Abstract
Asphyxia, with its attendant hypotension, is the most common cause for neonatal cerebral infarction. We have demonstrated uncoupling of cerebral blood flow & metabolism in a hemorrhagic hypotension(HH) model for cerebral infarction in the newborn beagle pup. We report the effects of HH on regional cerebral prostaglandin (PG) levels in newborn beagle pups exposed to a similar insult. Pups were randomized to (HH) or no insult (C). HH was induced by slow venous hemorrhage to maintain MABP 20-30 mm Hg. Fifteen minutes following HH/C, the animals underwent in vivo freezing of brain. PG determinations for 6-keto PGF1α, the stable metabolite of PGI2, TXB2, the stable breakdown product of TXA2, & PGE2 were performed using radioimmunoassays. MABP of HH group was 74 prior to & 26 mm Hg following insult; the MABP of the C group remained 71 mm Hg. The PG levels & ratios of 6-ketoPGF1α/TXB2(ratio) were as follows:
The alterations in the cerebral PGI2/TXA2 balance may in part be responsible for the changes found in cerebral blood flow & metabolism & the neuropathological consequences of perinatal ischemia.
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Ment, L., Duncan, C., Stewart, W. et al. 1691 ASSOCIATION OF CEREBRAL PROSTAGLANDIN IMBALANCE WITH PERINMAL STROKE. Pediatr Res 19, 392 (1985). https://doi.org/10.1203/00006450-198504000-01715
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DOI: https://doi.org/10.1203/00006450-198504000-01715