The cyclooxygenase-2 product prostaglandin E 2 modulates cardiac contractile function in adult rat ventricular cardiomyocytes

Abstract

Prostaglandin E 2 (PGE 2), a product of the cyclooxygenase-2 pathway, has been shown to increase cardiac output and modulate cardiac contractile function. However, whether the cardiac contractile response of PGE 2 is due to its action on single ventricular myocytes has not been elucidated. To assess the mechanical effect of PGE 2 at the cellular level, adult rat ventricular myocytes were isolated and stimulated to contract at 0.5 Hz. Mechanical and intracellular Ca 2+ properties were evaluated using an IonOptix Myocam ® analog-to-digital optical detection system. Contractile and intracellular Ca 2+ properties were evaluated as peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR 90), maximal velocity of shortening or relengthening (±d L/d t) and Ca 2+-induced intracellular Ca 2+ fluorescence release (CICR), baseline intracellular Ca 2+ levels and intracellular Ca 2+ decay rate ( τ). PGE 2 (10 −8 to 10 −3 M) elicited an augmentation in PS but had no effect on TPS, TR 90, ±d L/d t, CICR and τ. High concentration of PGE 2 (10 −5 M or higher) reduced the baseline intracellular Ca 2+ levels. These data indicate that the myocardial contractile response of PGE 2 may be due to its direct cardiac contractile action at the single ventricular myocyte level, probably through a mechanism independent of intracellular Ca 2+ release.