Haberl R L, Heizer M L, Ellis E F
Stroke. 1987 Jul-Aug;18(4):796-800. doi: 10.1161/01.str.18.4.796.
Our previous experiments have shown that thromboxane A2 is a strong contractor of cerebral arterial smooth muscle strips. The objective of these experiments was to determine if U 46619, a stable thromboxane A2 mimetic, affects the cerebral microcirculation in vivo. Pial arteriole diameter in rabbits and rats was measured with a microscope using the closed cranial window technique. Topical application of 10(-11) to 10(-6) M U 46619 induced dose-dependent arteriole vasoconstriction in both species. In rabbits and rats the maximum vasoconstriction was 9.7 +/- 1.3% (mean +/- SEM) and 14.0 +/- 0.5%, respectively. In rats, 10(-7) and 10(-6) M U 46619 induced intravascular platelet aggregation accompanied by a further decrease in diameter and transient occlusion of the arterioles and venules. U 46619 had no significant effect on rabbit pial arterioles that were predilated by hypercapnia or hypercapnia plus hypoxia. Our data suggest that in animals with a normal vasculature, thromboxane A2 may be a moderate constrictor of cerebral arterioles and that this constrictor effect is prevented by hypercapnia and hypoxia.
我们之前的实验表明，血栓素A2是脑动脉平滑肌条的强力收缩剂。这些实验的目的是确定稳定的血栓素A2模拟物U 46619是否会影响体内的脑微循环。使用闭合颅骨开窗技术，通过显微镜测量兔和大鼠软脑膜小动脉的直径。局部应用10(-11)至10(-6) M的U 46619在两种动物中均诱导出剂量依赖性的小动脉血管收缩。在兔和大鼠中，最大血管收缩分别为9.7 +/- 1.3%（平均值 +/- 标准误）和14.0 +/- 0.5%。在大鼠中，10(-7)和10(-6) M的U 46619诱导血管内血小板聚集，伴随小动脉和小静脉直径进一步减小以及短暂闭塞。U 46619对因高碳酸血症或高碳酸血症加缺氧而预扩张的兔软脑膜小动脉没有显著影响。我们的数据表明，在血管系统正常的动物中，血栓素A2可能是脑小动脉的中度收缩剂，并且这种收缩作用可被高碳酸血症和缺氧所阻止。
