The effects of perivascular blood on pial arteriolar vasoreactivity to selected vasodilators and vasoconstrictors were examined in vivo in a newborn pig model. a-Chloraloseanesthetized newborn pigs were fitted with closed cranial windows 4 d after cortical subarachnoid injections of autologous blood. The responsiveness of pial arterioles to topical application of dilator agents [iloprost, prostaglandin E, (PGE,), histamine, and sodium nitroprusside (SNP)] and vasoconstrictor agents [leukotriene C4 and endothelin-1 (ET-1) in artificial cerebrospinal fluid was studied in control and blood-injected piglets. Pial arterioles dilated dose dependently in response to topical application of iloprost, PGE,, histamine, and SNP in the control group, with increases in diameter of 54,44,67, and 50% at lop8 M, lop5 M, lop5 M, and M, respectively. These dilations in response to iloprost, PG&, and histamine in the blood-injected piglets were significantly attenuated to 23, 18, and 34%, respectively, whereas the dilation in response to SNP was not changed (64%). Constrictions in response to lop8 M leukotriene C4 and ET-1 were 16 and 26% and were potentiated by hematoma to 36 and 43%, respectively. The lowest dose of ET-1 (10-l2 M) significantly dilated pial arterioles in the control but not in the blood-treated group. We conclude that prolonged exposure of pial arterioles to perivascular blood attenuates cerebrovascular dilation in response to selected vasoactive agents (iloprost, PGE;, and histamine) but not to SNP, suggesting that blood-induced attenuation of vasodilation and the generalized vasoconstriction may involve inhibiting the prostanoid/cAMP signaling pathway. Potentiation of vasoconstriction induced by ET-1 and leukotriene C, in the hematoma group could be due to loss of this dilator influence. (Pediatr Res 36: [589][590][591][592][593][594] 1994) Abbreviations aCSF, artificial cerebrospinal fluid ET-1, endothelin-1 LTC,, leukotriene C, PGF,, prostaglandin F,, PGE,, prostaglandin E, SNP, sodium nitroprusside Intraventricular and periventricular cerebral hemorrhages occur frequently in preterm babies, whereas subarachnoid hemorrhages occur in both term and preterm infants (1-3). In adults and children, subarachnoid hemorrhage can also result from trauma, asphyxia, brain injury, or rupture of an intracranial aneurysm (4-6). In adults, one of the major complications of cerebral hemorrhage is a delayed cerebral ischemia due to abnormal vasoconstriction of large cerebral arteries that usually presents itself 4-7 d after the hemorrhage. Alterations of cerebral circulation and metabolism can develop secondary to cerebral vasoconstriction, resulting in death or permanent cerebral dysfunction (4-8). Despite much research into the etiology of hemorrhage-induced vasoconstriction (4-8), our understanding of the mechanism by which cerebral arterial vasoconstriction occurs after cerebral hemorrhages is still limited. Much less information is available on the effects of hematoma on cerebral circulation in neonates.Vasodilator pr...