Acute Lead Exposure Weakens Myocardial Contractile Function and the Therapeutic Effect of Alpha Lipoic Acid

This study comprehensively utilized toad hearts and myocardial cell models to explore the effects of acute lead exposure on myocardial contractile function and the therapeutic effect of alpha lipoic acid (ALA). The results showed that lead acetate (PbAc) dose dependently inhibited the contractile function of toad hearts. Acute treatment with 50, 150, and 450 mM PbAc reduced the amplitude of heart contraction to 92.8%, 78.0%, and 69.7% of the control before medication (<I>P</I><0.01), respectively, and reduced heart rate to 92.4%, 92.5%, and 54.9% of the control before medication (<I>P</I><0.05). After treatment with a middle concentration of PbAc (150 mM) for 24 hours, the cell viability of H9c2 decreased to 71.9% of the control group (<I>P</I><0.05). Compared with the lead exposure group, ALA at a concentration of 10 μM significantly improved cardiac contractile function, increasing the amplitude of cardiac contractions and heart rate to 109.4% and 134.2% of the control, respectively (<I>P</I><0.05). Correspondingly, ALA at a concentration of 20 μM increased the cell viability of H9c2 to 112.6% of the control group (<I>P</I><0.05). This study indicates that PbAc can significantly inhibit myocardial contractility and reduce cell viability, while ALA can antagonize lead induced myocardial injury and has significant cardioprotective potential.