Cerebral arteriolar dilation to hypoxia: role of prostanoids .
Leffler, Charles W., and Helena Parfenova.
Laboratory for Research in Neonatal Physiology, Departments of
Physiology/Biophysics and of Pediatrics, University of Tennessee,
Memphis, Memphis, TN 38163
APStracts 3:0380H, 1996.
Experiments addressed the hypothesis that dilator prostanoids
contribute to maintenance of low cerebral microvascular tone during
hypoxia in the newborn. Anesthetized newborn pigs equipped with
closed cranial windows were used to measure responses of pial
arterioles (approximately 60 m) to treatments. Hypoxia (PaO2 ( 25
mmHg) caused dilation of pial arterioles (about 50% increase in
diameter). Hypoxia (5 min) caused an increase in cortical CSF 6-keto
-PGF1( concentration from 907 171 (normoxia) to 1408 213 pg/ml
(hypoxia). Pretreatment with indomethacin (5 mg/kg) did not affect
pial arteriolar dilation to hypoxia. Conversely, indomethacin
treatment during hypoxia caused a rapid decrease in arteriolar
diameter to nearly the normoxia diameter within 3 min, returning to
the original hypoxia diameter by 10 min. Ibuprofen treatment (30
mg/kg) had no effect on pial arteriolar diameter during normoxia or
hypoxia and pretreatment did not alter dilation to hypoxia. However,
pretreatment with ibuprofen abolished the constrictor effect of
indomethacin given during hypoxia. These data suggest that the
primary mechanism by which hypoxia produces cerebral vasodilation
does not involve prostanoids but prostanoids can contribute to
cerebral vasodilation in response to hypoxia.
Received 19 April 1996; accepted in final form 31 July 1996.
APS Manuscript Number H349-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996