Prostaglandin Release From Isolated Rabbit Cerebral Cortex Micro-Vessels — Comparison of 6-Keto PGFla and PGE2 Release From Micro-Vessels Incubated in 100% O2, Room Air and 95% N2:5% CO2

Prostaglandin release from microvessels isolated from the rabbit cerebral cortex was determined under three different atmospheric conditions: 100% O2 ("O2") room air, and 95% N2=5% CO2 ("N2-COj"). Initial studies with homogenates prepared from rabbit cerebral microvessels (RCMV) indicated two pathways of enzymatic PGH2 transformation, namely PGI2 synthase and GSH-dependent PGHPGE isomerase. We measured the release of the principal products of these pathways, 6-keto PGF|a and PGE, from freshly prepared RCMV. The release of 6-keto PGF|a exceeded that of PGE^ in all three protocols. RCMV incubated in "N2-CO2" exhibited a reduction in the release of 6-keto PGFla compared to room air or "O2" incubated RCMV, evident at 30-60 min of incubation. No significant differences in the release of PGE2 were observed among the three incubation protocols. In all three incubation protocols the ratio of 6-keto PGF|a to PGE2 did not differ during the initial 10 minutes of each incubation. After 30 to 60 min of incubation, this ratio did not change from the "O2" or room air treated RCMV, but decreased significantly for the "N2-CO2" treated group. To determine the reversibility of the apparent "N2-CO2" induced decline in 6-keto PGF|a release, microvessels were removed from the nitrogen atmosphere and incubated in room air. Release was measured during the initial 10 min following reintroduction to room air and was compared to room air pretreated controls treated in an identical manner. Complete recovery of 6keto PGF|a production was observed, and an enhanced ratio of 6-keto PGFlo to PGE2 observed in the "N2CO2" treated RCMV. In view of the opposing actions of PGI2 (vasodilator) and PGE2 (mild vasoconstrictor) on cerebrovascular tone, this study suggests that release of prostaglandins by the microvasculature may participate in the cerebrovascular response to ischemia. In addition, this study suggests that the release of 6keto PGF|n and PGE2 by cerebral microvessels may be regulated independently. Stroke Vol 15, No 4, 1984