The aim of study was to assess acute effects of the divalent manganese ion (Mn2+) in an intact but isolated heart preparation. Rat hearts were perfused in the Langendorff mode at constant flow rate. Left ventricular (LV) developed pressure (LVDP), LV pressure first derivatives (LVdp/dtmax and min), heart rate (HR) and aortic pressure (AoP) were recorded. Ventricular contents of high energy phosphate compounds (HEP) and Mn metal were measured at the end of experiment. Infusion of MnCl2for 5 min with perfusate concentrations 1–3000 μMinduced an immediate depression of contractile function at and above 30 μMand negative chronotropy at and above 300 μM. These EC50values were found (μM): LVDP 250; LVdp/dtmax 160; LVdp/dpmin 120; HR 1000; and increase in AoP 80. Recovery of function during a 14 min washout period was rapid and extensive, except for Mn2+3000 μM. Somewhat unexpected, Mn2+30–1000 μMraised coronary vascular resistance up to about twice the control level, whereas the vasoconstrictory response was overcome at 3000 μM. Mn2+3000 μMreduced tissue HEP. Ventricular Mn content rose stepwise for perfusate Mn2+above 1 μMup to about 55 times the control level for perfusate Mn2+3000 μM. It is concluded that: acute effects of Mn2+like depression of contractility and rate is rapidly reversible; and rat hearts accumulate and buffer large amounts of Mn2+without affecting cardiac function or energy metabolism in th