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- W2000806505 abstract "ABSTRACT: The dilator stimuli that contribute to postasphyxial increases in cerebral blood flow in the neonate are unclear. To assess the possible role of cyclooxygenase products in these responses, we measured pial arteriolar diameter in six piglets and determined levels of prostaglan -din (PG) E2 and 6-keto-PG F1α (hydrolysis product of PGI2) in cerebrospinal fluid (CSF) bathing the parietal cortex during control conditions, after 4–10 min of complete respiratory arrest (asphyxia), and after 5–12 min of reventilation. Pial arterioles are important resistance vessels in the cerebral circulation. Baseline pial arteriolar diameter was 220 ± 40 μm (mean ± SEM) and increased to a maximum of 252 ± 49 and 267 ± 56 μm after asphyxia and reventilation, respectively. During control conditions, CSF PGE2 (n = 6) and 6-keto-PGF1α (n = 4) levels were 1947 ± 310 and 794 ± 147 pg/ml, respectively. During asphyxia, CSF levels of PGE2 did not increase, whereas 6-keto-PGF1α increased modestly. During reventilation, CSF PGE2 increased to 3576 ± 499 pg/ml, and 6-keto-PGF1α, increased to 2846 ± 123 pg/ml. In other experiments, we determined that these CSF levels of PGE2 and PGI2 (as 6-keto-PGF1α) were within the vasodilator range for pial arterioles. We conclude that postasphyxial increases in pial arteriolar diameter are associated with a rise in CSF levels of dilator prostanoids." @default.
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- W2000806505 date "1988-08-01" @default.
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- W2000806505 title "Postasphyxial Increases in Prostanoids in Cerebrospinal Fluid of Piglets" @default.
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- W2000806505 doi "https://doi.org/10.1203/00006450-198808000-00018" @default.
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