Does thromboxane mediate the fetal acth response to acidemia.
Cudd, Timothy A., and Charles E. Wood.
Department of Physiology, University of Florida College of
Medicine
APStracts 2:0273R, 1995.
Intravenous mineral acid infusions into fetal sheep stimulate
increases in plasma ACTH and cortisol concentrations which correlate
to the induced changes in arterial pH. We have recently demonstrated
that ACTH and cortisol responses to mineral acid infusion in adult
sheep are mediated by thromboxane A2 (TxA2). We designed the present
experiments to test the hypothesis that fetal ACTH and cortisol
responses are also mediated by TxA2. We infused chronically
-instrumented fetal sheep with 1N HCl (0.5 mL/min, iv) for 60 min,
with or without pretreatment with the cyclooxygenase inhibitor,
flunixin-N-methylglucamine. HCl infusion significantly decreased pHa
and significantly increased PaO2 and PaCO2. Flunixin pretreatment
significantly decreased fetal plasma thromboxane B2 (TxB2)
concentrations but did not significantly alter the blood gas and pH
response to HCl. TxB2 is a stable metabolite of TxA2 and was measured
as an index of TxA2 generation. HCl increased fetal heart rate only
in the flunixin group. Plasma ACTH and cortisol concentrations were
increased significantly in both groups; flunixin did not
significantly alter the responses. HCl infusion did not signficantly
alter plasma thromboxane B2 (TxB2) concentrations. We conclude that
the fetal ACTH and cortisol responses to HCl infusion are not
mediated by TxA2 or other prostanoids whose synthesis depends upon
cyclooxygenase activity.
Received 13 February 1995; accepted in final form 19 September
1995.
APS Manuscript Number R106-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95