Ellis E F, Wei E P, Cockrell C S, Choi S, Kontos H A
Prostaglandins. 1983 Dec;26(6):917-23. doi: 10.1016/0090-6980(83)90154-5.
We compared the effect of topical application of PGF2 alpha on cerebral arterioles in cats and rats equipped with an acutely implanted cranial window. Arterial diameter was measured using a microscope and image splitting device. PGF2 alpha in a concentration ranging from 10(-7) to 10(-5) M had no effect on large (greater than or equal to 100 microns) or small (less than 100 microns) cat pial arterioles, but induced a dose dependent constriction of rat pial arterioles with a maximum constriction to 76% of control diameter. Dilation of cat large cerebral arterioles by topically applied PGE2 was not affected by simultaneous application of PGF2 alpha and PGE2 induced dilation of small arterioles was decreased 3% by PGF2 alpha. While we and others have previously shown that both cat and rat brain can synthesize PGF2 alpha, it appears that PGF2 alpha is not likely to normally be a major modulator of cerebral arteriolar resistance in all species.
我们比较了在急性植入颅骨视窗的猫和大鼠中，局部应用前列腺素F2α（PGF2α）对脑小动脉的影响。使用显微镜和图像分割装置测量动脉直径。浓度范围为10^(-7)至10^(-5)M的PGF2α对大型（大于或等于100微米）或小型（小于100微米）猫软脑膜小动脉没有影响，但可引起大鼠软脑膜小动脉剂量依赖性收缩，最大收缩至对照直径的76%。局部应用前列腺素E2（PGE2）引起的猫大脑大动脉扩张不受同时应用PGF2α的影响，而PGE2引起的小动脉扩张被PGF2α降低了3%。虽然我们和其他人之前已经表明猫和大鼠的大脑都可以合成PGF2α，但PGF2α似乎不太可能在所有物种中正常地成为脑小动脉阻力的主要调节因子。
