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The Journal of Thoracic and Cardiovascular Surgery, Vol 82, 245-247, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
O Ylikorkala, E Saarela and L Viinikka
To study the effect of the cardiopulmonary bypass (CPB) on the productions
of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2
(TxA2), we collected serial plasma samples from seven patients before,
during, and after CPB and assayed them for 6-keto-PGF 1 alpha and
thromboxane B2, the main metabolites of PGI2 and TxA2, respectively. The
PGI2 production rose significantly (p less than 0.05) following cannulation
of the large vessels and remained elevated during the CPB. After
discontinuation of CPB, the PGI2 decreased progressively. The TxB2
production also rose during CPB, but later than the increase in PGI2. There
was a significant correlation between 6- keto-PGF 1 alpha and TxB2 levels
(r = 0.429, p less than 0.001, n = 77). Thus the deficient PGI2 production,
or an imbalance between PGI2 and TxA2, does not seem to be responsible for
the platelet loss during CPB. By contrast, the human body appears to be
protected from platelet aggregation by a surge in endogenous PGI2 during
CPB.
ARTICLES
Increased prostacyclin and thromboxane production in man during cardiopulmonary bypass
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