Leffler C W, Mirro R, Armstead W M, Shibata M
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
Am J Physiol. 1992 Sep;263(3 Pt 2):H746-51. doi: 10.1152/ajpheart.1992.263.3.H746.
In the newborn pig, cerebral vasodilator responses to hypercapnia are lost after cerebral ischemia. We examined the effect of topical application of arachidonic acid (30 micrograms/ml, 20 min) to the postischemic piglet brain on subsequent pial arteriolar dilated in response to hypercapnia (10% CO2 ventilation) and topical isoproterenol (10(-6), 10(-7) M). After 20 min cerebral ischemia, pial arterioles did not dilate to hypercapnia but responded to isoproterenol in a fashion similar to before ischemia. Treatment with arachidonic acid after ischemia restored pial arteriolar dilation to hypercapnia. Hypercapnia caused an increase in cortical periarachnoid concentration of 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) before but not after ischemia. After postischemic treatment with arachidonic acid, the increase in cortical periarachnoid fluid 6-keto-PGF1 alpha during hypercapnia was restored. Therefore, topical application of arachidonic acid to cerebral vessels restores cerebral prostanoid synthesis and pial arteriolar dilation in response to hypercapnia that has been abolished by ischemia.
在新生猪中,脑缺血后脑血管对高碳酸血症的舒张反应丧失。我们研究了在缺血后的仔猪脑局部应用花生四烯酸(30微克/毫升,20分钟)对随后软脑膜小动脉对高碳酸血症(10%二氧化碳通气)和局部应用异丙肾上腺素(10⁻⁶、10⁻⁷摩尔)舒张反应的影响。脑缺血20分钟后,软脑膜小动脉对高碳酸血症不发生舒张,但对异丙肾上腺素的反应方式与缺血前相似。缺血后用花生四烯酸治疗可恢复软脑膜小动脉对高碳酸血症的舒张。高碳酸血症在缺血前可使皮质蛛网膜下腔6-酮前列腺素F1α(6-酮-PGF1α)浓度升高,但缺血后则不然。缺血后用花生四烯酸治疗后,高碳酸血症期间皮质蛛网膜下腔液中6-酮-PGF1α的升高得以恢复。因此局部应用花生四烯酸于脑血管可恢复脑前列腺素合成以及缺血后已消失的软脑膜小动脉对高碳酸血症的舒张。