Komatsu H, Shoji K, Suzuki M
Department of Emergency Medicine, Akita University School of Medicine.
Masui. 1995 May;44(5):633-42.
The aim of this study is to clarify whether thromboxane mediates hemodynamic and airway changes induced by PAF in rabbits. Rabbits were divided into 4 groups. In No group rabbits (n = 5), PAF was intravenously injected. In Indo group rabbits (n = 5), indomethacin was infused intravenously 20 min prior to PAF administration. In KT2 group rabbits (n = 4), selective thromboxane antagonist; KT2-962, or in CV group rabbits (n = 3), selective PAF antagonist; CV6209 was injected intravenously 5 min prior to PAF administration. After PAF administration, pulmonary arterial and airway pressures increased transiently, and blood pressure, and leukocyte as well as platelet counts decreased. These hemodynamic and airway changes induced by PAF were almost totally blocked by CV6209 administration, but not by indomethacin and KT2-962 administrations. Similarly, decreases in leukocyte and platelet counts induced by PAF were blocked by CV6209 and KT2-962, but not by indomethacin. We conclude that thromboxane does not mediate hemodynamic and airway changes induced by PAF. PAF is likely to directly induce these changes.
本研究的目的是阐明血栓素是否介导了血小板活化因子(PAF)诱导的家兔血流动力学和气道变化。将家兔分为4组。在无处理组家兔(n = 5)中,静脉注射PAF。在吲哚美辛组家兔(n = 5)中,在给予PAF前20分钟静脉输注吲哚美辛。在KT2组家兔(n = 4)中,在给予PAF前5分钟静脉注射选择性血栓素拮抗剂KT2-962,或在对照血管组家兔(n = 3)中,静脉注射选择性PAF拮抗剂CV6209。给予PAF后,肺动脉压和气道压短暂升高,血压、白细胞计数和血小板计数降低。PAF诱导的这些血流动力学和气道变化几乎完全被CV6209给药阻断,但未被吲哚美辛和KT2-962给药阻断。同样,PAF诱导的白细胞计数和血小板计数降低被CV6209和KT2-962阻断,但未被吲哚美辛阻断。我们得出结论,血栓素不介导PAF诱导的血流动力学和气道变化。PAF可能直接诱导这些变化。