The effect of O2 and CO2 on prostaglandin levels in the cat cerebral cortex.

We measured the effect of arterial hypercapnia, arterial hypocapnia, and arterial hypoxia on the concentrations of PGE2, PGF20, and 6-keto-PGFio in quickly frozen cortical tissue from anesthetized cats. In order to correlate PG levels with the effects of these alterations in blood gases on the cerebral circulation, pial arteriolar diameters were measured with a microscope during normoxic and normocapnic conditions and then after blood gas intervention, immediately before tissue freezing. PGs were analyzed by high pressure liquid chromatography , deuterated standards, and gas chromatography/mass spectrometry. During control conditions with normal arterial blood gases (Pao2 = 87 mm Hg and Paco2 = 30 mm Hg) the levels of PGE2, PGF2a, and 6-keto-PGFia were 193 ± 57, 169 ± 34, and 31 ± 4 ng/g wet weight. Lowering Paco2 to 17 mm Hg had no significant effect on PG levels and decreased arteriolar diameter by 12%. Increasing Paco2 to 56 mm Hg was associated with a significant 60% reduction on PGE2 (P < 0.05), a statistically marginal 38% reduction in PGF&, (P < 0.1), and no change in 6-keto-PGFia, while pial arterioles dilated 32%. Arterial hypoxia (Pao2 = 21 mm Hg) was associated with 45% reduction in E2 which approached statistical significance (P < 0.1), and no change in PGF2,, or 6-keto-PGFi,,, while vessel diameter increased by 32%. The results show that PG levels in brain tissue do not increase during severe arterial hypoxia or during arterial hypocapnia, while during moderate hypercapnia the level of PGE2 decreases. The results do not support previous reports that prostaglandins are mediators of the vascular responses associated with these conditions. (Ore Res 51: 652-656, 1982)