Uyama O, Nagatsuka K, Fukunaga R, Kusunoki M, Takano T, Yoneda S, Kimura K, Abe H
Brain Res. 1983 Jan 24;259(2):344-7. doi: 10.1016/0006-8993(83)91272-6.
The prostacyclin (PGI2) formation in cerebral vessels, as reflected by the difference in concentration of internal carotid arterial and internal jugular venous radioimmunoassayed 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), was determined under normocapnic and hypercapnic conditions in 5 patients with mild cerebral thrombotic infarction. There was no evidence that endogenous PGI formation in cerebral vessels was stimulated at mild hypercapnia, while an increase of cerebral blood flow (CBF) induced by hypercapnia was observed. These results suggest that endogenous PGI2 may not be a mediator for the response of CBF to CO2.
通过放射免疫法测定5例轻度脑血栓形成性梗死患者在正常碳酸血症和高碳酸血症条件下，颈内动脉和颈内静脉中6-酮-前列腺素F1α（6-keto-PGF1α）浓度差异所反映的脑血管中前列环素（PGI2）的生成情况。没有证据表明在轻度高碳酸血症时脑血管内源性PGI生成受到刺激，而观察到高碳酸血症可诱导脑血流量（CBF）增加。这些结果提示内源性PGI2可能不是CBF对CO2反应的介质。
