Effects of iodoacetate and anoxia on phosphate metabolism in isolated perfused rat hearts.

When perfused with a solution equilibrated with 95% N2 and 5% CO2, the isolated rat heart was gradually depressed but continued to beat for longer than 30 min. Creatine phosphate content strikingly decreased, but lactate content was markedly elevated. When perfused with a fully oxygenated solution containing 0.5 mM of sodium iodoacetate (IAA) of the myocardial contractile force was almost unaltered and the heart rate decreased slightly within 10 min. Thereafter, the heart rate rapidly decreased, and soon cardiac arrest followed. Myocardial content of high-energy phosphates still remained at a considerably high level. The heart arrested by IAA responded to electrical stimulation, contracted and high-energy phosphates were well utilized. Addition of lactate to an oxygenated perfusate containing IAA improved myocardial performance. Citrate and palmitate did not restore the IAA-treated cardiac impairment. The results show that IAA disturbed cardiac conduction more markedly than contractility by blocking cytoplasmic glycolysis and that lactate, unlike citrate and palmitate, produced enough energy to recover cardiac activities in IAA-treated hearts.