Effects of adenine nucleotides on contractility of normal and postischemic myocardium

Abstract Effects of adenine nucleotides on contractile force of normal and postischemic ventricular muscle were studied. Experiments were performed at room temperature on Langendorff perfused feline right ventricular papillary muscle preparation remaining in situ. Peak systolic force developed by normal muscles was not significantly altered by adenine nucleotides in the concentrations used. Complete cessation of coronary perfusion (“ischemia”) for 30 minutes caused severe contractile failure which was not completely reversed on resumption of perfusion with oxygenated Tyrode solution. ATP (0.5 mM) and ADP (2.0 mM) caused significant recovery of force of failing postischemic muscles while 0.5 mM ADP, 0.5 mM AMP, 2.5 mM AMP, 0.5 mM adenosine, and 2.5 mM adenosine did not. These findings show that the contractile failure of ventricular muscle subjected to acute ischemia can be reversed by administration of high-energy phosphates. The recovery, however, is not sustained after nucleotide perfusion is stopped. There is suggestive evidence that ATP does not enter the cell intact but may enter the cell in the form of ADP.