Abstract
Increases in fatal cardiopulmonary dysfunction in cities with high levels of air pollution may be caused by the exacerbation of underlying heart conditions. The effect of Diesel Exhaust Particulates (DEP) in vitro on cardiomyocyte function was observed to determine if increased susceptibility occurs in heart failure animals. Aortocaval fistula (ACF) surgery was performed on rats to induce volume overload heart failure after 21 weeks. Myocytes were isolated 4 weeks post‐surgery, treated one hour with 1 μg/ml DEP, stimulated at 1 Hz, and analyzed based on sarcomere length and cytosolic calcium levels. No significant changes were observed during the cell contractile phase. DEP exposed ACF myocytes released significantly more calcium from the sarcoplasmic reticulum (SR) during contraction than Sham cells. Thus, Ryanodine receptors in strained ACF cells may be more sensitive to hyper‐phosphorylation. Calcium reuptake by the SR was also significantly faster in myoctyes from Sham versus ACF animals when treated with DEP. This indicates a possible decrease in SERCA2a function or expression. Unexpectedly, alterations in calcium transients did not correspond with changes in overall contractility. Future studies will be performed to investigate a compensatory mechanism involving the affinity of Troponin C for cytosolic calcium during contraction.Funding was provided by the American Physiological Society.
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