Basal and ethanol-induced cardiac contractile response in lean and obese Zucker rat hearts

Obesity plays a pivotal role in metabolic and cardiovascular diseases. Certain types of obesity may be related to alcohol ingestion, which itself leads to impaired cardiac function. This study analyzed basal and ethanol-induced cardiac contractile response using left-ventricular papillary muscles and myocytes from lean and obese Zucker rats. Contractile properties analyzed include: peak tension development (PTD), peak shortening amplitude (PS), time to PTD/PS (TPT/TPS), time to 90% relaxation/relengthening (RT90/TR90) and maximal velocities of contraction/shortening and relaxation/relengthening (+/-VT and +/-dL/dt). Intracellular Ca2+ transients were measured as fura-2 fluorescence intensity (Delta FFI) changes and fluorescence decay time (FDT), In papillary muscles from obese rats, the baseline TPT and RT90 were significantly prolonged accompanied with low to normal PTD and +/-VT compared to those in lean rats. Muscles from obese hearts also exhibited reduced responsiveness to postrest potentiation, increase in extracellular Ca2+ concentration, and norepinephrine, By contrast, in isolated myocytes, obesity reduced PS associated with a significant prolonged TR90, normal TPS and +/-dL/dt. Intracellular Ca2+ recording revealed decreased resting Ca2+ levels and prolonged FDT, Acute ethanol exposure (80-640 mg/dl) caused comparable concentration-dependent inhibitions of PTD/PS and Delta FFI, associated with reduced +/-VT in both groups. Collectively, these results suggest altered cardiac contractile function and unchanged ethanol-induced depression in obesity. Copyright (C) 2000 National Science Council, ROC and S. Karger AG, Basel.