Purinergic Modulation of LPS-induced Cardiac Dysfunction and TNF-alpha Expression

We used a gravity perfusion rat isolated heart model in which hearts were exposed to LPS to promote TNF-alpha mRNA expression and cardiac dysfunction. We inhibited ADA activity using 2'-deoxycoformycin, xanthine oxides (a producer of ROS) with allopurinol and adenosine signaling using 8-p-sulphyphenlytheophylline during LPS-insult. We measured indices of left ventricular function, ADA activity and ADA1 and TNF-alpha mRNA expression to determine the relative contributions of endogenous ADA, XO and adenosine to LPS-induced cardiac dysfunction and TNF-alpha mRNA expression.