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Synthesis of prostaglandins and thromboxane B2 by cerebral arteries.
Author(s) -
A. Ainsworth Hagen,
Richard P. White,
James T. Robertson
Publication year - 1979
Publication title -
stroke
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.397
H-Index - 319
eISSN - 1524-4628
pISSN - 0039-2499
DOI - 10.1161/01.str.10.3.306
Subject(s) - medicine , thromboxane , thromboxane a2 , cerebral arteries , thromboxane a synthase , cardiology , platelet
The capacity of cerebral arteries to synthesize prostaglandins was studied by 2 procedures. In one, bovine cerebral arteries were incubated with 0.1 μC (l-14C)-arachidonic acid for 3 hours. Using thin layer chromatography, 5 products of this arachidonic acid were isolated: prostaglandin E2 (PGE2), prostaglandin F2α; (PGF2α), 6-keto prostaglandin F1α (6-keto PGFlα), prostaglandin D2 (PGD2), and thromboxane B2 (TxB2). In the second group of experiments the biosynthesis of these lipids from endogenous substrate was confirmed, except for PGD2, by means of gas liquid chromatography-mass spectroscopy. In addition, the production of PGE2 and PGF2α was quantified. An average of 196 ng PGE2 and 172 ng PGF2α were synthesized per gram tissue in one hour. Meclofenamate inhibited the formation of these 2 prostaglandins while serotonin stimulated synthesis approximately 20-25%. The present finding demonstrates that cerebral arteries form several prostaglandins and, likely, thromboxane B2. It is hypothesized that these lipids may play a role in the vasomotion of cerebral blood vessels in health and disease. The relative rates of synthesis of these lipids may be important for maintaining normal cerebral circulation. However, in cerebrovascular disease the normal balance between the rate of synthesis of those prostaglandins which constrict and those which dilate may be disturbed.

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