Wolfe L S, Pappius H M, Marion J
Adv Prostaglandin Thromboxane Res. 1976;1:345-55.
Brain tissue slices in vitro synthesize both PGF2alpha and PGE2 from endogenous precursors at almost linear rates over the first hour. PGF2alpha biosynthesis predominates except for the cat cerebellum. Catecholamines and adrenochrome greatly activate the formation of PGF2alpha in slices and homogenates. The mechanism appears related to endoperoxide reduction rather than increased availability of precursor. The arachidonic acid for prostaglandin biosynthesis in slices is derived from an intracellular pool that forms immediately after animal death and is sufficient to saturate by cyclooxygenase completely and account for the linear kinetics. Biosynthesis of prostaglandins in vivo must be orders of magnitude less than that found in vitro, unless there is local tissue damaged. PGF2 alpha catabolism by cerebral cortex is very small; however, PGE2 is converted to PGF2alpha by brain slices by a 9-keto reductase activity in significant amounts when added in pharmacological amounts.
体外培养的脑组织切片在最初一小时内,能以内源性前体物质几乎呈线性的速率合成前列腺素F2α(PGF2α)和前列腺素E2(PGE2)。除猫的小脑外,PGF2α生物合成占主导地位。儿茶酚胺和肾上腺色素能极大地激活切片和匀浆中PGF2α的形成。其机制似乎与内过氧化物还原有关,而非前体物质可用性的增加。切片中用于前列腺素生物合成的花生四烯酸来自动物死亡后立即形成的细胞内池,该池足以完全被环氧化酶饱和,并解释线性动力学。除非存在局部组织损伤,否则体内前列腺素的生物合成量必定比体外发现的量低几个数量级。大脑皮层对PGF2α的分解代谢非常少;然而,当以药理剂量添加时,脑切片能通过9 - 酮还原酶活性将大量PGE2转化为PGF2α。