REDUCED RESPONSES OF RETINAL-VESSELS OF THE NEWBORN PIG TO PROSTAGLANDINS BUT NOT TO THROMBOXANE

The upper blood pressure limit of retinal blood flow autoregulation is lower in the newborn than in the adult; this suggests an insufficient vasoconstrictor response in the newborn when perfusion pressure is increased. Because prostaglandins (PGs) have an important role in autoregulation of retinal blood flow, we compared the effects of PGE(2), PGF(2 alpha), carbacyclin (PGI(2) analogue), and U46619 (thromboxane analogue), as well as that of agonists for the three different PGE(2) receptor subtypes, 17-phenyl trinor PGE(2) (EP(1)), butaprost (EP(2)), and M&B 28,767 (EP(3)), on the retinal vasculature of newborn and adult pigs, using isolated eyecup preparations. PGF(2 alpha) and PGE(2) caused a markedly greater constriction of retinal arteries and veins of the adult than of the newborn animals. Further analysis of the response to PGE(2), using receptor subtype agonists, revealed that the EP(1) receptor agonist, 17-phenyl trinor PGE(2), and the EP(3) receptor agonist, M&B 28,767, caused a significant constriction of adult arteries and veins but produced minimal effects on newborn vessels; the EP(2) receptor agonist, butaprost, caused a small and comparable dilation of newborn and adult arteries and veins. The PGI(2) analogue, carbacyclin, caused a greater dilation of the adult than of the newborn arteries, but produced comparable dilation of veins from both newborn and adult animals. In contrast to the effects of PGF2 alpha and PGE(2), the thromboxane analogue, U46619, as well as the alpha(1)-adrenoceptor agonist, phenylephrine, significantly constricted newborn arteries and veins, and this effect was comparable with that observed on retinal vessels of the adult. Our findings indicate that the retinal vasculature of the newborn responds minimally to prostaglandins, primarily PGF(2 alpha) and PGE(2), compared with the adult, but constricts effectively to thromboxane. Since prostaglandins play an important role in the autoregulation of retinal blood flow, our observations provide an explanation for the inability of the newborn to limit blood flow when perfusion pressure is raised.