Janero D R, Burghardt C
Department of Pharmacology and Chemotherapy, Roche Research Center, Hoffmann-La Roche Inc., Nutley, New Jersey 07110.
Res Commun Chem Pathol Pharmacol. 1990 Feb;67(2):201-18.
The potential of the injured heart-muscle cell (cardiomyocyte) to produce platelet-activating factor (PAF) has been evaluated. Beating rat myocytes in primary monolayer culture were used as the study-object, and metabolic inhibition served as the injury stimulus. Coincident with the development of irreversible injury, myocytes evidenced a rapid, net production of PAF which was sustained for some 3-6 h and reached, maximally, low-ng levels within approximately 0.5 h of injury. In the presence of serum, much of the PAF was released from the injured myocytes, whereas under serum-free conditions the PAF remained largely intracellular. Cardiomyocyte-derived PAF was pro-aggregatory to platelets and displayed the chromatographic properties and chemical reactivity of authentic PAF. However, PAF itself did not elicit myocyte injury, and a specific PAF antagonist could not attenuate the myocyte damage associated with metabolic inhibition. These results suggest that the cardiomyocyte may constitute a cellular source of PAF during heart injury, although the cell itself is not directly responsive to PAF.
