Basal and Ethanol-Induced Cardiac Contractile Response in Lean and Obese Zucker Rat Hearts

Abstract

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 (ΔFFI) 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 ΔFFI, associated with reduced ±VT in both groups. Collectively, these results suggest altered cardiac contractile function and unchanged ethanol-induced depression in obesity.