Background and Aims: Heart failure is relatively common in our part of the world, and the prevalence is increasing. Further research is necessary to improve the treatment, and prevent progression of heart failure for the patient. Research has shown hypertrophy of cardiomyocytes, change in the transport of sodium and calcium and reduced contractility in a failing heart. Cytokines are thought to be one important factor to initiate and continue the pathophysiologic processes (hypertrophy, contractile failure and phenotypic change) in the cardiomyocytes of a failing heart. Studies show a direct relationship between levels of TNFalpha and the NYHA class the patient is in. Research at UUS have shown that rats with induced post-infarction heart failure react different than “sham”-operated rats, under hypoxy-reoxygenating trials.
Our hypothesis is that cytokines like TNFalpha lead to a change in phenotype of cardiomyocytes, with reduced levels of ATP, reduced uptake of sodium- and calcium when hypoxy-reoxygenating conditions, and reduced uptake of glucose after hypoxy. It is difficult to predict how TNFalpha influence levels of LD.
Methods: We isolated cardiomyocytes from adult rats, and grew the cell cultures with or without TNFalpha. The cultures were studied under hypoxy/reoxygenating or normoxic conditions.
Results: The results confirmed partly our hypothesis regarding uptake of calcium and glucose. However, the results varied, and the differences between the two groups were insignificant. In our trials, TNFalpha lead to reduced levels of LD after hypoxic conditions. This may imply that TNFalpha in certain settings can protect the cell against hypoxy.
Conclusions: Further experiments are necessary to conclude the effects TNFalpha have on cardiomyocytes