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 0.5Hz. Mechanical and intracellular Ca 2 + properties were evaluated using an IonOptix Myocam ( R) 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 9 0 ), maximal velocity of shortening or relengthening (+/-dL/dt) 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 9 0 , +/-dL/dt, 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.