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The isolated perfused rat heart was used to study if arachidonic acid (AA) release affected prostaglandin (PG) production. The perfused heart avidly absorbed and esterified exogenous AA, mostly into polar lipids. The administration of bradykinin (BK) after prelabeling with 1-C14-AA caused a two-fold increase in the amount of AA released. Bovine serum albumin (BSA) stimulated release 2.5-fold. Perfusion with AA saturated BSA enhanced the release of 1-14C-AA 23-fold indicating the presence of an active deacylation/reacylation system in rat heart.
BK caused a four-fold increase whereas BSA had no effect on the amount of prostaglandins released from perfused heart indicating that BK acted on a specific AA pool available to cyclooxygenase whereas the BSA stimulated a separate pool of AA which apparently was not available to the cyclooxygenase.
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