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Cardiac formation of prostacyclin during cardioplegia in man

1982; Elsevier BV; Volume: 24; Issue: 1 Linguagem: Inglês

10.1016/0090-6980(82)90173-3

1878-416X

A. Edlund, W. Bomfin, L. Kaijser, Christian Olin, Carlo Patrono, E Pinca, A Wennmalm,

Cancer, Hypoxia, and Metabolism

In patients undergoing aortic valve surgery during cardioplegia (a condition characterized by extra-corporal circulation, potassium-induced cardiac arrest and cardiac hypothermia) cardiac release or uptake of 6-keto-PGF1α, and in some cases also of 6,15-diketo-13,14-dihydro-PGF1α were determined, using radioimmunoassay with specific antibodies for determination of the arterial and coronary sinus plasma levels of these PGI2 metabolites. The aim of the study was to find out whether cardiac hypoxia, as evidenced by anaerobic glycolysis in the heart, resulted in stimulation of it PGI2 production. Before cardioplegia the uptake of oxygen (23 ml/min) and the arterio-coronary sinus concentration difference (a-cs) of lactate (0.3 mM) were within the normal range, indicating that the O2 supply to the heart was sufficient for aerobic metabolism. During cardioplegia the oxygen uptake fell, to less than 3 % of the basal value. The uptake of lactate was significantly reversed into a small release inicating that myocardial hypoxia developed. No release of 6-keto-PGF1α took place before cardioplegia, implying that the hearts' PGI2 productino was low or absent when its O2 supply was sufficient. During cardioplegia a significant (a-cs) of 6-keto-PGF1α developed, amounting to −75 pg/ml. Since no evidence of a hypoxia-induced decrease in the metabolic breakdown of PGI2 or 6-keto-PGF1α in the heart could be demonstrated - as shown by a continued, or even augmented liberation of 6,15-diketo-13,14-dihydro-PGF1α during cardioplegia - the cardiac release of 6-keto-PGF1α indicated that the PGI2 production in the heart was stimulated during the cardioplegia/hypoxia. From these data we suggest that human cardiac formation of PGI2 is low or absent when the O2 supply is sufficient. Furthermore, cardiac hypoxia, as evidenced by release of lactate, results in stimulation of cardiac PGI2 formation.